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  • Male  (307)
  • 2015-2019
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  • 2010  (307)
  • 1
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    Sex bias blights drug studies (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Check Hayden, Erika -- England -- Nature. 2010 Mar 18;464(7287):332-3. doi: 10.1038/464332b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bias (Epidemiology) ; Biomedical Research/*methods ; Clinical Trials as Topic/methods ; Drug Evaluation/*methods ; Female ; Humans ; Male ; Patient Selection ; Prejudice ; *Sex Characteristics ; Sex Distribution
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    The primate connection (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trivedi, Bijal -- England -- Nature. 2010 Jul 15;466(7304):S5. doi: 10.1038/nature09236.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631704" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/immunology ; Animals ; Chronic Disease ; Disease Models, Animal ; Disease Progression ; Female ; Genome, Viral/genetics ; HIV Infections/*immunology/physiopathology/virology ; HIV-1/genetics/growth & development/immunology ; Host-Pathogen Interactions/immunology ; Immunity, Innate/immunology ; Inflammation/immunology/pathology ; Interleukin-17/immunology ; Macaca/immunology/virology ; Male ; Physiology, Comparative/methods ; Primates/*immunology/metabolism/*virology ; Receptors, HIV/metabolism ; Simian Acquired Immunodeficiency Syndrome/*immunology/metabolism/virology ; Simian Immunodeficiency Virus/classification/genetics/pathogenicity/*physiology ; T-Lymphocytes, Helper-Inducer/immunology/pathology ; Viral Load
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Males still dominate animal studies (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zucker, Irving -- Beery, Annaliese K -- England -- Nature. 2010 Jun 10;465(7299):690. doi: 10.1038/465690a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departmentsof Psychology, Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720, USA. irvzuck@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bias (Epidemiology) ; Biomedical Research/ethics/*methods/trends ; *Disease Models, Animal ; Female ; Humans ; Male ; Prevalence ; *Sex Characteristics ; Sex Distribution ; Sex Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Foot strike patterns and collision forces in habitually barefoot versus shod runners (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-30
    Description: Humans have engaged in endurance running for millions of years, but the modern running shoe was not invented until the 1970s. For most of human evolutionary history, runners were either barefoot or wore minimal footwear such as sandals or moccasins with smaller heels and little cushioning relative to modern running shoes. We wondered how runners coped with the impact caused by the foot colliding with the ground before the invention of the modern shoe. Here we show that habitually barefoot endurance runners often land on the fore-foot (fore-foot strike) before bringing down the heel, but they sometimes land with a flat foot (mid-foot strike) or, less often, on the heel (rear-foot strike). In contrast, habitually shod runners mostly rear-foot strike, facilitated by the elevated and cushioned heel of the modern running shoe. Kinematic and kinetic analyses show that even on hard surfaces, barefoot runners who fore-foot strike generate smaller collision forces than shod rear-foot strikers. This difference results primarily from a more plantarflexed foot at landing and more ankle compliance during impact, decreasing the effective mass of the body that collides with the ground. Fore-foot- and mid-foot-strike gaits were probably more common when humans ran barefoot or in minimal shoes, and may protect the feet and lower limbs from some of the impact-related injuries now experienced by a high percentage of runners.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lieberman, Daniel E -- Venkadesan, Madhusudhan -- Werbel, William A -- Daoud, Adam I -- D'Andrea, Susan -- Davis, Irene S -- Mang'eni, Robert Ojiambo -- Pitsiladis, Yannis -- England -- Nature. 2010 Jan 28;463(7280):531-5. doi: 10.1038/nature08723.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Evolutionary Biology, 11 Divinity Avenue, Harvard University, Cambridge, Massachusetts 02138, USA. danlieb@fas.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20111000" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Biomechanical Phenomena ; Child ; Female ; Foot/*physiology ; Forefoot, Human/physiology ; Gait/physiology ; Humans ; Kenya ; Male ; Running/*physiology ; *Shoes/standards ; *Stress, Mechanical ; United States ; Weight-Bearing/physiology ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Amygdalar and hippocampal substrates of anxious temperament differ in their heritability (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-13
    Description: Anxious temperament (AT) in human and non-human primates is a trait-like phenotype evident early in life that is characterized by increased behavioural and physiological reactivity to mildly threatening stimuli. Studies in children demonstrate that AT is an important risk factor for the later development of anxiety disorders, depression and comorbid substance abuse. Despite its importance as an early predictor of psychopathology, little is known about the factors that predispose vulnerable children to develop AT and the brain systems that underlie its expression. To characterize the neural circuitry associated with AT and the extent to which the function of this circuit is heritable, we studied a large sample of rhesus monkeys phenotyped for AT. Using 238 young monkeys from a multigenerational single-family pedigree, we simultaneously assessed brain metabolic activity and AT while monkeys were exposed to the relevant ethological condition that elicits the phenotype. High-resolution (18)F-labelled deoxyglucose positron-emission tomography (FDG-PET) was selected as the imaging modality because it provides semi-quantitative indices of absolute glucose metabolic rate, allows for simultaneous measurement of behaviour and brain activity, and has a time course suited for assessing temperament-associated sustained brain responses. Here we demonstrate that the central nucleus region of the amygdala and the anterior hippocampus are key components of the neural circuit predictive of AT. We also show significant heritability of the AT phenotype by using quantitative genetic analysis. Additionally, using voxelwise analyses, we reveal significant heritability of metabolic activity in AT-associated hippocampal regions. However, activity in the amygdala region predictive of AT is not significantly heritable. Furthermore, the heritabilities of the hippocampal and amygdala regions significantly differ from each other. Even though these structures are closely linked, the results suggest differential influences of genes and environment on how these brain regions mediate AT and the ongoing risk of developing anxiety and depression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998538/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998538/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oler, Jonathan A -- Fox, Andrew S -- Shelton, Steven E -- Rogers, Jeffrey -- Dyer, Thomas D -- Davidson, Richard J -- Shelledy, Wendy -- Oakes, Terrence R -- Blangero, John -- Kalin, Ned H -- MH018931/MH/NIMH NIH HHS/ -- MH046729/MH/NIMH NIH HHS/ -- MH059490/MH/NIMH NIH HHS/ -- MH081884/MH/NIMH NIH HHS/ -- MH084051/MH/NIMH NIH HHS/ -- P50 MH084051/MH/NIMH NIH HHS/ -- P50 MH084051-030001/MH/NIMH NIH HHS/ -- R01 MH046729/MH/NIMH NIH HHS/ -- R01 MH046729-17/MH/NIMH NIH HHS/ -- R01 MH081884/MH/NIMH NIH HHS/ -- R01 MH081884-04/MH/NIMH NIH HHS/ -- R37 MH059490/MH/NIMH NIH HHS/ -- R37 MH059490-13/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Aug 12;466(7308):864-8. doi: 10.1038/nature09282.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Wisconsin-Madison, Madison, Wisconsin 53719, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703306" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*metabolism ; Animals ; Anxiety/*genetics/*physiopathology ; Depression/genetics ; Female ; Freezing Reaction, Cataleptic ; Genetic Predisposition to Disease/*genetics ; Glucose/metabolism ; *Heredity ; Hippocampus/*metabolism ; Macaca mulatta/genetics/physiology ; Male ; Models, Animal ; Neural Pathways/physiology ; Pedigree ; Phenotype ; Positron-Emission Tomography ; Stress, Psychological ; Temperament/*physiology ; Temporal Lobe/metabolism ; Vocalization, Animal
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Forgotten lessons (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Basu, Paroma -- England -- Nature. 2010 Jul 15;466(7304):S14-5. doi: 10.1038/nature09241.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631697" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/drug therapy/epidemiology/prevention & ; control/psychology/transmission ; Adult ; Child ; Chronic Disease/drug therapy/epidemiology/prevention & control/psychology ; Community-Institutional Relations ; Developed Countries/*statistics & numerical data ; Female ; HIV Infections/drug therapy/*epidemiology/prevention & ; control/*psychology/transmission ; Health Education ; Humans ; Incidence ; Male ; Patient Compliance/psychology/statistics & numerical data ; Risk-Taking ; Safe Sex/*psychology/*statistics & numerical data ; Viral Load/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Competition drives cooperation among closely related sperm of deer mice (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-22
    Description: Among the extraordinary adaptations driven by sperm competition is the cooperative behaviour of spermatozoa. By forming cooperative groups, sperm can increase their swimming velocity and thereby gain an advantage in intermale sperm competition. Accordingly, selection should favour cooperation of the most closely related sperm to maximize fitness. Here we show that sperm of deer mice (genus Peromyscus) form motile aggregations, then we use this system to test predictions of sperm cooperation. We find that sperm aggregate more often with conspecific than heterospecific sperm, suggesting that individual sperm can discriminate on the basis of genetic relatedness. Next, we provide evidence that the cooperative behaviour of closely related sperm is driven by sperm competition. In a monogamous species lacking sperm competition, Peromyscus polionotus, sperm indiscriminately group with unrelated conspecific sperm. In contrast, in the highly promiscuous deer mouse, Peromyscus maniculatus, sperm are significantly more likely to aggregate with those obtained from the same male than with sperm from an unrelated conspecific donor. Even when we test sperm from sibling males, we continue to see preferential aggregations of related sperm in P. maniculatus. These results suggest that sperm from promiscuous deer mice discriminate among relatives and thereby cooperate with the most closely related sperm, an adaptation likely to have been driven by sperm competition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824558/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824558/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, Heidi S -- Hoekstra, Hopi E -- F32 GM084719/GM/NIGMS NIH HHS/ -- F32 GM084719-02/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Feb 11;463(7282):801-3. doi: 10.1038/nature08736. Epub 2010 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismic and Evolutionary Biology, Museum of Comparative Zoology, Cambridge, Massachusetts 02138, USA. hfisher@oeb.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20090679" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aggregation ; Competitive Behavior/*physiology ; *Cooperative Behavior ; Copulation/physiology ; Female ; Male ; Peromyscus/*classification/*physiology ; Sexual Behavior, Animal/*physiology ; Species Specificity ; Sperm Motility/physiology ; Spermatozoa/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Neuroscience: Sexy circuits (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benton, Richard -- England -- Nature. 2010 Dec 2;468(7324):638-40. doi: 10.1038/468638a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124442" target="_blank"〉PubMed〈/a〉
    Keywords: Acetates/pharmacology ; Animals ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/anatomy & histology/*cytology/*drug effects/physiology ; Female ; Gene Expression Regulation ; Male ; Nerve Tissue Proteins/genetics/metabolism ; Neuroanatomical Tract-Tracing Techniques/methods ; Oleic Acids/pharmacology ; Olfactory Pathways/anatomy & histology/cytology/*drug effects ; Olfactory Perception/drug effects/physiology ; Pheromones/*pharmacology ; Sensory Receptor Cells/drug effects/physiology ; *Sex Characteristics ; Sexual Behavior, Animal/physiology ; Transcription Factors/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Lkb1 regulates quiescence and metabolic homeostasis of haematopoietic stem cells (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-03
    Description: The capacity to fine-tune cellular bioenergetics with the demands of stem-cell maintenance and regeneration is central to normal development and ageing, and to organismal survival during periods of acute stress. How energy metabolism and stem-cell homeostatic processes are coordinated is not well understood. Lkb1 acts as an evolutionarily conserved regulator of cellular energy metabolism in eukaryotic cells and functions as the major upstream kinase to phosphorylate AMP-activated protein kinase (AMPK) and 12 other AMPK-related kinases. Whether Lkb1 regulates stem-cell maintenance remains unknown. Here we show that Lkb1 has an essential role in haematopoietic stem cell (HSC) homeostasis. We demonstrate that ablation of Lkb1 in adult mice results in severe pancytopenia and subsequent lethality. Loss of Lkb1 leads to impaired survival and escape from quiescence of HSCs, resulting in exhaustion of the HSC pool and a marked reduction of HSC repopulating potential in vivo. Lkb1 deletion has an impact on cell proliferation in HSCs, but not on more committed compartments, pointing to context-specific functions for Lkb1 in haematopoiesis. The adverse impact of Lkb1 deletion on haematopoiesis was predominantly cell-autonomous and mTOR complex 1 (mTORC1)-independent, and involves multiple mechanisms converging on mitochondrial apoptosis and possibly downregulation of PGC-1 coactivators and their transcriptional network, which have critical roles in mitochondrial biogenesis and function. Thus, Lkb1 serves as an essential regulator of HSCs and haematopoiesis, and more generally, points to the critical importance of coupling energy metabolism and stem-cell homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058342/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058342/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gan, Boyi -- Hu, Jian -- Jiang, Shan -- Liu, Yingchun -- Sahin, Ergun -- Zhuang, Li -- Fletcher-Sananikone, Eliot -- Colla, Simona -- Wang, Y Alan -- Chin, Lynda -- Depinho, Ronald A -- 01CA141508/CA/NCI NIH HHS/ -- R21 CA135057/CA/NCI NIH HHS/ -- R21 CA135057-01/CA/NCI NIH HHS/ -- R21CA135057/CA/NCI NIH HHS/ -- U01 CA141508/CA/NCI NIH HHS/ -- U01 CA141508-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):701-4. doi: 10.1038/nature09595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Cycle/*physiology ; Cell Proliferation ; Cell Survival ; *Energy Metabolism ; Female ; Gene Deletion ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism/pathology ; *Homeostasis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Pancytopenia/genetics ; Phenotype ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/metabolism ; Survival Analysis ; TOR Serine-Threonine Kinases ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Secrets of the shaking palsy (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schnabel, Jim -- England -- Nature. 2010 Aug 26;466(7310):S2-5. doi: 10.1038/466S2b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20739933" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/metabolism ; Female ; Humans ; Male ; Mitochondria/pathology ; Neurons/*pathology ; Parkinson Disease/diagnosis/genetics/*pathology ; alpha-Synuclein/genetics/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Chemical genetics strategy identifies an HCV NS5A inhibitor with a potent clinical effect (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-23
    Description: The worldwide prevalence of chronic hepatitis C virus (HCV) infection is estimated to be approaching 200 million people. Current therapy relies upon a combination of pegylated interferon-alpha and ribavirin, a poorly tolerated regimen typically associated with less than 50% sustained virological response rate in those infected with genotype 1 virus. The development of direct-acting antiviral agents to treat HCV has focused predominantly on inhibitors of the viral enzymes NS3 protease and the RNA-dependent RNA polymerase NS5B. Here we describe the profile of BMS-790052, a small molecule inhibitor of the HCV NS5A protein that exhibits picomolar half-maximum effective concentrations (EC(50)) towards replicons expressing a broad range of HCV genotypes and the JFH-1 genotype 2a infectious virus in cell culture. In a phase I clinical trial in patients chronically infected with HCV, administration of a single 100-mg dose of BMS-790052 was associated with a 3.3 log(10) reduction in mean viral load measured 24 h post-dose that was sustained for an additional 120 h in two patients infected with genotype 1b virus. Genotypic analysis of samples taken at baseline, 24 and 144 h post-dose revealed that the major HCV variants observed had substitutions at amino-acid positions identified using the in vitro replicon system. These results provide the first clinical validation of an inhibitor of HCV NS5A, a protein with no known enzymatic function, as an approach to the suppression of virus replication that offers potential as part of a therapeutic regimen based on combinations of HCV inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, Min -- Nettles, Richard E -- Belema, Makonen -- Snyder, Lawrence B -- Nguyen, Van N -- Fridell, Robert A -- Serrano-Wu, Michael H -- Langley, David R -- Sun, Jin-Hua -- O'Boyle, Donald R 2nd -- Lemm, Julie A -- Wang, Chunfu -- Knipe, Jay O -- Chien, Caly -- Colonno, Richard J -- Grasela, Dennis M -- Meanwell, Nicholas A -- Hamann, Lawrence G -- England -- Nature. 2010 May 6;465(7294):96-100. doi: 10.1038/nature08960. Epub 2010 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology, Bristol-Myers Squibb Research and Development, 5 Research Parkway, Wallingford, Connecticut 06492, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20410884" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antiviral Agents/blood/chemistry/*pharmacology/therapeutic use ; Cell Line ; Cercopithecus aethiops ; Drug Resistance, Viral ; Female ; Genotype ; HeLa Cells ; Hepacivirus/*drug effects ; Hepatitis C/drug therapy/virology ; Humans ; Imidazoles/blood/chemistry/*pharmacology ; Inhibitory Concentration 50 ; Male ; Middle Aged ; Time Factors ; Vero Cells ; Viral Load/drug effects ; Viral Nonstructural Proteins/*antagonists & inhibitors ; Young Adult
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Evolutionary biology: Oh sibling, who art thou? (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cockburn, Andrew -- England -- Nature. 2010 Aug 19;466(7309):930-1. doi: 10.1038/466930a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20725030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/classification/genetics/*physiology ; *Cooperative Behavior ; Fathers ; Female ; Male ; Models, Biological ; Mothers ; Phylogeny ; Reproduction/genetics/physiology ; Sexual Behavior, Animal/*physiology ; *Siblings
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    Higher rates of sex evolve in spatially heterogeneous environments (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-15
    Description: The evolution and maintenance of sexual reproduction has puzzled biologists for decades. Although this field is rich in hypotheses, experimental evidence is scarce. Some important experiments have demonstrated differences in evolutionary rates between sexual and asexual populations; other experiments have documented evolutionary changes in phenomena related to genetic mixing, such as recombination and selfing. However, direct experiments of the evolution of sex within populations are extremely rare (but see ref. 12). Here we use the rotifer, Brachionus calyciflorus, which is capable of both sexual and asexual reproduction, to test recent theory predicting that there is more opportunity for sex to evolve in spatially heterogeneous environments. Replicated experimental populations of rotifers were maintained in homogeneous environments, composed of either high- or low-quality food habitats, or in heterogeneous environments that consisted of a mix of the two habitats. For populations maintained in either type of homogeneous environment, the rate of sex evolves rapidly towards zero. In contrast, higher rates of sex evolve in populations experiencing spatially heterogeneous environments. The data indicate that the higher level of sex observed under heterogeneity is not due to sex being less costly or selection against sex being less efficient; rather sex is sufficiently advantageous in heterogeneous environments to overwhelm its inherent costs. Counter to some alternative theories for the evolution of sex, there is no evidence that genetic drift plays any part in the evolution of sex in these populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Becks, Lutz -- Agrawal, Aneil F -- England -- Nature. 2010 Nov 4;468(7320):89-92. doi: 10.1038/nature09449. Epub 2010 Oct 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology & Evolutionary Biology, University of Toronto, Toronto, Ontario M5S 3B2, Canada. lutz.becks@utoronto.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20944628" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Migration/physiology ; Animals ; *Biological Evolution ; Diet/veterinary ; *Ecosystem ; Female ; *Food ; Genetic Drift ; Male ; Meiosis/genetics ; Models, Biological ; Ovum/physiology ; Population Density ; Reproduction/physiology ; Reproduction, Asexual/physiology ; Rotifera/cytology/genetics/*physiology ; Selection, Genetic ; *Sex
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    Epigenetic silencing of engineered L1 retrotransposition events in human embryonic carcinoma cells (2010)
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    Publication Date: 2010-08-06
    Description: Long interspersed element-1 (LINE-1 or L1) retrotransposition continues to affect human genome evolution. L1s can retrotranspose in the germline, during early development and in select somatic cells; however, the host response to L1 retrotransposition remains largely unexplored. Here we show that reporter genes introduced into the genome of various human embryonic carcinoma-derived cell lines (ECs) by L1 retrotransposition are rapidly and efficiently silenced either during or immediately after their integration. Treating ECs with histone deacetylase inhibitors rapidly reverses this silencing, and chromatin immunoprecipitation experiments revealed that reactivation of the reporter gene was correlated with changes in chromatin status at the L1 integration site. Under our assay conditions, rapid silencing was also observed when reporter genes were delivered into ECs by mouse L1s and a zebrafish LINE-2 element, but not when similar reporter genes were delivered into ECs by Moloney murine leukaemia virus or human immunodeficiency virus, suggesting that these integration events are silenced by distinct mechanisms. Finally, we demonstrate that subjecting ECs to culture conditions that promote differentiation attenuates the silencing of reporter genes delivered by L1 retrotransposition, but that differentiation, in itself, is not sufficient to reactivate previously silenced reporter genes. Thus, our data indicate that ECs differ from many differentiated cells in their ability to silence reporter genes delivered by L1 retrotransposition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3034402/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3034402/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia-Perez, Jose L -- Morell, Maria -- Scheys, Joshua O -- Kulpa, Deanna A -- Morell, Santiago -- Carter, Christoph C -- Hammer, Gary D -- Collins, Kathleen L -- O'Shea, K Sue -- Menendez, Pablo -- Moran, John V -- 5 P30 CA46592/CA/NCI NIH HHS/ -- GM-069985/GM/NIGMS NIH HHS/ -- GM060518/GM/NIGMS NIH HHS/ -- GM082970/GM/NIGMS NIH HHS/ -- NS-048187/NS/NINDS NIH HHS/ -- R01 DK62027/DK/NIDDK NIH HHS/ -- R01 GM060518/GM/NIGMS NIH HHS/ -- R01 GM060518-12/GM/NIGMS NIH HHS/ -- R01 GM082970/GM/NIGMS NIH HHS/ -- R01 GM082970-04/GM/NIGMS NIH HHS/ -- R01AI051198/AI/NIAID NIH HHS/ -- T32-GM08322/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Aug 5;466(7307):769-73. doi: 10.1038/nature09209.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, 1241 East Catherine Street, University of Michigan Medical School, Ann Arbor, Michigan 48109-5618, USA. josel.garcia.perez@juntadeandalucia.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20686575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/genetics/physiology ; Cell Line, Tumor ; Chromatin/drug effects/genetics/metabolism ; Chromatin Immunoprecipitation ; Embryonal Carcinoma Stem Cells/*metabolism/pathology ; Epigenesis, Genetic/drug effects/*genetics ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; *Gene Silencing/drug effects ; Genes, Reporter/genetics ; Genetic Engineering ; Genetic Vectors/genetics ; Genome, Human/genetics ; HIV/genetics ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Long Interspersed Nucleotide Elements/genetics ; Male ; Mice ; Models, Genetic ; Moloney murine leukemia virus/genetics ; Retroelements/*genetics ; Zebrafish/genetics
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    A population-specific HTR2B stop codon predisposes to severe impulsivity (2010)
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    Publication Date: 2010-12-24
    Description: Impulsivity, describing action without foresight, is an important feature of several psychiatric diseases, suicidality and violent behaviour. The complex origins of impulsivity hinder identification of the genes influencing it and the diseases with which it is associated. Here we perform exon-focused sequencing of impulsive individuals in a founder population, targeting fourteen genes belonging to the serotonin and dopamine domain. A stop codon in HTR2B was identified that is common (minor allele frequency 〉 1%) but exclusive to Finnish people. Expression of the gene in the human brain was assessed, as well as the molecular functionality of the stop codon, which was associated with psychiatric diseases marked by impulsivity in both population and family-based analyses. Knockout of Htr2b increased impulsive behaviours in mice, indicative of predictive validity. Our study shows the potential for identifying and tracing effects of rare alleles in complex behavioural phenotypes using founder populations, and indicates a role for HTR2B in impulsivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevilacqua, Laura -- Doly, Stephane -- Kaprio, Jaakko -- Yuan, Qiaoping -- Tikkanen, Roope -- Paunio, Tiina -- Zhou, Zhifeng -- Wedenoja, Juho -- Maroteaux, Luc -- Diaz, Silvina -- Belmer, Arnaud -- Hodgkinson, Colin A -- Dell'osso, Liliana -- Suvisaari, Jaana -- Coccaro, Emil -- Rose, Richard J -- Peltonen, Leena -- Virkkunen, Matti -- Goldman, David -- AA-09203/AA/NIAAA NIH HHS/ -- AA-12502/AA/NIAAA NIH HHS/ -- Z01 AA000301-09/Intramural NIH HHS/ -- Z01 AA000301-10/Intramural NIH HHS/ -- Z99 AA999999/Intramural NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1061-6. doi: 10.1038/nature09629.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Rockville, Maryland 20852, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Case-Control Studies ; Cell Line ; Female ; Finland ; Founder Effect ; Gene Expression Regulation ; Gene Knockout Techniques ; Genotype ; Humans ; Impulsive Behavior/*genetics ; Male ; Mental Disorders/genetics ; Mice ; Mice, 129 Strain ; Mice, Knockout ; Pedigree ; Polymorphism, Single Nucleotide/genetics ; Receptor, Serotonin, 5-HT2B/*genetics/*metabolism ; Testosterone/blood/cerebrospinal fluid
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    Bone progenitor dysfunction induces myelodysplasia and secondary leukaemia (2010)
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    Publication Date: 2010-03-23
    Description: Mesenchymal cells contribute to the 'stroma' of most normal and malignant tissues, with specific mesenchymal cells participating in the regulatory niches of stem cells. By examining how mesenchymal osteolineage cells modulate haematopoiesis, here we show that deletion of Dicer1 specifically in mouse osteoprogenitors, but not in mature osteoblasts, disrupts the integrity of haematopoiesis. Myelodysplasia resulted and acute myelogenous leukaemia emerged that had acquired several genetic abnormalities while having intact Dicer1. Examining gene expression altered in osteoprogenitors as a result of Dicer1 deletion showed reduced expression of Sbds, the gene mutated in Schwachman-Bodian-Diamond syndrome-a human bone marrow failure and leukaemia pre-disposition condition. Deletion of Sbds in mouse osteoprogenitors induced bone marrow dysfunction with myelodysplasia. Therefore, perturbation of specific mesenchymal subsets of stromal cells can disorder differentiation, proliferation and apoptosis of heterologous cells, and disrupt tissue homeostasis. Furthermore, primary stromal dysfunction can result in secondary neoplastic disease, supporting the concept of niche-induced oncogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422863/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422863/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raaijmakers, Marc H G P -- Mukherjee, Siddhartha -- Guo, Shangqin -- Zhang, Siyi -- Kobayashi, Tatsuya -- Schoonmaker, Jesse A -- Ebert, Benjamin L -- Al-Shahrour, Fatima -- Hasserjian, Robert P -- Scadden, Edward O -- Aung, Zinmar -- Matza, Marc -- Merkenschlager, Matthias -- Lin, Charles -- Rommens, Johanna M -- Scadden, David T -- MC_U120027516/Medical Research Council/United Kingdom -- R01 DK050234/DK/NIDDK NIH HHS/ -- R01 HL044851/HL/NHLBI NIH HHS/ -- R01 HL097794/HL/NHLBI NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- U54 HL081030/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Apr 8;464(7290):852-7. doi: 10.1038/nature08851. Epub 2010 Mar 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Regenerative Medicine, Massachusetts General Hospital and Harvard Medical School CPZN, USA. hraaijmakers@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20305640" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/metabolism/pathology ; Bone and Bones/metabolism/*pathology ; Cell Differentiation ; Cell Lineage ; Female ; Gene Deletion ; Hematopoiesis/genetics ; Leukemia, Myeloid, Acute/genetics/metabolism/*pathology ; Male ; Mesoderm/cytology ; Mice ; Myelodysplastic Syndromes/genetics/metabolism/*pathology ; Osteoblasts/metabolism/pathology ; Phenotype ; Proteins/genetics/metabolism ; Ribonuclease III/deficiency/genetics/metabolism ; Sarcoma, Myeloid/genetics/metabolism/pathology ; Stem Cell Niche/metabolism/pathology ; Stem Cells/metabolism/*pathology ; Stromal Cells/metabolism/pathology
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    The evolution of eusociality (2010)
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    Publication Date: 2010-08-27
    Description: Eusociality, in which some individuals reduce their own lifetime reproductive potential to raise the offspring of others, underlies the most advanced forms of social organization and the ecologically dominant role of social insects and humans. For the past four decades kin selection theory, based on the concept of inclusive fitness, has been the major theoretical attempt to explain the evolution of eusociality. Here we show the limitations of this approach. We argue that standard natural selection theory in the context of precise models of population structure represents a simpler and superior approach, allows the evaluation of multiple competing hypotheses, and provides an exact framework for interpreting empirical observations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279739/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279739/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, Martin A -- Tarnita, Corina E -- Wilson, Edward O -- R01 GM078986/GM/NIGMS NIH HHS/ -- R01 GM078986-04/GM/NIGMS NIH HHS/ -- R01GM078986/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Aug 26;466(7310):1057-62. doi: 10.1038/nature09205.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program for Evolutionary Dynamics, Department of Mathematics, Harvard University, Cambridge, Massachusetts 02138, USA. martin_nowak@harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20740005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*physiology ; *Biological Evolution ; Female ; Humans ; Insects/physiology ; Male ; Models, Biological ; Selection, Genetic ; *Social Behavior
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    Support for a synaptic chain model of neuronal sequence generation (2010)
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    Publication Date: 2010-10-26
    Description: In songbirds, the remarkable temporal precision of song is generated by a sparse sequence of bursts in the premotor nucleus HVC. To distinguish between two possible classes of models of neural sequence generation, we carried out intracellular recordings of HVC neurons in singing zebra finches (Taeniopygia guttata). We found that the subthreshold membrane potential is characterized by a large, rapid depolarization 5-10 ms before burst onset, consistent with a synaptically connected chain of neurons in HVC. We found no evidence for the slow membrane potential modulation predicted by models in which burst timing is controlled by subthreshold dynamics. Furthermore, bursts ride on an underlying depolarization of approximately 10-ms duration, probably the result of a regenerative calcium spike within HVC neurons that could facilitate the propagation of activity through a chain network with high temporal precision. Our results provide insight into the fundamental mechanisms by which neural circuits can generate complex sequential behaviours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998755/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998755/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, Michael A -- Jin, Dezhe Z -- Fee, Michale S -- DC009280/DC/NIDCD NIH HHS/ -- MH067105/MH/NIMH NIH HHS/ -- R01 MH067105/MH/NIMH NIH HHS/ -- R01 MH067105-06/MH/NIMH NIH HHS/ -- R01 MH067105-07/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Nov 18;468(7322):394-9. doi: 10.1038/nature09514. Epub 2010 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20972420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Channels, L-Type/metabolism ; Calcium Signaling/drug effects ; Finches/*physiology ; Male ; Membrane Potentials/drug effects ; *Models, Neurological ; Neural Pathways/drug effects/*physiology ; Neurons/drug effects/*metabolism ; Sleep/physiology ; Synapses/*metabolism ; Vocalization, Animal/physiology
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    CD95 promotes tumour growth (2010)
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    Publication Date: 2010-05-28
    Description: CD95 (also called Fas and APO-1) is a prototypical death receptor that regulates tissue homeostasis mainly in the immune system through the induction of apoptosis. During cancer progression CD95 is frequently downregulated or cells are rendered apoptosis resistant, raising the possibility that loss of CD95 is part of a mechanism for tumour evasion. However, complete loss of CD95 is rarely seen in human cancers and many cancer cells express large quantities of CD95 and are highly sensitive to CD95-mediated apoptosis in vitro. Furthermore, cancer patients frequently have elevated levels of the physiological ligand for CD95, CD95L. These data raise the possibility that CD95 could actually promote the growth of tumours through its non-apoptotic activities. Here we show that cancer cells in general, regardless of their CD95 apoptosis sensitivity, depend on constitutive activity of CD95, stimulated by cancer-produced CD95L, for optimal growth. Consistently, loss of CD95 in mouse models of ovarian cancer and liver cancer reduces cancer incidence as well as the size of the tumours. The tumorigenic activity of CD95 is mediated by a pathway involving JNK and Jun. These results demonstrate that CD95 has a growth-promoting role during tumorigenesis and indicate that efforts to inhibit its activity rather than to enhance it should be considered during cancer therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879093/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879093/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Lina -- Park, Sun-Mi -- Tumanov, Alexei V -- Hau, Annika -- Sawada, Kenjiro -- Feig, Christine -- Turner, Jerrold R -- Fu, Yang-Xin -- Romero, Iris L -- Lengyel, Ernst -- Peter, Marcus E -- CA112240/CA/NCI NIH HHS/ -- K12 HD000849/HD/NICHD NIH HHS/ -- L30 CA153336/CA/NCI NIH HHS/ -- R01 CA095319/CA/NCI NIH HHS/ -- R01 CA11182/CA/NCI NIH HHS/ -- R01 CA112240/CA/NCI NIH HHS/ -- R01 CA112240-01A1/CA/NCI NIH HHS/ -- R01 CA112240-02/CA/NCI NIH HHS/ -- R01 CA112240-03/CA/NCI NIH HHS/ -- R01 CA112240-04/CA/NCI NIH HHS/ -- R01 CA112240-05/CA/NCI NIH HHS/ -- England -- Nature. 2010 May 27;465(7297):492-6. doi: 10.1038/nature09075.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Ben May Department for Cancer Research, The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20505730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/deficiency/genetics/*metabolism ; Apoptosis ; Carcinoma, Endometrioid/metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation ; Fas Ligand Protein/antagonists & inhibitors/immunology/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Hepatocytes/enzymology/metabolism/pathology ; Humans ; Liver Neoplasms/enzymology/metabolism/pathology ; Male ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/metabolism ; Neoplasms/*metabolism/*pathology ; Ovarian Neoplasms/metabolism/pathology
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    Altruism researchers must cooperate (2010)
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    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okasha, Samir -- England -- Nature. 2010 Oct 7;467(7316):653-5. doi: 10.1038/467653a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Philosophy, University of Bristol, Bristol BS8 1TB, UK. Samir.Okasha@bristol.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20930821" target="_blank"〉PubMed〈/a〉
    Keywords: *Altruism ; Animals ; Biological Evolution ; *Cooperative Behavior ; Female ; Group Processes ; Male ; Models, Biological ; *Research Personnel ; Selection, Genetic ; Social Behavior
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    Sex determination: An avian sexual revolution (2010)
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    Publication Date: 2010-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barske, Lindsey A -- Capel, Blanche -- England -- Nature. 2010 Mar 11;464(7286):171-2. doi: 10.1038/464171a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220830" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/genetics/*physiology ; Chick Embryo ; Chickens ; Female ; Genotype ; Humans ; Male ; Mice ; Mosaicism ; Phenotype ; Sex Characteristics ; Sex Chromosomes/genetics ; *Sex Determination Processes
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    Blindsight depends on the lateral geniculate nucleus (2010)
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    Publication Date: 2010-06-25
    Description: Injury to the primary visual cortex (V1) leads to the loss of visual experience. Nonetheless, careful testing shows that certain visually guided behaviours can persist even in the absence of visual awareness. The neural circuits supporting this phenomenon, which is often termed blindsight, remain uncertain. Here we demonstrate that the thalamic lateral geniculate nucleus (LGN) has a causal role in V1-independent processing of visual information. By comparing functional magnetic resonance imaging (fMRI) and behavioural measures with and without temporary LGN inactivation, we assessed the contribution of the LGN to visual functions of macaque monkeys (Macaca mulatta) with chronic V1 lesions. Before LGN inactivation, high-contrast stimuli presented to the lesion-affected visual field (scotoma) produced significant V1-independent fMRI activation in the extrastriate cortical areas V2, V3, V4, V5/middle temporal (MT), fundus of the superior temporal sulcus (FST) and lateral intraparietal area (LIP) and the animals correctly located the stimuli in a detection task. However, following reversible inactivation of the LGN in the V1-lesioned hemisphere, fMRI responses and behavioural detection were abolished. These results demonstrate that direct LGN projections to the extrastriate cortex have a critical functional contribution to blindsight. They suggest a viable pathway to mediate fast detection during normal vision.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904843/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904843/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmid, Michael C -- Mrowka, Sylwia W -- Turchi, Janita -- Saunders, Richard C -- Wilke, Melanie -- Peters, Andrew J -- Ye, Frank Q -- Leopold, David A -- Z01 MH002838-05/Intramural NIH HHS/ -- England -- Nature. 2010 Jul 15;466(7304):373-7. doi: 10.1038/nature09179. Epub 2010 Jun 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA. schmidmicha@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20574422" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Geniculate Bodies/*physiology/physiopathology ; Macaca mulatta/*physiology ; Male ; Models, Neurological ; Photic Stimulation ; Visual Cortex/physiology/physiopathology ; Visual Pathways/*physiology/physiopathology ; Visual Perception/*physiology
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    Animal behaviour: An ill wind for finches (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lincoln, Tim -- England -- Nature. 2010 Feb 18;463(7283):888. doi: 10.1038/463888a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164914" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bird Diseases/*epidemiology/microbiology/transmission ; Cues ; Feeding Behavior/*physiology ; Female ; Finches/*physiology ; Male ; Mycoplasma Infections/epidemiology/microbiology/transmission/*veterinary ; *Mycoplasma gallisepticum/pathogenicity ; Sex Factors
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    Multiple personal genomes await (2010)
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    Publication Date: 2010-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venter, J Craig -- England -- Nature. 2010 Apr 1;464(7289):676-7. doi: 10.1038/464676a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. Craig Venter Institute, La Jolla, California 92121, USA. jcventer@jcvi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Continental Population Groups/genetics ; Diploidy ; Female ; Genetic Predisposition to Disease/genetics ; Genetic Variation/genetics ; Genetics, Medical/*trends ; Genome, Human/*genetics ; Genomics/economics/history/*trends ; Haploidy ; Haplotypes/genetics ; History, 20th Century ; History, 21st Century ; Human Genome Project/economics/history ; Humans ; Male ; Phenotype ; Precision Medicine/*trends ; Sequence Analysis, DNA/economics/history/instrumentation/methods
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    In vivo imaging of haematopoietic cells emerging from the mouse aortic endothelium (2010)
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    Publication Date: 2010-02-16
    Description: Haematopoietic stem cells (HSCs), responsible for blood production in the adult mouse, are first detected in the dorsal aorta starting at embryonic day 10.5 (E10.5). Immunohistological analysis of fixed embryo sections has revealed the presence of haematopoietic cell clusters attached to the aortic endothelium where HSCs might localize. The origin of HSCs has long been controversial and several candidates of the direct HSC precursors have been proposed (for review see ref. 7), including a specialized endothelial cell population with a haemogenic potential. Such cells have been described both in vitro in the embryonic stem cell (ESC) culture system and retrospectively in vivo by endothelial lineage tracing and conditional deletion experiments. Whether the transition from haemogenic endothelium to HSC actually occurs in the mouse embryonic aorta is still unclear and requires direct and real-time in vivo observation. To address this issue we used time-lapse confocal imaging and a new dissection procedure to visualize the deeply located aorta. Here we show the dynamic de novo emergence of phenotypically defined HSCs (Sca1(+), c-kit(+), CD41(+)) directly from ventral aortic haemogenic endothelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boisset, Jean-Charles -- van Cappellen, Wiggert -- Andrieu-Soler, Charlotte -- Galjart, Niels -- Dzierzak, Elaine -- Robin, Catherine -- R37 DKO54077/PHS HHS/ -- England -- Nature. 2010 Mar 4;464(7285):116-20. doi: 10.1038/nature08764. Epub 2010 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Erasmus Medical Center, Department of Cell Biology, CA Rotterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20154729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/*cytology/embryology/surgery ; *Cell Differentiation ; *Cell Lineage ; Core Binding Factor Alpha 2 Subunit/deficiency/genetics/metabolism ; Dissection ; Embryo, Mammalian/cytology ; Endothelial Cells/cytology ; Endothelium, Vascular/*cytology/embryology ; Female ; Hematopoietic Stem Cells/*cytology ; Male ; Mice ; Microscopy, Confocal ; Phenotype ; Pregnancy
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    Start/stop signals emerge in nigrostriatal circuits during sequence learning (2010)
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    Publication Date: 2010-07-24
    Description: Learning new action sequences subserves a plethora of different abilities such as escaping a predator, playing the piano, or producing fluent speech. Proper initiation and termination of each action sequence is critical for the organization of behaviour, and is compromised in nigrostriatal disorders like Parkinson's and Huntington's diseases. Using a self-paced operant task in which mice learn to perform a particular sequence of actions to obtain an outcome, we found neural activity in nigrostriatal circuits specifically signalling the initiation or the termination of each action sequence. This start/stop activity emerged during sequence learning, was specific for particular actions, and did not reflect interval timing, movement speed or action value. Furthermore, genetically altering the function of striatal circuits disrupted the development of start/stop activity and selectively impaired sequence learning. These results have important implications for understanding the functional organization of actions and the sequence initiation and termination impairments observed in basal ganglia disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477867/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477867/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jin, Xin -- Costa, Rui M -- 243393/European Research Council/International -- Z01 AA000416-02/Intramural NIH HHS/ -- England -- Nature. 2010 Jul 22;466(7305):457-62. doi: 10.1038/nature09263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5625 Fishers Lane, Bethesda, Maryland 20892-9412, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651684" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Behavior, Animal/physiology ; Dopamine/metabolism ; Glutamic Acid/metabolism ; Learning/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Neostriatum/*physiology ; Neural Pathways/*physiology ; Receptors, N-Methyl-D-Aspartate/deficiency/genetics/metabolism ; Substantia Nigra/*physiology
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    A novel pathway regulates memory and plasticity via SIRT1 and miR-134 (2010)
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    Publication Date: 2010-07-14
    Description: The NAD-dependent deacetylase Sir2 was initially identified as a mediator of replicative lifespan in budding yeast and was subsequently shown to modulate longevity in worms and flies. Its mammalian homologue, SIRT1, seems to have evolved complex systemic roles in cardiac function, DNA repair and genomic stability. Recent studies suggest a functional relevance of SIRT1 in normal brain physiology and neurological disorders. However, it is unknown if SIRT1 has a role in higher-order brain functions. We report that SIRT1 modulates synaptic plasticity and memory formation via a microRNA-mediated mechanism. Activation of SIRT1 enhances, whereas its loss-of-function impairs, synaptic plasticity. Surprisingly, these effects were mediated via post-transcriptional regulation of cAMP response binding protein (CREB) expression by a brain-specific microRNA, miR-134. SIRT1 normally functions to limit expression of miR-134 via a repressor complex containing the transcription factor YY1, and unchecked miR-134 expression following SIRT1 deficiency results in the downregulated expression of CREB and brain-derived neurotrophic factor (BDNF), thereby impairing synaptic plasticity. These findings demonstrate a new role for SIRT1 in cognition and a previously unknown microRNA-based mechanism by which SIRT1 regulates these processes. Furthermore, these results describe a separate branch of SIRT1 signalling, in which SIRT1 has a direct role in regulating normal brain function in a manner that is disparate from its cell survival functions, demonstrating its value as a potential therapeutic target for the treatment of central nervous system disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928875/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928875/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, Jun -- Wang, Wen-Yuan -- Mao, Ying-Wei -- Graff, Johannes -- Guan, Ji-Song -- Pan, Ling -- Mak, Gloria -- Kim, Dohoon -- Su, Susan C -- Tsai, Li-Huei -- P01 AG027916/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Aug 26;466(7310):1105-9. doi: 10.1038/nature09271. Epub 2010 Jul 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20622856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/metabolism ; CREB-Binding Protein/metabolism ; Electrical Synapses/genetics/pathology ; Gene Expression Regulation ; Gene Knockdown Techniques ; Long-Term Potentiation/genetics ; Male ; Memory/*physiology ; Memory Disorders/genetics/physiopathology ; Mice ; MicroRNAs/*genetics/*metabolism ; Neuronal Plasticity/*genetics ; Protein Binding ; Sequence Deletion ; Sirtuin 1/*genetics/*metabolism
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    Gender agenda: sex bias can be justified in animal research (2010)
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    Publication Date: 2010-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolon, Brad -- England -- Nature. 2010 Jul 1;466(7302):28. doi: 10.1038/466028d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595991" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Experimentation/standards ; Animals ; Animals, Laboratory ; *Bias (Epidemiology) ; Clinical Trials as Topic ; Editorial Policies ; Female ; Humans ; Male ; *Models, Animal ; *Research Design ; *Sex Characteristics
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    Climate-driven population divergence in sex-determining systems (2010)
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    Publication Date: 2010-10-29
    Description: Sex determination is a fundamental biological process, yet its mechanisms are remarkably diverse. In vertebrates, sex can be determined by inherited genetic factors or by the temperature experienced during embryonic development. However, the evolutionary causes of this diversity remain unknown. Here we show that live-bearing lizards at different climatic extremes of the species' distribution differ in their sex-determining mechanisms, with temperature-dependent sex determination in lowlands and genotypic sex determination in highlands. A theoretical model parameterized with field data accurately predicts this divergence in sex-determining systems and the consequence thereof for variation in cohort sex ratios among years. Furthermore, we show that divergent natural selection on sex determination across altitudes is caused by climatic effects on lizard life history and variation in the magnitude of between-year temperature fluctuations. Our results establish an adaptive explanation for intra-specific divergence in sex-determining systems driven by phenotypic plasticity and ecological selection, thereby providing a unifying framework for integrating the developmental, ecological and evolutionary basis for variation in vertebrate sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pen, Ido -- Uller, Tobias -- Feldmeyer, Barbara -- Harts, Anna -- While, Geoffrey M -- Wapstra, Erik -- England -- Nature. 2010 Nov 18;468(7322):436-8. doi: 10.1038/nature09512. Epub 2010 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Theoretical Biology Group, University of Groningen, PO Box 14, 9750 AA Haren, the Netherlands. i.r.pen@rug.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20981009" target="_blank"〉PubMed〈/a〉
    Keywords: Altitude ; Animals ; Biological Evolution ; *Climate ; Female ; Genotype ; Lizards/*genetics/*physiology ; Male ; Models, Biological ; Phenotype ; Selection, Genetic ; Sex Chromosomes ; *Sex Determination Processes/genetics/physiology ; *Sex Differentiation/genetics/physiology ; Sex Ratio ; *Temperature ; Time Factors ; Viviparity, Nonmammalian/physiology
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    Neuroscience: A mine of imprinted genes (2010)
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    Publication Date: 2010-08-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keverne, Eric B -- England -- Nature. 2010 Aug 12;466(7308):823-4. doi: 10.1038/466823a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703293" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Bias (Epidemiology) ; Brain/cytology/*metabolism ; Fathers ; Female ; Genomic Imprinting/*genetics ; Male ; Mice ; Models, Genetic ; Mothers ; X Chromosome/genetics
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    Strange lesions after stem-cell therapy (2010)
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    Publication Date: 2010-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2010 Jun 24;465(7301):997. doi: 10.1038/465997a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20577182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Child ; Fatal Outcome ; Female ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Humans ; Lupus Nephritis/*complications/*therapy ; Male ; Thailand
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    Gene therapy: Targeting beta-thalassaemia (2010)
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    Publication Date: 2010-09-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Persons, Derek A -- England -- Nature. 2010 Sep 16;467(7313):277-8. doi: 10.1038/467277a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20844523" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Blood Cells/cytology/metabolism ; Blood Transfusion ; Clone Cells/metabolism ; *Genetic Therapy ; HMGA2 Protein/genetics/*metabolism ; Humans ; Male ; Time Factors ; Transcriptional Activation ; Young Adult ; beta-Globins/*genetics/*metabolism ; beta-Thalassemia/*genetics/metabolism/*therapy
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    Toxicology: The big test for bisphenol A (2010)
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    Publication Date: 2010-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borrell, Brendan -- England -- Nature. 2010 Apr 22;464(7292):1122-4. doi: 10.1038/4641122a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20414285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzhydryl Compounds ; Chemical Industry/methods/standards ; Endocrine Disruptors/adverse effects/toxicity ; Estrogens, Non-Steroidal/adverse effects/toxicity ; Female ; Guidelines as Topic ; Humans ; Infant ; Male ; Mice ; National Institute of Environmental Health Sciences (U.S.) ; Neoplasms/chemically induced/etiology ; Phenols/adverse effects/*toxicity ; Rats ; Toxicity Tests/methods/standards ; Toxicology/economics/*methods/*standards ; United States ; United States Environmental Protection Agency ; Validation Studies as Topic
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    Sex bias in trials and treatment must end (2010)
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    Publication Date: 2010-06-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Alison M -- Tingen, Candace M -- Woodruff, Teresa K -- England -- Nature. 2010 Jun 10;465(7299):688-9. doi: 10.1038/465688a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535184" target="_blank"〉PubMed〈/a〉
    Keywords: Bias (Epidemiology) ; Biomedical Research/methods/*trends ; Clinical Trials as Topic/methods/*trends ; Drug Dosage Calculations ; Female ; Genomic Imprinting ; Humans ; Male ; Precision Medicine/trends ; *Sex Characteristics ; Sex Distribution ; Sex Factors
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    Role of conserved non-coding DNA elements in the Foxp3 gene in regulatory T-cell fate (2010)
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    Publication Date: 2010-01-15
    Description: Immune homeostasis is dependent on tight control over the size of a population of regulatory T (T(reg)) cells capable of suppressing over-exuberant immune responses. The T(reg) cell subset is comprised of cells that commit to the T(reg) lineage by upregulating the transcription factor Foxp3 either in the thymus (tT(reg)) or in the periphery (iT(reg)). Considering a central role for Foxp3 in T(reg) cell differentiation and function, we proposed that conserved non-coding DNA sequence (CNS) elements at the Foxp3 locus encode information defining the size, composition and stability of the T(reg) cell population. Here we describe the function of three Foxp3 CNS elements (CNS1-3) in T(reg) cell fate determination in mice. The pioneer element CNS3, which acts to potently increase the frequency of T(reg) cells generated in the thymus and the periphery, binds c-Rel in in vitro assays. In contrast, CNS1, which contains a TGF-beta-NFAT response element, is superfluous for tT(reg) cell differentiation, but has a prominent role in iT(reg) cell generation in gut-associated lymphoid tissues. CNS2, although dispensable for Foxp3 induction, is required for Foxp3 expression in the progeny of dividing T(reg) cells. Foxp3 binds to CNS2 in a Cbf-beta-Runx1 and CpG DNA demethylation-dependent manner, suggesting that Foxp3 recruitment to this 'cellular memory module' facilitates the heritable maintenance of the active state of the Foxp3 locus and, therefore, T(reg) lineage stability. Together, our studies demonstrate that the composition, size and maintenance of the T(reg) cell population are controlled by Foxp3 CNS elements engaged in response to distinct cell-extrinsic or -intrinsic cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884187/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, Ye -- Josefowicz, Steven -- Chaudhry, Ashutosh -- Peng, Xiao P -- Forbush, Katherine -- Rudensky, Alexander Y -- R37 AI034206/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 11;463(7282):808-12. doi: 10.1038/nature08750. Epub 2010 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunology, University of Washington, Seattle, Washington 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20072126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage/*genetics ; Chromatin Assembly and Disassembly ; Conserved Sequence/*genetics ; CpG Islands/genetics ; DNA Methylation ; Female ; Forkhead Transcription Factors/*genetics/metabolism ; Gene Expression Regulation ; Lymphocyte Count ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-rel/metabolism ; Regulatory Sequences, Nucleic Acid/*genetics ; Response Elements/genetics ; T-Lymphocytes, Regulatory/*cytology/immunology/*metabolism ; Thymus Gland/cytology/immunology/metabolism
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    Science in court: head case (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Virginia -- England -- Nature. 2010 Mar 18;464(7287):340-2. doi: 10.1038/464340a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237536" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antisocial Personality Disorder/physiopathology/psychology ; Child ; Female ; Forensic Sciences/ethics/*methods/trends ; Homicide/*legislation & jurisprudence/*psychology ; Humans ; Insanity Defense ; Magnetic Resonance Imaging/standards/*utilization ; Male ; *Neurosciences ; Positron-Emission Tomography/utilization ; Rape/legislation & jurisprudence/psychology ; Reproducibility of Results
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    Genome, epigenome and RNA sequences of monozygotic twins discordant for multiple sclerosis (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-30
    Description: Monozygotic or 'identical' twins have been widely studied to dissect the relative contributions of genetics and environment in human diseases. In multiple sclerosis (MS), an autoimmune demyelinating disease and common cause of neurodegeneration and disability in young adults, disease discordance in monozygotic twins has been interpreted to indicate environmental importance in its pathogenesis. However, genetic and epigenetic differences between monozygotic twins have been described, challenging the accepted experimental model in disambiguating the effects of nature and nurture. Here we report the genome sequences of one MS-discordant monozygotic twin pair, and messenger RNA transcriptome and epigenome sequences of CD4(+) lymphocytes from three MS-discordant, monozygotic twin pairs. No reproducible differences were detected between co-twins among approximately 3.6 million single nucleotide polymorphisms (SNPs) or approximately 0.2 million insertion-deletion polymorphisms. Nor were any reproducible differences observed between siblings of the three twin pairs in HLA haplotypes, confirmed MS-susceptibility SNPs, copy number variations, mRNA and genomic SNP and insertion-deletion genotypes, or the expression of approximately 19,000 genes in CD4(+) T cells. Only 2 to 176 differences in the methylation of approximately 2 million CpG dinucleotides were detected between siblings of the three twin pairs, in contrast to approximately 800 methylation differences between T cells of unrelated individuals and several thousand differences between tissues or between normal and cancerous tissues. In the first systematic effort to estimate sequence variation among monozygotic co-twins, we did not find evidence for genetic, epigenetic or transcriptome differences that explained disease discordance. These are the first, to our knowledge, female, twin and autoimmune disease individual genome sequences reported.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862593/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862593/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baranzini, Sergio E -- Mudge, Joann -- van Velkinburgh, Jennifer C -- Khankhanian, Pouya -- Khrebtukova, Irina -- Miller, Neil A -- Zhang, Lu -- Farmer, Andrew D -- Bell, Callum J -- Kim, Ryan W -- May, Gregory D -- Woodward, Jimmy E -- Caillier, Stacy J -- McElroy, Joseph P -- Gomez, Refujia -- Pando, Marcelo J -- Clendenen, Leonda E -- Ganusova, Elena E -- Schilkey, Faye D -- Ramaraj, Thiruvarangan -- Khan, Omar A -- Huntley, Jim J -- Luo, Shujun -- Kwok, Pui-Yan -- Wu, Thomas D -- Schroth, Gary P -- Oksenberg, Jorge R -- Hauser, Stephen L -- Kingsmore, Stephen F -- P20 RR016480/RR/NCRR NIH HHS/ -- P20 RR016480-09/RR/NCRR NIH HHS/ -- R01 NS026799/NS/NINDS NIH HHS/ -- R01 NS026799-20A1/NS/NINDS NIH HHS/ -- R01 NS046297/NS/NINDS NIH HHS/ -- R01 NS046297-06/NS/NINDS NIH HHS/ -- R01NS26799/NS/NINDS NIH HHS/ -- R01NS46297/NS/NINDS NIH HHS/ -- RR016480/RR/NCRR NIH HHS/ -- U01 AI066569/AI/NIAID NIH HHS/ -- U01 AI066569-05/AI/NIAID NIH HHS/ -- U19 HD077693/HD/NICHD NIH HHS/ -- England -- Nature. 2010 Apr 29;464(7293):1351-6. doi: 10.1038/nature08990.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California at San Francisco, San Francisco, California 94143, USA. sebaran@cgl.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20428171" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Allelic Imbalance/genetics ; Breast/metabolism ; Breast Neoplasms/genetics ; CD4-Positive T-Lymphocytes/metabolism ; Case-Control Studies ; CpG Islands/genetics ; DNA Copy Number Variations/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic/*genetics ; Female ; Genetic Predisposition to Disease/genetics ; Genome, Human/*genetics ; Haplotypes/genetics ; Heterozygote ; Humans ; INDEL Mutation/genetics ; Lung/metabolism ; Lung Neoplasms/genetics ; Male ; Multiple Sclerosis/*genetics ; Polymorphism, Genetic/genetics ; Quantitative Trait Loci/genetics ; RNA, Messenger/analysis/*genetics/metabolism ; Twins, Monozygotic/*genetics
    Print ISSN: 0028-0836
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    Convergent evolution of chicken Z and human X chromosomes by expansion and gene acquisition (2010)
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    Publication Date: 2010-07-14
    Description: In birds, as in mammals, one pair of chromosomes differs between the sexes. In birds, males are ZZ and females ZW. In mammals, males are XY and females XX. Like the mammalian XY pair, the avian ZW pair is believed to have evolved from autosomes, with most change occurring in the chromosomes found in only one sex--the W and Y chromosomes. By contrast, the sex chromosomes found in both sexes--the Z and X chromosomes--are assumed to have diverged little from their autosomal progenitors. Here we report findings that challenge this assumption for both the chicken Z chromosome and the human X chromosome. The chicken Z chromosome, which we sequenced essentially to completion, is less gene-dense than chicken autosomes but contains a massive tandem array containing hundreds of duplicated genes expressed in testes. A comprehensive comparison of the chicken Z chromosome with the finished sequence of the human X chromosome demonstrates that each evolved independently from different portions of the ancestral genome. Despite this independence, the chicken Z and human X chromosomes share features that distinguish them from autosomes: the acquisition and amplification of testis-expressed genes, and a low gene density resulting from an expansion of intergenic regions. These features were not present on the autosomes from which the Z and X chromosomes originated but were instead acquired during the evolution of Z and X as sex chromosomes. We conclude that the avian Z and mammalian X chromosomes followed convergent evolutionary trajectories, despite their evolving with opposite (female versus male) systems of heterogamety. More broadly, in birds and mammals, sex chromosome evolution involved not only gene loss in sex-specific chromosomes, but also marked expansion and gene acquisition in sex chromosomes common to males and females.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943333/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943333/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bellott, Daniel W -- Skaletsky, Helen -- Pyntikova, Tatyana -- Mardis, Elaine R -- Graves, Tina -- Kremitzki, Colin -- Brown, Laura G -- Rozen, Steve -- Warren, Wesley C -- Wilson, Richard K -- Page, David C -- R01 HG000257/HG/NHGRI NIH HHS/ -- R01 HG000257-21/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jul 29;466(7306):612-6. doi: 10.1038/nature09172. Epub 2010 Jul 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20622855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens/*genetics ; Chromosomes, Human, X/*genetics ; *Evolution, Molecular ; Female ; Gene Deletion ; Genes/*genetics ; Genome/genetics ; Humans ; Male ; Multigene Family/genetics ; Sex Characteristics ; Sex Chromosomes/*genetics ; Testis/metabolism
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    Learning from the elite (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trivedi, Bijal -- England -- Nature. 2010 Jul 15;466(7304):S4. doi: 10.1038/nature09235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631703" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/*immunology/prevention & ; control/virology ; Alleles ; *Disease Progression ; Female ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; HIV/genetics/immunology ; HIV Infections/genetics/*immunology/prevention & control/virology ; *HIV Long-Term Survivors/statistics & numerical data ; HLA-B Antigens/genetics/immunology ; Humans ; Immunity, Innate/genetics/*immunology ; Major Histocompatibility Complex/genetics ; Male ; Polymorphism, Single Nucleotide/genetics ; RNA, Viral/blood
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    Encoding of conditioned fear in central amygdala inhibitory circuits (2010)
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    Publication Date: 2010-11-12
    Description: The central amygdala (CEA), a nucleus predominantly composed of GABAergic inhibitory neurons, is essential for fear conditioning. How the acquisition and expression of conditioned fear are encoded within CEA inhibitory circuits is not understood. Using in vivo electrophysiological, optogenetic and pharmacological approaches in mice, we show that neuronal activity in the lateral subdivision of the central amygdala (CEl) is required for fear acquisition, whereas conditioned fear responses are driven by output neurons in the medial subdivision (CEm). Functional circuit analysis revealed that inhibitory CEA microcircuits are highly organized and that cell-type-specific plasticity of phasic and tonic activity in the CEl to CEm pathway may gate fear expression and regulate fear generalization. Our results define the functional architecture of CEA microcircuits and their role in the acquisition and regulation of conditioned fear behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciocchi, Stephane -- Herry, Cyril -- Grenier, Francois -- Wolff, Steffen B E -- Letzkus, Johannes J -- Vlachos, Ioannis -- Ehrlich, Ingrid -- Sprengel, Rolf -- Deisseroth, Karl -- Stadler, Michael B -- Muller, Christian -- Luthi, Andreas -- England -- Nature. 2010 Nov 11;468(7321):277-82. doi: 10.1038/nature09559.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068837" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Amygdala/anatomy & histology/cytology/*physiology ; Animals ; Conditioning, Classical/*physiology ; Fear/*physiology ; Freezing Reaction, Cataleptic ; Male ; Mice ; Mice, Inbred C57BL ; Neural Inhibition/*physiology ; Neural Pathways/cytology/*physiology ; Neuronal Plasticity/physiology ; Neurons/physiology ; gamma-Aminobutyric Acid/metabolism
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    Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke (2010)
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    Publication Date: 2010-11-05
    Description: Stroke is a leading cause of disability, but no pharmacological therapy is currently available for promoting recovery. The brain region adjacent to stroke damage-the peri-infarct zone-is critical for rehabilitation, as it shows heightened neuroplasticity, allowing sensorimotor functions to re-map from damaged areas. Thus, understanding the neuronal properties constraining this plasticity is important for the development of new treatments. Here we show that after a stroke in mice, tonic neuronal inhibition is increased in the peri-infarct zone. This increased tonic inhibition is mediated by extrasynaptic GABA(A) receptors and is caused by an impairment in GABA (gamma-aminobutyric acid) transporter (GAT-3/GAT-4) function. To counteract the heightened inhibition, we administered in vivo a benzodiazepine inverse agonist specific for alpha5-subunit-containing extrasynaptic GABA(A) receptors at a delay after stroke. This treatment produced an early and sustained recovery of motor function. Genetically lowering the number of alpha5- or delta-subunit-containing GABA(A) receptors responsible for tonic inhibition also proved beneficial for recovery after stroke, consistent with the therapeutic potential of diminishing extrasynaptic GABA(A) receptor function. Together, our results identify new pharmacological targets and provide the rationale for a novel strategy to promote recovery after stroke and possibly other brain injuries.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058798/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058798/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarkson, Andrew N -- Huang, Ben S -- Macisaac, Sarah E -- Mody, Istvan -- Carmichael, S Thomas -- NS30549/NS/NINDS NIH HHS/ -- R01 NS030549/NS/NINDS NIH HHS/ -- R01 NS030549-18/NS/NINDS NIH HHS/ -- England -- Nature. 2010 Nov 11;468(7321):305-9. doi: 10.1038/nature09511. Epub 2010 Nov 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, The David Geffen School of Medicine at UCLA, 635 Charles Young Drive South, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21048709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepines/pharmacology ; Cerebral Infarction/metabolism/pathology/physiopathology ; Disease Models, Animal ; Drug Inverse Agonism ; GABA Antagonists/pharmacology ; GABA Plasma Membrane Transport Proteins/metabolism ; Imidazoles/pharmacology ; Male ; Membrane Potentials/drug effects ; Mice ; Mice, Inbred C57BL ; Motor Cortex/metabolism/pathology/*physiology/*physiopathology ; Neuronal Plasticity/physiology ; Receptors, GABA/deficiency/genetics/metabolism ; Recovery of Function/*physiology ; Stroke/drug therapy/*metabolism/pathology ; Synapses/metabolism ; Time Factors ; gamma-Aminobutyric Acid/*metabolism
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    Cancer: a lower bar for senescence (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Serrano, Manuel -- England -- Nature. 2010 Mar 18;464(7287):363-4. doi: 10.1038/464363a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *Cell Aging/drug effects ; Cyclin-Dependent Kinase 2/deficiency/*metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Leukemia/metabolism/pathology ; Male ; Mice ; Neoplasms/drug therapy/metabolism/*pathology/prevention & control ; PTEN Phosphohydrolase/deficiency/genetics/metabolism ; Prostatic Neoplasms/metabolism/pathology ; S-Phase Kinase-Associated Proteins/antagonists & inhibitors/genetics/*metabolism
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    Putting gender on the agenda (2010)
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    Publication Date: 2010-06-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2010 Jun 10;465(7299):665. doi: 10.1038/465665a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535156" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bias (Epidemiology) ; Biomedical Research/*methods/*trends ; Clinical Trials as Topic/*methods/*trends ; Evidence-Based Medicine/methods/trends ; Female ; Humans ; Male ; Precision Medicine/methods/trends ; Pregnancy ; *Sex Characteristics ; Sex Factors
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    Evolutionary biology: pregnant fathers in charge (2010)
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    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berglund, Anders -- England -- Nature. 2010 Mar 18;464(7287):364-5. doi: 10.1038/464364a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237558" target="_blank"〉PubMed〈/a〉
    Keywords: Abortion, Eugenic/veterinary ; Animals ; *Biological Evolution ; Body Size/physiology ; *Conflict (Psychology) ; Embryo, Nonmammalian/embryology/physiology ; Embryonic Development/*physiology ; Female ; Male ; Mating Preference, Animal/*physiology ; Paternal Behavior ; Selection, Genetic ; *Sex ; Sex Characteristics ; Smegmamorpha/anatomy & histology/embryology/*physiology ; Survival Rate
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    Staphylococcus epidermidis Esp inhibits Staphylococcus aureus biofilm formation and nasal colonization (2010)
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    Publication Date: 2010-05-21
    Description: Commensal bacteria are known to inhibit pathogen colonization; however, complex host-microbe and microbe-microbe interactions have made it difficult to gain a detailed understanding of the mechanisms involved in the inhibition of colonization. Here we show that the serine protease Esp secreted by a subset of Staphylococcus epidermidis, a commensal bacterium, inhibits biofilm formation and nasal colonization by Staphylococcus aureus, a human pathogen. Epidemiological studies have demonstrated that the presence of Esp-secreting S. epidermidis in the nasal cavities of human volunteers correlates with the absence of S. aureus. Purified Esp inhibits biofilm formation and destroys pre-existing S. aureus biofilms. Furthermore, Esp enhances the susceptibility of S. aureus in biofilms to immune system components. In vivo studies have shown that Esp-secreting S. epidermidis eliminates S. aureus nasal colonization. These findings indicate that Esp hinders S. aureus colonization in vivo through a novel mechanism of bacterial interference, which could lead to the development of novel therapeutics to prevent S. aureus colonization and infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwase, Tadayuki -- Uehara, Yoshio -- Shinji, Hitomi -- Tajima, Akiko -- Seo, Hiromi -- Takada, Koji -- Agata, Toshihiko -- Mizunoe, Yoshimitsu -- England -- Nature. 2010 May 20;465(7296):346-9. doi: 10.1038/nature09074.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, The Jikei University School of Medicine, Tokyo, 105-8461 Japan. iwase.tadayuki@jikei.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485435" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/chemistry/isolation & purification/*metabolism/pharmacology ; Biofilms/*growth & development ; Female ; Humans ; Male ; Nose/*microbiology ; Odds Ratio ; Serine Proteases/chemistry/deficiency/isolation & purification/*metabolism ; Staphylococcal Infections/microbiology/prevention & control/therapy ; Staphylococcus aureus/*growth & development/immunology ; Staphylococcus epidermidis/*enzymology/genetics/*physiology ; Superinfection/immunology/microbiology/prevention & control/therapy ; Young Adult ; beta-Defensins/immunology/pharmacology
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    Korean deaths spark inquiry (2010)
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    Publication Date: 2010-11-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2010 Nov 25;468(7323):485. doi: 10.1038/468485a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107396" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Male ; *Medical Tourism/economics/ethics/legislation & jurisprudence ; Republic of Korea ; Stem Cell Transplantation/*ethics/*legislation & jurisprudence/mortality ; *Travel
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    Production of p53 gene knockout rats by homologous recombination in embryonic stem cells (2010)
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    Publication Date: 2010-08-13
    Description: The use of homologous recombination to modify genes in embryonic stem (ES) cells provides a powerful means to elucidate gene function and create disease models. Application of this technology to engineer genes in rats has not previously been possible because of the absence of germline-competent ES cells in this species. We have recently established authentic rat ES cells. Here we report the generation of gene knockout rats using the ES-cell-based gene targeting technology. We designed a targeting vector to disrupt the tumour suppressor gene p53 (also known as Tp53) in rat ES cells by means of homologous recombination. p53 gene-targeted rat ES cells can be routinely generated. Furthermore, the p53 gene-targeted mutation in the rat ES-cell genome can transmit through the germ line via ES-cell rat chimaeras to create p53 gene knockout rats. The rat is the most widely used animal model in biological research. The establishment of gene targeting technology in rat ES cells, in combination with advances in genomics and the vast amount of research data on physiology and pharmacology in this species, now provide a powerful new platform for the study of human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937076/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937076/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tong, Chang -- Li, Ping -- Wu, Nancy L -- Yan, Youzhen -- Ying, Qi-Long -- 1R01 RR025881/RR/NCRR NIH HHS/ -- R01 OD010926/OD/NIH HHS/ -- R01 RR025881/RR/NCRR NIH HHS/ -- R01 RR025881-01A2/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Sep 9;467(7312):211-3. doi: 10.1038/nature09368. Epub 2010 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Culture Techniques ; Embryo, Mammalian/cytology ; Embryonic Stem Cells/*cytology ; Female ; Gene Knockout Techniques/*methods ; *Genes, p53 ; Germ-Line Mutation ; Male ; Mice ; Molecular Sequence Data ; Rats/*genetics ; Rats, Inbred F344 ; Rats, Sprague-Dawley ; Recombination, Genetic
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    Systematic genetic analysis of muscle morphogenesis and function in Drosophila (2010)
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    Publication Date: 2010-03-12
    Description: Systematic genetic approaches have provided deep insight into the molecular and cellular mechanisms that operate in simple unicellular organisms. For multicellular organisms, however, the pleiotropy of gene function has largely restricted such approaches to the study of early embryogenesis. With the availability of genome-wide transgenic RNA interference (RNAi) libraries in Drosophila, it is now possible to perform a systematic genetic dissection of any cell or tissue type at any stage of the lifespan. Here we apply these methods to define the genetic basis for formation and function of the Drosophila muscle. We identify a role in muscle for 2,785 genes, many of which we assign to specific functions in the organization of muscles, myofibrils or sarcomeres. Many of these genes are phylogenetically conserved, including genes implicated in mammalian sarcomere organization and human muscle diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schnorrer, Frank -- Schonbauer, Cornelia -- Langer, Christoph C H -- Dietzl, Georg -- Novatchkova, Maria -- Schernhuber, Katharina -- Fellner, Michaela -- Azaryan, Anna -- Radolf, Martin -- Stark, Alexander -- Keleman, Krystyna -- Dickson, Barry J -- England -- Nature. 2010 Mar 11;464(7286):287-91. doi: 10.1038/nature08799.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany. schnorrer@biochem.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Computational Biology ; Drosophila melanogaster/*embryology ; Genes, Insect/*genetics ; Genome-Wide Association Study ; Genomic Library ; Larva ; Male ; Muscles/embryology ; RNA Interference
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    Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-22
    Description: Two forms of X-chromosome inactivation (XCI) ensure the selective silencing of female sex chromosomes during mouse embryogenesis. Imprinted XCI begins with the detection of Xist RNA expression on the paternal X chromosome (Xp) at about the four-cell stage of embryonic development. In the embryonic tissues of the inner cell mass, a random form of XCI occurs in blastocysts that inactivates either Xp or the maternal X chromosome (Xm). Both forms of XCI require the non-coding Xist RNA that coats the inactive X chromosome from which it is expressed. Xist has crucial functions in the silencing of X-linked genes, including Rnf12 (refs 3, 4) encoding the ubiquitin ligase RLIM (RING finger LIM-domain-interacting protein). Here we show, by targeting a conditional knockout of Rnf12 to oocytes where RLIM accumulates to high levels, that the maternal transmission of the mutant X chromosome (Deltam) leads to lethality in female embryos as a result of defective imprinted XCI. We provide evidence that in Deltam female embryos the initial formation of Xist clouds and Xp silencing are inhibited. In contrast, embryonic stem cells lacking RLIM are able to form Xist clouds and silence at least some X-linked genes during random XCI. These results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted XCI.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967734/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967734/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, Jongdae -- Bossenz, Michael -- Chung, Young -- Ma, Hong -- Byron, Meg -- Taniguchi-Ishigaki, Naoko -- Zhu, Xiaochun -- Jiao, Baowei -- Hall, Lisa L -- Green, Michael R -- Jones, Stephen N -- Hermans-Borgmeyer, Irm -- Lawrence, Jeanne B -- Bach, Ingolf -- 5 P30 DK32520/DK/NIDDK NIH HHS/ -- DK32520/DK/NIDDK NIH HHS/ -- GM053234/GM/NIGMS NIH HHS/ -- R01 CA131158/CA/NCI NIH HHS/ -- R01 CA131158-04/CA/NCI NIH HHS/ -- R01 GM033977/GM/NIGMS NIH HHS/ -- R01 GM053234/GM/NIGMS NIH HHS/ -- R01CA131158/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Oct 21;467(7318):977-81. doi: 10.1038/nature09457.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS), Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962847" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Congenic ; Blastocyst/metabolism ; Cell Line ; Chromosomes, Mammalian/*genetics ; Embryo Loss/genetics ; Fathers ; Female ; Gene Silencing ; *Genomic Imprinting ; Male ; Mice ; Mice, Transgenic ; *Mothers ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Repressor Proteins/deficiency/genetics/*metabolism ; Ubiquitin-Protein Ligases ; X Chromosome/*genetics ; X Chromosome Inactivation/*genetics
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    Haematopoietic stem cells derive directly from aortic endothelium during development (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-02-16
    Description: A major goal of regenerative medicine is to instruct formation of multipotent, tissue-specific stem cells from induced pluripotent stem cells (iPSCs) for cell replacement therapies. Generation of haematopoietic stem cells (HSCs) from iPSCs or embryonic stem cells (ESCs) is not currently possible, however, necessitating a better understanding of how HSCs normally arise during embryonic development. We previously showed that haematopoiesis occurs through four distinct waves during zebrafish development, with HSCs arising in the final wave in close association with the dorsal aorta. Recent reports have suggested that murine HSCs derive from haemogenic endothelial cells (ECs) lining the aortic floor. Additional in vitro studies have similarly indicated that the haematopoietic progeny of ESCs arise through intermediates with endothelial potential. Here we have used the unique strengths of the zebrafish embryo to image directly the generation of HSCs from the ventral wall of the dorsal aorta. Using combinations of fluorescent reporter transgenes, confocal time-lapse microscopy and flow cytometry, we have identified and isolated the stepwise intermediates as aortic haemogenic endothelium transitions to nascent HSCs. Finally, using a permanent lineage tracing strategy, we demonstrate that the HSCs generated from haemogenic endothelium are the lineal founders of the adult haematopoietic system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858358/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858358/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bertrand, Julien Y -- Chi, Neil C -- Santoso, Buyung -- Teng, Shutian -- Stainier, Didier Y R -- Traver, David -- DK074482/DK/NIDDK NIH HHS/ -- F32DK752433/DK/NIDDK NIH HHS/ -- HL074891/HL/NHLBI NIH HHS/ -- HL54737/HL/NHLBI NIH HHS/ -- R01 DK074482/DK/NIDDK NIH HHS/ -- R01 DK074482-04/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Mar 4;464(7285):108-11. doi: 10.1038/nature08738. Epub 2010 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, California 92093-0380, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20154733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Aorta/*cytology/*embryology ; *Cell Differentiation ; *Cell Lineage ; Cell Separation ; Endothelial Cells/cytology ; Endothelium, Vascular/*cytology/embryology ; Female ; Flow Cytometry ; Genes, Reporter/genetics ; Hematopoietic Stem Cells/*cytology ; Male ; Microscopy, Confocal ; Microscopy, Fluorescence ; Transgenes/genetics ; Zebrafish/blood/*embryology
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    Palaeogenetics: Icy resolve (2010)
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    Publication Date: 2010-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalton, Rex -- England -- Nature. 2010 Feb 11;463(7282):724-5. doi: 10.1038/463724a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20148008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arctic Regions ; Cryopreservation ; DNA/genetics/isolation & purification ; DNA, Mitochondrial/analysis/genetics ; Denmark ; Emigration and Immigration/*history ; Feces ; Fossils ; Genetics, Medical/history ; Genome, Human/*genetics ; Greenland/ethnology ; History, 20th Century ; History, 21st Century ; History, Ancient ; Humans ; Inuits/*ethnology/*history ; Male ; Paleontology/*history ; Phylogeny ; Reproducibility of Results ; Sequence Analysis, DNA ; Siberia/ethnology
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    Metabolic disorders: Fathers' nutritional legacy (2010)
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    Publication Date: 2010-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skinner, Michael K -- England -- Nature. 2010 Oct 21;467(7318):922-3. doi: 10.1038/467922a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962833" target="_blank"〉PubMed〈/a〉
    Keywords: Adiposity/drug effects ; Animals ; Body Weight/drug effects ; DNA Methylation ; Diabetes Mellitus, Type 2/etiology/genetics/pathology/physiopathology ; Diet/*adverse effects ; Dietary Fats/*administration & dosage/*adverse effects ; Epigenesis, Genetic/drug effects ; *Fathers ; Female ; Gene Expression Profiling ; Glucose Intolerance/etiology/pathology/physiopathology ; Insulin/secretion ; Insulin-Secreting Cells/metabolism/*pathology/secretion ; Male ; Obesity/etiology/genetics/pathology/physiopathology ; Paternal Exposure/*adverse effects ; Rats ; Spermatozoa/drug effects/metabolism
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    Promiscuity and the evolutionary transition to complex societies (2010)
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    Publication Date: 2010-08-21
    Description: Theory predicts that the evolution of cooperative behaviour is favoured by low levels of promiscuity leading to high within-group relatedness. However, in vertebrates, cooperation often occurs between non-relatives and promiscuity rates are among the highest recorded. Here we resolve this apparent inconsistency with a phylogenetic analysis of 267 bird species, demonstrating that cooperative breeding is associated with low promiscuity; that in cooperative species, helping is more common when promiscuity is low; and that intermediate levels of promiscuity favour kin discrimination. Overall, these results suggest that promiscuity is a unifying feature across taxa in explaining transitions to and from cooperative societies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cornwallis, Charlie K -- West, Stuart A -- Davis, Katie E -- Griffin, Ashleigh S -- England -- Nature. 2010 Aug 19;466(7309):969-72. doi: 10.1038/nature09335.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Edward Grey Institute, Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20725039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/classification/genetics/*physiology ; *Cooperative Behavior ; Fathers ; Female ; Male ; Models, Biological ; Mothers ; Phylogeny ; Reproduction/genetics/physiology ; Sexual Behavior, Animal/*physiology ; *Siblings
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    Rekindling the gender-bias debate (2010)
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    Publication Date: 2010-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, Karen -- England -- Nature. 2009 Dec 17;462(7275):947.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20108406" target="_blank"〉PubMed〈/a〉
    Keywords: *Aptitude ; Biomedical Research/manpower ; Engineering/*manpower ; Female ; Femininity ; Humans ; Male ; Masculinity ; Mathematics/*manpower ; Models, Psychological ; Motivation ; *Prejudice ; Science/*manpower ; *Sex Characteristics ; Sex Factors ; Workload
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    Allelic variation in a fatty-acyl reductase gene causes divergence in moth sex pheromones (2010)
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    Publication Date: 2010-07-02
    Description: Pheromone-based behaviours are crucial in animals from insects to mammals, and reproductive isolation is often based on pheromone differences. However, the genetic mechanisms by which pheromone signals change during the evolution of new species are largely unknown. In the sexual communication system of moths (Insecta: Lepidoptera), females emit a species-specific pheromone blend that attracts males over long distances. The European corn borer, Ostrinia nubilalis, consists of two sex pheromone races, Z and E, that use different ratios of the cis and trans isomers of acetate pheromone components. This subtle difference leads to strong reproductive isolation in the field between the two races, which could represent a first step in speciation. Female sex pheromone production and male behavioural response are under the control of different major genes, but the identity of these genes is unknown. Here we show that allelic variation in a fatty-acyl reductase gene essential for pheromone biosynthesis accounts for the phenotypic variation in female pheromone production, leading to race-specific signals. Both the cis and trans isomers of the pheromone precursors are produced by both races, but the precursors are differentially reduced to yield opposite ratios in the final pheromone blend as a result of the substrate specificity of the enzymes encoded by the Z and E alleles. This is the first functional characterization of a gene contributing to intraspecific behavioural reproductive isolation in moths, highlighting the importance of evolutionary diversification in a lepidopteran-specific family of reductases. Accumulation of substitutions in the coding region of a single biosynthetic enzyme can produce pheromone differences resulting in reproductive isolation, with speciation as a potential end result.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lassance, Jean-Marc -- Groot, Astrid T -- Lienard, Marjorie A -- Antony, Binu -- Borgwardt, Christin -- Andersson, Fredrik -- Hedenstrom, Erik -- Heckel, David G -- Lofstedt, Christer -- England -- Nature. 2010 Jul 22;466(7305):486-9. doi: 10.1038/nature09058. Epub 2010 Jun 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Lund University, 22362 Lund, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20592730" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Female ; Isomerism ; Male ; Molecular Sequence Data ; Moths/classification/enzymology/genetics/*physiology ; Oxidoreductases/*genetics/*metabolism ; Phylogeny ; RNA/analysis/genetics/metabolism ; Sex Attractants/biosynthesis/chemistry/*metabolism ; Substrate Specificity
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    Genetic dissection of an amygdala microcircuit that gates conditioned fear (2010)
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    Publication Date: 2010-11-12
    Description: The role of different amygdala nuclei (neuroanatomical subdivisions) in processing Pavlovian conditioned fear has been studied extensively, but the function of the heterogeneous neuronal subtypes within these nuclei remains poorly understood. Here we use molecular genetic approaches to map the functional connectivity of a subpopulation of GABA-containing neurons, located in the lateral subdivision of the central amygdala (CEl), which express protein kinase C-delta (PKC-delta). Channelrhodopsin-2-assisted circuit mapping in amygdala slices and cell-specific viral tracing indicate that PKC-delta(+) neurons inhibit output neurons in the medial central amygdala (CEm), and also make reciprocal inhibitory synapses with PKC-delta(-) neurons in CEl. Electrical silencing of PKC-delta(+) neurons in vivo suggests that they correspond to physiologically identified units that are inhibited by the conditioned stimulus, called CEl(off) units. This correspondence, together with behavioural data, defines an inhibitory microcircuit in CEl that gates CEm output to control the level of conditioned freezing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597095/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597095/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haubensak, Wulf -- Kunwar, Prabhat S -- Cai, Haijiang -- Ciocchi, Stephane -- Wall, Nicholas R -- Ponnusamy, Ravikumar -- Biag, Jonathan -- Dong, Hong-Wei -- Deisseroth, Karl -- Callaway, Edward M -- Fanselow, Michael S -- Luthi, Andreas -- Anderson, David J -- 1 R01 MH085082-01A1/MH/NIMH NIH HHS/ -- R01 MH063912/MH/NIMH NIH HHS/ -- R01 MH063912-09/MH/NIMH NIH HHS/ -- R01 MH063912-09S1/MH/NIMH NIH HHS/ -- R01 MH063912-10/MH/NIMH NIH HHS/ -- R01 MH085082/MH/NIMH NIH HHS/ -- R01 MH085082-01A1/MH/NIMH NIH HHS/ -- RC2 NS069464/NS/NINDS NIH HHS/ -- RC2 NS069464-01/NS/NINDS NIH HHS/ -- RC2 NS069464-02/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 11;468(7321):270-6. doi: 10.1038/nature09553.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068836" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/anatomy & histology/cytology/enzymology/*physiology ; Animals ; Axonal Transport ; Cells, Cultured ; Conditioning, Classical/*physiology ; Fear/*physiology ; Female ; Freezing Reaction, Cataleptic ; Genetic Techniques ; Humans ; Male ; Mice ; Mice, Transgenic ; Neural Inhibition/*physiology ; Neural Pathways/cytology/enzymology/*physiology ; Neurons/enzymology/metabolism ; Protein Kinase C-delta/deficiency/genetics/metabolism ; Synapses/metabolism ; gamma-Aminobutyric Acid/metabolism
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    L1 retrotransposition in neurons is modulated by MeCP2 (2010)
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    Publication Date: 2010-11-19
    Description: Long interspersed nuclear elements-1 (LINE-1 or L1s) are abundant retrotransposons that comprise approximately 20% of mammalian genomes. Active L1 retrotransposons can impact the genome in a variety of ways, creating insertions, deletions, new splice sites or gene expression fine-tuning. We have shown previously that L1 retrotransposons are capable of mobilization in neuronal progenitor cells from rodents and humans and evidence of massive L1 insertions was observed in adult brain tissues but not in other somatic tissues. In addition, L1 mobility in the adult hippocampus can be influenced by the environment. The neuronal specificity of somatic L1 retrotransposition in neural progenitors is partially due to the transition of a Sox2/HDAC1 repressor complex to a Wnt-mediated T-cell factor/lymphoid enhancer factor (TCF/LEF) transcriptional activator. The transcriptional switch accompanies chromatin remodelling during neuronal differentiation, allowing a transient stimulation of L1 transcription. The activity of L1 retrotransposons during brain development can have an impact on gene expression and neuronal function, thereby increasing brain-specific genetic mosaicism. Further understanding of the molecular mechanisms that regulate L1 expression should provide new insights into the role of L1 retrotransposition during brain development. Here we show that L1 neuronal transcription and retrotransposition in rodents are increased in the absence of methyl-CpG-binding protein 2 (MeCP2), a protein involved in global DNA methylation and human neurodevelopmental diseases. Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that patients with Rett syndrome (RTT), carrying MeCP2 mutations, have increased susceptibility for L1 retrotransposition. Our data demonstrate that L1 retrotransposition can be controlled in a tissue-specific manner and that disease-related genetic mutations can influence the frequency of neuronal L1 retrotransposition. Our findings add a new level of complexity to the molecular events that can lead to neurological disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059197/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059197/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muotri, Alysson R -- Marchetto, Maria C N -- Coufal, Nicole G -- Oefner, Ruth -- Yeo, Gene -- Nakashima, Kinichi -- Gage, Fred H -- 1-DP2-OD006495-01/OD/NIH HHS/ -- DP2 OD006495/OD/NIH HHS/ -- DP2 OD006495-01/OD/NIH HHS/ -- R01 MH088485/MH/NIMH NIH HHS/ -- R01 MH088485-03/MH/NIMH NIH HHS/ -- R01MH088485/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Nov 18;468(7322):443-6. doi: 10.1038/nature09544.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California San Diego, School of Medicine, Department of Pediatrics/Rady Children's Hospital San Diego, La Jolla, California 92093-0695, USA. muotri@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21085180" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/genetics ; Animals ; Brain/cytology/metabolism ; DNA Methylation ; Gene Silencing ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Long Interspersed Nucleotide Elements/*genetics ; Male ; Methyl-CpG-Binding Protein 2/deficiency/genetics/*metabolism ; Methylation ; Mice ; Neuroepithelial Cells/metabolism ; Neurons/*metabolism ; Organ Specificity ; Promoter Regions, Genetic/genetics ; Rats ; Recombination, Genetic/*genetics ; Rett Syndrome/genetics/pathology ; Transcription, Genetic/genetics
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    Cognitive remediation therapy needs funding (2010)
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    Publication Date: 2010-11-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wykes, Til -- England -- Nature. 2010 Nov 11;468(7321):165-6. doi: 10.1038/468165a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Psychiatry, King's College London. til.wykes@kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068807" target="_blank"〉PubMed〈/a〉
    Keywords: Cognitive Therapy/*economics ; Delusions/complications/prevention & control ; Employment/statistics & numerical data ; Hallucinations/complications/prevention & control ; Humans ; Male ; Quality of Life ; Schizophrenia/complications/economics/*physiopathology/*therapy ; Schizophrenic Psychology ; Treatment Outcome
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    TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs (2010)
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    Publication Date: 2010-10-22
    Description: Aberrant expression of microRNAs (miRNAs) and the enzymes that control their processing have been reported in multiple biological processes including primary and metastatic tumours, but the mechanisms governing this are not clearly understood. Here we show that TAp63, a p53 family member, suppresses tumorigenesis and metastasis, and coordinately regulates Dicer and miR-130b to suppress metastasis. Metastatic mouse and human tumours deficient in TAp63 express Dicer at very low levels, and we found that modulation of expression of Dicer and miR-130b markedly affected the metastatic potential of cells lacking TAp63. TAp63 binds to and transactivates the Dicer promoter, demonstrating direct transcriptional regulation of Dicer by TAp63. These data provide a novel understanding of the roles of TAp63 in tumour and metastasis suppression through the coordinate transcriptional regulation of Dicer and miR-130b and may have implications for the many processes regulated by miRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055799/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055799/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Xiaohua -- Chakravarti, Deepavali -- Cho, Min Soon -- Liu, Lingzhi -- Gi, Young Jin -- Lin, Yu-Li -- Leung, Marco L -- El-Naggar, Adel -- Creighton, Chad J -- Suraokar, Milind B -- Wistuba, Ignacio -- Flores, Elsa R -- 01DE019765/DE/NIDCR NIH HHS/ -- CA16672/CA/NCI NIH HHS/ -- P30 CA016672-27/CA/NCI NIH HHS/ -- P50 CA070907/CA/NCI NIH HHS/ -- P50 CA070907-10/CA/NCI NIH HHS/ -- P50 CA091846/CA/NCI NIH HHS/ -- P50 CA091846-10/CA/NCI NIH HHS/ -- P50CA070907/CA/NCI NIH HHS/ -- P50CA091846/CA/NCI NIH HHS/ -- U01 DE019765/DE/NIDCR NIH HHS/ -- U01 DE019765-03/DE/NIDCR NIH HHS/ -- England -- Nature. 2010 Oct 21;467(7318):986-90. doi: 10.1038/nature09459.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aging ; Cell Line ; Cell Line, Tumor ; DEAD-box RNA Helicases/biosynthesis/deficiency/genetics/*metabolism ; Endoribonucleases/genetics/*metabolism ; Female ; *Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor/physiology ; Genomic Instability ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*biosynthesis/genetics/metabolism ; Neoplasm Metastasis/*genetics ; Neoplasms/genetics/pathology/secretion ; Phosphoproteins/deficiency/genetics/*metabolism ; Promoter Regions, Genetic/genetics ; Ribonuclease III/biosynthesis/deficiency/genetics/*metabolism ; Trans-Activators/deficiency/genetics/*metabolism ; Transcription Factors ; Transcriptional Activation ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism
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    The ploidy conveyor of mature hepatocytes as a source of genetic variation (2010)
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    Publication Date: 2010-09-24
    Description: Mononucleated and binucleated polyploid hepatocytes (4n, 8n, 16n and higher) are found in all mammalian species, but the functional significance of this conserved phenomenon remains unknown. Polyploidization occurs through failed cytokinesis, begins at weaning in rodents and increases with age. Previously, we demonstrated that the opposite event, ploidy reversal, also occurs in polyploid hepatocytes generated by artificial cell fusion. This raised the possibility that somatic 'reductive mitoses' can also happen in normal hepatocytes. Here we show that multipolar mitotic spindles form frequently in mouse polyploid hepatocytes and can result in one-step ploidy reversal to generate offspring with halved chromosome content. Proliferating hepatocytes produce a highly diverse population of daughter cells with multiple numerical chromosome imbalances as well as uniparental origins. Our findings support a dynamic model of hepatocyte polyploidization, ploidy reversal and aneuploidy, a phenomenon that we term the 'ploidy conveyor'. We propose that this mechanism evolved to generate genetic diversity and permits adaptation of hepatocytes to xenobiotic or nutritional injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967727/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967727/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duncan, Andrew W -- Taylor, Matthew H -- Hickey, Raymond D -- Hanlon Newell, Amy E -- Lenzi, Michelle L -- Olson, Susan B -- Finegold, Milton J -- Grompe, Markus -- DK56338/DK/NIDDK NIH HHS/ -- F32 DK076232-01/DK/NIDDK NIH HHS/ -- F32DK076232/DK/NIDDK NIH HHS/ -- R01 DK067636/DK/NIDDK NIH HHS/ -- R01 DK067636-01/DK/NIDDK NIH HHS/ -- R01DK067636/DK/NIDDK NIH HHS/ -- S10-RR023432/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Oct 7;467(7316):707-10. doi: 10.1038/nature09414. Epub 2010 Sep 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oregon Stem Cell Center, Pape Family Pediatric Research Institute, Oregon Health & Science University, Portland, Oregon 97239, USA. duncanan@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20861837" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Aneuploidy ; Animals ; Chromosome Segregation ; Flow Cytometry ; *Genetic Variation ; Hepatocytes/*cytology/*metabolism ; In Situ Hybridization, Fluorescence ; Karyotyping ; Male ; Mice ; Mitosis ; *Models, Genetic ; *Polyploidy ; Spindle Apparatus/metabolism
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    Heteroplasmic mitochondrial DNA mutations in normal and tumour cells (2010)
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    Publication Date: 2010-03-05
    Description: The presence of hundreds of copies of mitochondrial DNA (mtDNA) in each human cell poses a challenge for the complete characterization of mtDNA genomes by conventional sequencing technologies. Here we describe digital sequencing of mtDNA genomes with the use of massively parallel sequencing-by-synthesis approaches. Although the mtDNA of human cells is considered to be homogeneous, we found widespread heterogeneity (heteroplasmy) in the mtDNA of normal human cells. Moreover, the frequency of heteroplasmic variants varied considerably between different tissues in the same individual. In addition to the variants identified in normal tissues, cancer cells harboured further homoplasmic and heteroplasmic mutations that could also be detected in patient plasma. These studies provide insights into the nature and variability of mtDNA sequences and have implications for mitochondrial processes during embryogenesis, cancer biomarker development and forensic analysis. In particular, they demonstrate that individual humans are characterized by a complex mixture of related mitochondrial genotypes rather than a single genotype.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176451/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176451/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yiping -- Wu, Jian -- Dressman, Devin C -- Iacobuzio-Donahue, Christine -- Markowitz, Sanford D -- Velculescu, Victor E -- Diaz, Luis A Jr -- Kinzler, Kenneth W -- Vogelstein, Bert -- Papadopoulos, Nickolas -- CA 43460/CA/NCI NIH HHS/ -- CA 62924/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- P50 CA062924/CA/NCI NIH HHS/ -- P50 CA062924-06/CA/NCI NIH HHS/ -- R01 CA057345/CA/NCI NIH HHS/ -- R01 CA057345-08/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-04/CA/NCI NIH HHS/ -- R37 CA043460/CA/NCI NIH HHS/ -- R37 CA043460-16/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Mar 25;464(7288):610-4. doi: 10.1038/nature08802. Epub 2010 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Ludwig Center for Cancer Genetics and Therapeutics and The Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, Maryland 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20200521" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Child ; Colorectal Neoplasms/*pathology ; DNA, Mitochondrial/blood/*genetics ; Female ; Gene Frequency ; *Genetic Heterogeneity ; Genetic Variation ; Genotype ; Humans ; Intestinal Mucosa/cytology/pathology ; Male ; Middle Aged ; Mutation/*genetics
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    Whole-genome resequencing reveals loci under selection during chicken domestication (2010)
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    Publication Date: 2010-03-12
    Description: Domestic animals are excellent models for genetic studies of phenotypic evolution. They have evolved genetic adaptations to a new environment, the farm, and have been subjected to strong human-driven selection leading to remarkable phenotypic changes in morphology, physiology and behaviour. Identifying the genetic changes underlying these developments provides new insight into general mechanisms by which genetic variation shapes phenotypic diversity. Here we describe the use of massively parallel sequencing to identify selective sweeps of favourable alleles and candidate mutations that have had a prominent role in the domestication of chickens (Gallus gallus domesticus) and their subsequent specialization into broiler (meat-producing) and layer (egg-producing) chickens. We have generated 44.5-fold coverage of the chicken genome using pools of genomic DNA representing eight different populations of domestic chickens as well as red jungle fowl (Gallus gallus), the major wild ancestor. We report more than 7,000,000 single nucleotide polymorphisms, almost 1,300 deletions and a number of putative selective sweeps. One of the most striking selective sweeps found in all domestic chickens occurred at the locus for thyroid stimulating hormone receptor (TSHR), which has a pivotal role in metabolic regulation and photoperiod control of reproduction in vertebrates. Several of the selective sweeps detected in broilers overlapped genes associated with growth, appetite and metabolic regulation. We found little evidence that selection for loss-of-function mutations had a prominent role in chicken domestication, but we detected two deletions in coding sequences that we suggest are functionally important. This study has direct application to animal breeding and enhances the importance of the domestic chicken as a model organism for biomedical research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubin, Carl-Johan -- Zody, Michael C -- Eriksson, Jonas -- Meadows, Jennifer R S -- Sherwood, Ellen -- Webster, Matthew T -- Jiang, Lin -- Ingman, Max -- Sharpe, Ted -- Ka, Sojeong -- Hallbook, Finn -- Besnier, Francois -- Carlborg, Orjan -- Bed'hom, Bertrand -- Tixier-Boichard, Michele -- Jensen, Per -- Siegel, Paul -- Lindblad-Toh, Kerstin -- Andersson, Leif -- England -- Nature. 2010 Mar 25;464(7288):587-91. doi: 10.1038/nature08832. Epub 2010 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry and Microbiology, Uppsala University, Box 582, SE-75123 Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220755" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Evolution ; Chickens/*genetics ; Female ; Genetic Loci/*genetics ; Genome/*genetics ; Male ; Molecular Sequence Data ; Polymorphism, Single Nucleotide ; Selection, Genetic/*genetics ; Sequence Alignment ; Sequence Analysis, DNA ; Sequence Deletion
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    Lkb1 regulates cell cycle and energy metabolism in haematopoietic stem cells (2010)
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    Publication Date: 2010-12-03
    Description: Little is known about metabolic regulation in stem cells and how this modulates tissue regeneration or tumour suppression. We studied the Lkb1 tumour suppressor and its substrate AMP-activated protein kinase (AMPK), kinases that coordinate metabolism with cell growth. Deletion of the Lkb1 (also called Stk11) gene in mice caused increased haematopoietic stem cell (HSC) division, rapid HSC depletion and pancytopenia. HSCs depended more acutely on Lkb1 for cell-cycle regulation and survival than many other haematopoietic cells. HSC depletion did not depend on mTOR activation or oxidative stress. Lkb1-deficient HSCs, but not myeloid progenitors, had reduced mitochondrial membrane potential and ATP levels. HSCs deficient for two catalytic alpha-subunits of AMPK (AMPK-deficient HSCs) showed similar changes in mitochondrial function but remained able to reconstitute irradiated mice. Lkb1-deficient HSCs, but not AMPK-deficient HSCs, exhibited defects in centrosomes and mitotic spindles in culture, and became aneuploid. Lkb1 is therefore required for HSC maintenance through AMPK-dependent and AMPK-independent mechanisms, revealing differences in metabolic and cell-cycle regulation between HSCs and some other haematopoietic progenitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059717/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059717/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakada, Daisuke -- Saunders, Thomas L -- Morrison, Sean J -- CA46592/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Dec 2;468(7324):653-8. doi: 10.1038/nature09571.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Life Sciences Institute, Center for Stem Cell Biology, University of Michigan, Ann Arbor, Michigan 48109-2216, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124450" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/chemistry/deficiency/genetics/metabolism ; Aneuploidy ; Animals ; Catalytic Domain/genetics ; Cell Cycle/*physiology ; Cell Death ; Cell Division ; Cell Survival ; Centrosome/pathology ; Energy Metabolism/*physiology ; Enzyme Activation ; Female ; Gene Deletion ; Hematopoietic Stem Cells/*cytology/drug effects/*metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Pancytopenia/genetics ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/metabolism ; Regeneration ; Signal Transduction ; Sirolimus/pharmacology ; Spindle Apparatus/pathology ; TOR Serine-Threonine Kinases/metabolism
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    LRRC26 auxiliary protein allows BK channel activation at resting voltage without calcium (2010)
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    Publication Date: 2010-07-09
    Description: Large-conductance, voltage- and calcium-activated potassium (BK, or K(Ca)1.1) channels are ubiquitously expressed in electrically excitable and non-excitable cells, either as alpha-subunit (BKalpha) tetramers or together with tissue specific auxiliary beta-subunits (beta1-beta4). Activation of BK channels typically requires coincident membrane depolarization and elevation in free cytosolic Ca(2+) concentration ([Ca(2+)](i)), which are not physiological conditions for most non-excitable cells. Here we present evidence that in non-excitable LNCaP prostate cancer cells, BK channels can be activated at negative voltages without rises in [Ca(2+)](i) through their complex with an auxiliary protein, leucine-rich repeat (LRR)-containing protein 26 (LRRC26). LRRC26 modulates the gating of a BK channel by enhancing the allosteric coupling between voltage-sensor activation and the channel's closed-open transition. This finding reveals a novel auxiliary protein of a voltage-gated ion channel that gives an unprecedentedly large negative shift ( approximately -140 mV) in voltage dependence and provides a molecular basis for activation of BK channels at physiological voltages and calcium levels in non-excitable cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, Jiusheng -- Aldrich, Richard W -- England -- Nature. 2010 Jul 22;466(7305):513-6. doi: 10.1038/nature09162. Epub 2010 Jul 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Center for Learning and Memory, University of Texas, Austin, Texas 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20613726" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Amino Acid Sequence ; Animals ; *Calcium/analysis ; Cell Line, Tumor ; Humans ; Ion Channel Gating/*physiology ; Large-Conductance Calcium-Activated Potassium Channels/genetics/*metabolism ; Male ; Membrane Potentials ; Mice ; Molecular Sequence Data ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Prostatic Neoplasms/metabolism ; Rats
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    Molecular coupling of Tsix regulation and pluripotency (2010)
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    Publication Date: 2010-11-19
    Description: The reprogramming of X-chromosome inactivation during the acquisition of pluripotency in vivo and in vitro is accompanied by the repression of Xist, the trigger of X-inactivation, and the upregulation of its antisense counterpart Tsix. We have shown that key factors supporting pluripotency-Nanog, Oct4 and Sox2-bind within Xist intron 1 in undifferentiated embryonic stem cells (ESC) to repress Xist transcription. However, the relationship between transcription factors of the pluripotency network and Tsix regulation has remained unclear. Here we show that Tsix upregulation in embryonic stem cells depends on the recruitment of the pluripotent marker Rex1, and of the reprogramming-associated factors Klf4 and c-Myc, by the DXPas34 minisatellite associated with the Tsix promoter. Upon deletion of DXPas34, binding of the three factors is abrogated and the transcriptional machinery is no longer efficiently recruited to the Tsix promoter. Additional analyses including knockdown experiments further demonstrate that Rex1 is critically important for efficient transcription elongation of Tsix. Hence, distinct embryonic-stem-cell-specific complexes couple X-inactivation reprogramming and pluripotency, with Nanog, Oct4 and Sox2 repressing Xist to facilitate the reactivation of the inactive X, and Klf4, c-Myc and Rex1 activating Tsix to remodel Xist chromatin and ensure random X-inactivation upon differentiation. The holistic pattern of Xist/Tsix regulation by pluripotent factors that we have identified suggests a general direct governance of complex epigenetic processes by the machinery dedicated to pluripotency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Navarro, Pablo -- Oldfield, Andrew -- Legoupi, Julie -- Festuccia, Nicola -- Dubois, Agnes -- Attia, Mikael -- Schoorlemmer, Jon -- Rougeulle, Claire -- Chambers, Ian -- Avner, Philip -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Nov 18;468(7322):457-60. doi: 10.1038/nature09496.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite de Genetique Moleculaire Murine, URA 2578, Institut Pasteur, 75724 Paris Cedex 15, France. pablo.navarro@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21085182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryonic Stem Cells/cytology/*metabolism ; Female ; Homeodomain Proteins/metabolism ; Kruppel-Like Transcription Factors/metabolism ; Male ; Mice ; Minisatellite Repeats/genetics ; Octamer Transcription Factor-3/metabolism ; Pluripotent Stem Cells/cytology/*metabolism ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Long Noncoding ; RNA, Untranslated/*genetics ; SOXB1 Transcription Factors/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic/*genetics ; Up-Regulation/*genetics ; X Chromosome Inactivation/genetics
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    A dimorphic pheromone circuit in Drosophila from sensory input to descending output (2010)
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    Publication Date: 2010-12-03
    Description: Drosophila show innate olfactory-driven behaviours that are observed in naive animals without previous learning or experience, suggesting that the neural circuits that mediate these behaviours are genetically programmed. Despite the numerical simplicity of the fly nervous system, features of the anatomical organization of the fly brain often confound the delineation of these circuits. Here we identify a neural circuit responsive to cVA, a pheromone that elicits sexually dimorphic behaviours. We have combined neural tracing using an improved photoactivatable green fluorescent protein (PA-GFP) with electrophysiology, optical imaging and laser-mediated microlesioning to map this circuit from the activation of sensory neurons in the antennae to the excitation of descending neurons in the ventral nerve cord. This circuit is concise and minimally comprises four neurons, connected by three synapses. Three of these neurons are overtly dimorphic and identify a male-specific neuropil that integrates inputs from multiple sensory systems and sends outputs to the ventral nerve cord. This neural pathway suggests a means by which a single pheromone can elicit different behaviours in the two sexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruta, Vanessa -- Datta, Sandeep Robert -- Vasconcelos, Maria Luisa -- Freeland, Jessica -- Looger, Loren L -- Axel, Richard -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Dec 2;468(7324):686-90. doi: 10.1038/nature09554.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics and the Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124455" target="_blank"〉PubMed〈/a〉
    Keywords: Acetates/pharmacology ; Animals ; Arthropod Antennae/cytology/drug effects/innervation ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/anatomy & histology/*cytology/*drug effects ; Female ; Male ; Nerve Tissue Proteins/genetics/metabolism ; Neuroanatomical Tract-Tracing Techniques ; Odors ; Oleic Acids/pharmacology ; Olfactory Pathways/cytology/*drug effects ; Olfactory Perception/drug effects/physiology ; Pheromones/*pharmacology ; Physical Stimulation ; Sensory Receptor Cells/drug effects/physiology ; *Sex Characteristics ; Sexual Behavior, Animal/drug effects/physiology ; Transcription Factors/genetics/metabolism
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    The rise of the genome bloggers (2010)
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    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2010 Dec 16;468(7326):880-1. doi: 10.1038/468880a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164454" target="_blank"〉PubMed〈/a〉
    Keywords: *Blogging/trends/utilization ; Genetic Association Studies ; Genetic Privacy ; Genetics, Population/manpower ; Genome, Human/*genetics ; Genomics/*manpower/trends ; *Hobbies/statistics & numerical data ; Humans ; Jews/genetics ; Male ; Pedigree ; Precision Medicine
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    Long-term potentiation depends on release of D-serine from astrocytes (2010)
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    Publication Date: 2010-01-16
    Description: Long-term potentiation (LTP) of synaptic transmission provides an experimental model for studying mechanisms of memory. The classical form of LTP relies on N-methyl-D-aspartate receptors (NMDARs), and it has been shown that astroglia can regulate their activation through Ca(2+)-dependent release of the NMDAR co-agonist D-serine. Release of D-serine from glia enables LTP in cultures and explains a correlation between glial coverage of synapses and LTP in the supraoptic nucleus. However, increases in Ca(2+) concentration in astroglia can also release other signalling molecules, most prominently glutamate, ATP and tumour necrosis factor-alpha, whereas neurons themselves can synthesize and supply D-serine. Furthermore, loading an astrocyte with exogenous Ca(2+) buffers does not suppress LTP in hippocampal area CA1 (refs 14-16), and the physiological relevance of experiments in cultures or strong exogenous stimuli applied to astrocytes has been questioned. The involvement of glia in LTP induction therefore remains controversial. Here we show that clamping internal Ca(2+) in individual CA1 astrocytes blocks LTP induction at nearby excitatory synapses by decreasing the occupancy of the NMDAR co-agonist sites. This LTP blockade can be reversed by exogenous D-serine or glycine, whereas depletion of D-serine or disruption of exocytosis in an individual astrocyte blocks local LTP. We therefore demonstrate that Ca(2+)-dependent release of D-serine from an astrocyte controls NMDAR-dependent plasticity in many thousands of excitatory synapses nearby.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807667/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807667/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henneberger, Christian -- Papouin, Thomas -- Oliet, Stephane H R -- Rusakov, Dmitri A -- 084311/Wellcome Trust/United Kingdom -- G0600368/Medical Research Council/United Kingdom -- G0600368(77987)/Medical Research Council/United Kingdom -- G0802216/Medical Research Council/United Kingdom -- G0802216(89644)/Medical Research Council/United Kingdom -- G0900613/Medical Research Council/United Kingdom -- G0900613(91064)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jan 14;463(7278):232-6. doi: 10.1038/nature08673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UCL Institute of Neurology, University College London, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/drug effects/metabolism/*secretion ; Calcium/antagonists & inhibitors/metabolism ; Exocytosis/drug effects ; Glycine/pharmacology ; Hippocampus/cytology/drug effects/physiology ; Long-Term Potentiation/drug effects/*physiology ; Male ; Memory/drug effects/physiology ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/agonists/metabolism ; Serine/biosynthesis/metabolism/pharmacology/*secretion ; Synapses/drug effects/metabolism
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    Drug safety crackdown revs up (2010)
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    Publication Date: 2010-08-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2010 Aug 5;466(7307):677. doi: 10.1038/466677a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20686544" target="_blank"〉PubMed〈/a〉
    Keywords: Benzazepines/*adverse effects ; Female ; Humans ; Male ; *Product Surveillance, Postmarketing ; Quinoxalines/*adverse effects ; Risk Assessment ; Thiazolidinediones/adverse effects ; United States ; United States Food and Drug Administration/*legislation & jurisprudence ; Varenicline ; Violence
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    B-cell-derived lymphotoxin promotes castration-resistant prostate cancer (2010)
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    Publication Date: 2010-03-12
    Description: Prostate cancer (CaP) progresses from prostatic intraepithelial neoplasia through locally invasive adenocarcinoma to castration-resistant metastatic carcinoma. Although radical prostatectomy, radiation and androgen ablation are effective therapies for androgen-dependent CaP, metastatic castration-resistant CaP is a major complication with high mortality. Androgens stimulate growth and survival of prostate epithelium and early CaP. Although most patients initially respond to androgen ablation, many develop castration-resistant CaP within 12-18 months. Despite extensive studies, the mechanisms underlying the emergence of castration-resistant CaP remain poorly understood and their elucidation is critical for developing improved therapies. Curiously, castration-resistant CaP remains androgen-receptor dependent, and potent androgen-receptor antagonists induce tumour regression in castrated mice. The role of inflammation in castration-resistant CaP has not been addressed, although it was reported that intrinsic NF-kappaB activation supports its growth. Inflammation is a localized protective reaction to injury or infection, but it also has a pathogenic role in many diseases, including cancer. Whereas acute inflammation is critical for host defence, chronic inflammation contributes to tumorigenesis and metastatic progression. The inflammation-responsive IkappaB kinase (IKK)-beta and its target NF-kappaB have important tumour-promoting functions within malignant cells and inflammatory cells. The latter, including macrophages and lymphocytes, are important elements of the tumour microenvironment, but the mechanisms underlying their recruitment remain obscure, although they are thought to depend on chemokine and cytokine production. We found that CaP progression is associated with inflammatory infiltration and activation of IKK-alpha, which stimulates metastasis by an NF-kappaB-independent, cell autonomous mechanism. Here we show that androgen ablation causes infiltration of regressing androgen-dependent tumours with leukocytes, including B cells, in which IKK-beta activation results in production of cytokines that activate IKK-alpha and STAT3 in CaP cells to enhance hormone-free survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866639/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866639/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ammirante, Massimo -- Luo, Jun-Li -- Grivennikov, Sergei -- Nedospasov, Sergei -- Karin, Michael -- R01 CA127923/CA/NCI NIH HHS/ -- R01 CA127923-04/CA/NCI NIH HHS/ -- England -- Nature. 2010 Mar 11;464(7286):302-5. doi: 10.1038/nature08782.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology and Cancer Center, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0723, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220849" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/metabolism ; Animals ; B-Lymphocytes/*metabolism ; Humans ; I-kappa B Kinase/genetics/metabolism ; Lymphotoxin-alpha/*metabolism ; Male ; Mice ; Orchiectomy ; Prostate/metabolism/pathology ; Prostatic Neoplasms/*metabolism/*pathology/physiopathology ; Survival Analysis
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    Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS (2010)
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    Publication Date: 2010-08-27
    Description: The causes of amyotrophic lateral sclerosis (ALS), a devastating human neurodegenerative disease, are poorly understood, although the protein TDP-43 has been suggested to have a critical role in disease pathogenesis. Here we show that ataxin 2 (ATXN2), a polyglutamine (polyQ) protein mutated in spinocerebellar ataxia type 2, is a potent modifier of TDP-43 toxicity in animal and cellular models. ATXN2 and TDP-43 associate in a complex that depends on RNA. In spinal cord neurons of ALS patients, ATXN2 is abnormally localized; likewise, TDP-43 shows mislocalization in spinocerebellar ataxia type 2. To assess the involvement of ATXN2 in ALS, we analysed the length of the polyQ repeat in the ATXN2 gene in 915 ALS patients. We found that intermediate-length polyQ expansions (27-33 glutamines) in ATXN2 were significantly associated with ALS. These data establish ATXN2 as a relatively common ALS susceptibility gene. Furthermore, these findings indicate that the TDP-43-ATXN2 interaction may be a promising target for therapeutic intervention in ALS and other TDP-43 proteinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965417/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965417/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elden, Andrew C -- Kim, Hyung-Jun -- Hart, Michael P -- Chen-Plotkin, Alice S -- Johnson, Brian S -- Fang, Xiaodong -- Armakola, Maria -- Geser, Felix -- Greene, Robert -- Lu, Min Min -- Padmanabhan, Arun -- Clay-Falcone, Dana -- McCluskey, Leo -- Elman, Lauren -- Juhr, Denise -- Gruber, Peter J -- Rub, Udo -- Auburger, Georg -- Trojanowski, John Q -- Lee, Virginia M-Y -- Van Deerlin, Vivianna M -- Bonini, Nancy M -- Gitler, Aaron D -- 1DP2OD004417-01/OD/NIH HHS/ -- 1R01NS065317-01/NS/NINDS NIH HHS/ -- AG-10124/AG/NIA NIH HHS/ -- AG-17586/AG/NIA NIH HHS/ -- DP2 OD004417/OD/NIH HHS/ -- DP2 OD004417-01/OD/NIH HHS/ -- K08 AG-033101-01/AG/NIA NIH HHS/ -- P01 AG-09215/AG/NIA NIH HHS/ -- R01 NS065317/NS/NINDS NIH HHS/ -- R01 NS065317-01/NS/NINDS NIH HHS/ -- R01 NS065317-02/NS/NINDS NIH HHS/ -- R01 NS065317-03/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Aug 26;466(7310):1069-75. doi: 10.1038/nature09320.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20740007" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Amyotrophic Lateral Sclerosis/*genetics ; Animals ; Ataxins ; Cell Line ; DNA-Binding Proteins/metabolism/toxicity ; Drosophila/drug effects/genetics ; Female ; *Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Nerve Tissue Proteins/*genetics/*metabolism ; Neurons/pathology ; Peptides/chemistry/*genetics ; Repetitive Sequences, Amino Acid/*genetics ; Risk Factors ; Saccharomyces cerevisiae/drug effects/genetics/metabolism ; Young Adult
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    SIRT3 regulates mitochondrial fatty-acid oxidation by reversible enzyme deacetylation (2010)
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    Publication Date: 2010-03-06
    Description: Sirtuins are NAD(+)-dependent protein deacetylases. They mediate adaptive responses to a variety of stresses, including calorie restriction and metabolic stress. Sirtuin 3 (SIRT3) is localized in the mitochondrial matrix, where it regulates the acetylation levels of metabolic enzymes, including acetyl coenzyme A synthetase 2 (refs 1, 2). Mice lacking both Sirt3 alleles appear phenotypically normal under basal conditions, but show marked hyperacetylation of several mitochondrial proteins. Here we report that SIRT3 expression is upregulated during fasting in liver and brown adipose tissues. During fasting, livers from mice lacking SIRT3 had higher levels of fatty-acid oxidation intermediate products and triglycerides, associated with decreased levels of fatty-acid oxidation, compared to livers from wild-type mice. Mass spectrometry of mitochondrial proteins shows that long-chain acyl coenzyme A dehydrogenase (LCAD) is hyperacetylated at lysine 42 in the absence of SIRT3. LCAD is deacetylated in wild-type mice under fasted conditions and by SIRT3 in vitro and in vivo; and hyperacetylation of LCAD reduces its enzymatic activity. Mice lacking SIRT3 exhibit hallmarks of fatty-acid oxidation disorders during fasting, including reduced ATP levels and intolerance to cold exposure. These findings identify acetylation as a novel regulatory mechanism for mitochondrial fatty-acid oxidation and demonstrate that SIRT3 modulates mitochondrial intermediary metabolism and fatty-acid use during fasting.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841477/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841477/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirschey, Matthew D -- Shimazu, Tadahiro -- Goetzman, Eric -- Jing, Enxuan -- Schwer, Bjoern -- Lombard, David B -- Grueter, Carrie A -- Harris, Charles -- Biddinger, Sudha -- Ilkayeva, Olga R -- Stevens, Robert D -- Li, Yu -- Saha, Asish K -- Ruderman, Neil B -- Bain, James R -- Newgard, Christopher B -- Farese, Robert V Jr -- Alt, Frederick W -- Kahn, C Ronald -- Verdin, Eric -- DK019514-29/DK/NIDDK NIH HHS/ -- DK59637/DK/NIDDK NIH HHS/ -- K01 DK076573/DK/NIDDK NIH HHS/ -- K08 AG022325/AG/NIA NIH HHS/ -- K08 AG022325-01A1/AG/NIA NIH HHS/ -- P01 HL068758/HL/NHLBI NIH HHS/ -- P01 HL068758-06A1/HL/NHLBI NIH HHS/ -- P30 DK026743/DK/NIDDK NIH HHS/ -- P30 DK026743-26A1/DK/NIDDK NIH HHS/ -- R01 DK019514/DK/NIDDK NIH HHS/ -- R01 DK019514-29/DK/NIDDK NIH HHS/ -- R01 DK067509/DK/NIDDK NIH HHS/ -- R01 DK067509-04/DK/NIDDK NIH HHS/ -- U24 DK059637/DK/NIDDK NIH HHS/ -- U24 DK059637-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Mar 4;464(7285):121-5. doi: 10.1038/nature08778.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203611" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acyl-CoA Dehydrogenase, Long-Chain/chemistry/*metabolism ; Adenosine Triphosphate/biosynthesis/metabolism ; Adipose Tissue, Brown/enzymology/metabolism ; Animals ; Body Temperature Regulation ; Caloric Restriction ; Carnitine/analogs & derivatives/metabolism ; Cell Line ; Cold Temperature ; Fasting/metabolism ; Fatty Acids/*metabolism ; Humans ; Hypoglycemia/metabolism ; Liver/enzymology/metabolism ; Male ; Mass Spectrometry ; Mice ; Mitochondria/*enzymology/*metabolism ; Oxidation-Reduction ; Sirtuin 3/deficiency/genetics/*metabolism ; Triglycerides/metabolism ; Up-Regulation
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    Globe still in grip of addiction (2010)
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    Publication Date: 2010-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Samet, Jonathan M -- Wipfli, Heather L -- England -- Nature. 2010 Feb 25;463(7284):1020-1. doi: 10.1038/4631020a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Southern California, Keck School of Medicine, Department of Preventive Medicine and USC Institute for Global Health, Los Angeles, California 90033, USA. jsamet@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20182492" target="_blank"〉PubMed〈/a〉
    Keywords: Developed Countries/statistics & numerical data ; Developing Countries/*statistics & numerical data ; Female ; Global Health ; Humans ; International Cooperation ; Male ; Public Health ; Smoking/adverse effects/*epidemiology/legislation & jurisprudence/*prevention & ; control ; Tobacco/adverse effects ; Tobacco Smoke Pollution/adverse effects/legislation & jurisprudence/prevention & ; control ; Tobacco Use Disorder/*epidemiology/etiology/*prevention & control ; World Health Organization
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    Unexpected requirement for ELMO1 in clearance of apoptotic germ cells in vivo (2010)
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    Publication Date: 2010-09-17
    Description: Apoptosis and the subsequent clearance of dying cells occurs throughout development and adult life in many tissues. Failure to promptly clear apoptotic cells has been linked to many diseases. ELMO1 is an evolutionarily conserved cytoplasmic engulfment protein that functions downstream of the phosphatidylserine receptor BAI1, and, along with DOCK1 and the GTPase RAC1, promotes internalization of the dying cells. Here we report the generation of ELMO1-deficient mice, which we found to be unexpectedly viable and grossly normal. However, they had a striking testicular pathology, with disrupted seminiferous epithelium, multinucleated giant cells, uncleared apoptotic germ cells and decreased sperm output. Subsequent in vitro and in vivo analyses revealed a crucial role for ELMO1 in the phagocytic clearance of apoptotic germ cells by Sertoli cells lining the seminiferous epithelium. The engulfment receptor BAI1 and RAC1 (upstream and downstream of ELMO1, respectively) were also important for Sertoli-cell-mediated engulfment. Collectively, these findings uncover a selective requirement for ELMO1 in Sertoli-cell-mediated removal of apoptotic germ cells and make a compelling case for a relationship between engulfment and tissue homeostasis in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773546/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elliott, Michael R -- Zheng, Shuqiu -- Park, Daeho -- Woodson, Robin I -- Reardon, Michael A -- Juncadella, Ignacio J -- Kinchen, Jason M -- Zhang, Jun -- Lysiak, Jeffrey J -- Ravichandran, Kodi S -- R01 GM064709/GM/NIGMS NIH HHS/ -- R01 HD057242/HD/NICHD NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):333-7. doi: 10.1038/nature09356.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20844538" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/deficiency/genetics/*metabolism ; Angiogenic Proteins/metabolism ; Animals ; *Apoptosis ; Cell Line ; Homeostasis ; Male ; Mice ; Mice, Inbred C57BL ; Neuropeptides/metabolism ; Phagocytosis/*physiology ; Phosphatidylserines/metabolism ; Seminiferous Epithelium/cytology/pathology ; Sertoli Cells/*cytology/*metabolism/pathology ; Signal Transduction ; Spermatozoa/*cytology/pathology ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein
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    A shot in the arm for cancer vaccines? (2010)
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    Publication Date: 2010-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2010 Apr 22;464(7292):1110-1. doi: 10.1038/4641110a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20414279" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Phosphatase ; Antigens, Neoplasm/immunology ; Cancer Vaccines/*immunology/standards ; Dendritic Cells/immunology/transplantation ; Drug Approval/legislation & jurisprudence ; Humans ; Male ; Prostatic Neoplasms/*immunology/*therapy ; Protein Tyrosine Phosphatases/immunology ; United States ; United States Food and Drug Administration/*legislation & jurisprudence
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    Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring (2010)
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    Publication Date: 2010-10-22
    Description: The global prevalence of obesity is increasing across most ages in both sexes. This is contributing to the early emergence of type 2 diabetes and its related epidemic. Having either parent obese is an independent risk factor for childhood obesity. Although the detrimental impacts of diet-induced maternal obesity on adiposity and metabolism in offspring are well established, the extent of any contribution of obese fathers is unclear, particularly the role of non-genetic factors in the causal pathway. Here we show that paternal high-fat-diet (HFD) exposure programs beta-cell 'dysfunction' in rat F(1) female offspring. Chronic HFD consumption in Sprague-Dawley fathers induced increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had an early onset of impaired insulin secretion and glucose tolerance that worsened with time, and normal adiposity. Paternal HFD altered the expression of 642 pancreatic islet genes in adult female offspring (P 〈 0.01); genes belonged to 13 functional clusters, including cation and ATP binding, cytoskeleton and intracellular transport. Broader pathway analysis of 2,492 genes differentially expressed (P 〈 0.05) demonstrated involvement of calcium-, MAPK- and Wnt-signalling pathways, apoptosis and the cell cycle. Hypomethylation of the Il13ra2 gene, which showed the highest fold difference in expression (1.76-fold increase), was demonstrated. This is the first report in mammals of non-genetic, intergenerational transmission of metabolic sequelae of a HFD from father to offspring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, Sheau-Fang -- Lin, Ruby C Y -- Laybutt, D Ross -- Barres, Romain -- Owens, Julie A -- Morris, Margaret J -- England -- Nature. 2010 Oct 21;467(7318):963-6. doi: 10.1038/nature09491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medical Sciences, University of New South Wales, New South Wales, Sydney 2052, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962845" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Adiposity/drug effects ; Aging/genetics ; Animals ; Apoptosis/genetics ; Body Weight/drug effects ; Cations/metabolism ; Cell Cycle/genetics ; Cytoskeleton/metabolism ; DNA Methylation/drug effects ; Diabetes Mellitus, Type 2/etiology/pathology/physiopathology ; Diet/*adverse effects ; Dietary Fats/*administration & dosage/*adverse effects ; Epigenesis, Genetic/drug effects ; *Fathers ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Glucose/pharmacology ; Glucose Intolerance/etiology/pathology/physiopathology ; Glucose Tolerance Test ; Homeostasis/drug effects ; Insulin/secretion ; Insulin-Secreting Cells/metabolism/*pathology/secretion ; Litter Size ; Male ; Obesity/etiology/pathology/physiopathology ; Paternal Exposure/*adverse effects ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/genetics
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    Africa yields two full human genomes (2010)
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    Publication Date: 2010-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2010 Feb 18;463(7283):857. doi: 10.1038/463857a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164887" target="_blank"〉PubMed〈/a〉
    Keywords: African Continental Ancestry Group/*genetics ; Ethnic Groups/*genetics ; Genetic Variation/genetics ; Genome, Human/*genetics ; *Genomics/trends ; Humans ; Malaria, Vivax/genetics ; Male ; Minority Groups ; Phylogeny ; South Africa/ethnology
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    Striatal microRNA controls cocaine intake through CREB signalling (2010)
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    Publication Date: 2010-07-09
    Description: Cocaine addiction is characterized by a gradual loss of control over drug use, but the molecular mechanisms regulating vulnerability to this process remain unclear. Here we report that microRNA-212 (miR-212) is upregulated in the dorsal striatum of rats with a history of extended access to cocaine. Striatal miR-212 decreases responsiveness to the motivational properties of cocaine by markedly amplifying the stimulatory effects of the drug on cAMP response element binding protein (CREB) signalling. This action occurs through miR-212-enhanced Raf1 activity, resulting in adenylyl cyclase sensitization and increased expression of the essential CREB co-activator TORC (transducer of regulated CREB; also known as CRTC). Our findings indicate that striatal miR-212 signalling has a key role in determining vulnerability to cocaine addiction, reveal new molecular regulators that control the complex actions of cocaine in brain reward circuitries and provide an entirely new direction for the development of anti-addiction therapeutics based on the modulation of noncoding RNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916751/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916751/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hollander, Jonathan A -- Im, Heh-In -- Amelio, Antonio L -- Kocerha, Jannet -- Bali, Purva -- Lu, Qun -- Willoughby, David -- Wahlestedt, Claes -- Conkright, Michael D -- Kenny, Paul J -- F32 CA134121/CA/NCI NIH HHS/ -- F32 DA024932/DA/NIDA NIH HHS/ -- R01 DA025983/DA/NIDA NIH HHS/ -- R01 DA025983-03/DA/NIDA NIH HHS/ -- England -- Nature. 2010 Jul 8;466(7303):197-202. doi: 10.1038/nature09202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Behavioral and Molecular Neuroscience, Department of Molecular Therapeutics, The Scripps Research Institute, Scripps Florida, Jupiter, Florida 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20613834" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Cocaine/*metabolism/pharmacology ; Cocaine-Related Disorders/drug therapy/enzymology/*genetics/*metabolism ; Cyclic AMP Response Element-Binding Protein/*metabolism ; MAP Kinase Kinase Kinases/metabolism ; Male ; MicroRNAs/biosynthesis/genetics/*metabolism ; Neostriatum/drug effects/*metabolism ; Rats ; Rats, Wistar ; Reward ; *Signal Transduction/drug effects ; Transcription Factors/metabolism ; Up-Regulation/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 79
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    Gender agenda: positive steps taken in Germany (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeeb, Hajo -- Spallek, Jacob -- Jahn, Ingeborg -- England -- Nature. 2010 Jul 15;466(7304):315. doi: 10.1038/466315b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631777" target="_blank"〉PubMed〈/a〉
    Keywords: Bias (Epidemiology) ; Biomedical Research/standards ; Chronic Disease/*epidemiology ; Cohort Studies ; Female ; Germany ; Humans ; Male ; *Patient Selection ; Public Health/standards ; Research Personnel/*statistics & numerical data ; Sex Distribution
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Patient-specific induced pluripotent stem-cell-derived models of LEOPARD syndrome (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-11
    Description: The generation of reprogrammed induced pluripotent stem cells (iPSCs) from patients with defined genetic disorders holds the promise of increased understanding of the aetiologies of complex diseases and may also facilitate the development of novel therapeutic interventions. We have generated iPSCs from patients with LEOPARD syndrome (an acronym formed from its main features; that is, lentigines, electrocardiographic abnormalities, ocular hypertelorism, pulmonary valve stenosis, abnormal genitalia, retardation of growth and deafness), an autosomal-dominant developmental disorder belonging to a relatively prevalent class of inherited RAS-mitogen-activated protein kinase signalling diseases, which also includes Noonan syndrome, with pleomorphic effects on several tissues and organ systems. The patient-derived cells have a mutation in the PTPN11 gene, which encodes the SHP2 phosphatase. The iPSCs have been extensively characterized and produce multiple differentiated cell lineages. A major disease phenotype in patients with LEOPARD syndrome is hypertrophic cardiomyopathy. We show that in vitro-derived cardiomyocytes from LEOPARD syndrome iPSCs are larger, have a higher degree of sarcomeric organization and preferential localization of NFATC4 in the nucleus when compared with cardiomyocytes derived from human embryonic stem cells or wild-type iPSCs derived from a healthy brother of one of the LEOPARD syndrome patients. These features correlate with a potential hypertrophic state. We also provide molecular insights into signalling pathways that may promote the disease phenotype.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885001/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885001/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carvajal-Vergara, Xonia -- Sevilla, Ana -- D'Souza, Sunita L -- Ang, Yen-Sin -- Schaniel, Christoph -- Lee, Dung-Fang -- Yang, Lei -- Kaplan, Aaron D -- Adler, Eric D -- Rozov, Roye -- Ge, Yongchao -- Cohen, Ninette -- Edelmann, Lisa J -- Chang, Betty -- Waghray, Avinash -- Su, Jie -- Pardo, Sherly -- Lichtenbelt, Klaske D -- Tartaglia, Marco -- Gelb, Bruce D -- Lemischka, Ihor R -- 5R01GM078465/GM/NIGMS NIH HHS/ -- R01 GM078465/GM/NIGMS NIH HHS/ -- R01 GM078465-03/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Jun 10;465(7299):808-12. doi: 10.1038/nature09005.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Gene and Cell Medicine, Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, New York 10029, USA. xcarvajal@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535210" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cells, Cultured ; Embryonic Stem Cells/metabolism ; Enzyme Activation ; Female ; Fibroblasts/metabolism/pathology ; Gene Expression Profiling ; Homeodomain Proteins/genetics ; Humans ; Induced Pluripotent Stem Cells/enzymology/metabolism/*pathology ; LEOPARD Syndrome/drug therapy/metabolism/*pathology ; Male ; Mitogen-Activated Protein Kinases/metabolism ; *Models, Biological ; Myocytes, Cardiac/metabolism/pathology ; NFATC Transcription Factors/genetics/metabolism ; Octamer Transcription Factor-3/genetics ; Phosphoproteins/analysis ; Polymerase Chain Reaction ; *Precision Medicine ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/genetics/metabolism ; SOXB1 Transcription Factors/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Biological, clinical and population relevance of 95 loci for blood lipids (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-06
    Description: Plasma concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides are among the most important risk factors for coronary artery disease (CAD) and are targets for therapeutic intervention. We screened the genome for common variants associated with plasma lipids in 〉100,000 individuals of European ancestry. Here we report 95 significantly associated loci (P 〈 5 x 10(-8)), with 59 showing genome-wide significant association with lipid traits for the first time. The newly reported associations include single nucleotide polymorphisms (SNPs) near known lipid regulators (for example, CYP7A1, NPC1L1 and SCARB1) as well as in scores of loci not previously implicated in lipoprotein metabolism. The 95 loci contribute not only to normal variation in lipid traits but also to extreme lipid phenotypes and have an impact on lipid traits in three non-European populations (East Asians, South Asians and African Americans). Our results identify several novel loci associated with plasma lipids that are also associated with CAD. Finally, we validated three of the novel genes-GALNT2, PPP1R3B and TTC39B-with experiments in mouse models. Taken together, our findings provide the foundation to develop a broader biological understanding of lipoprotein metabolism and to identify new therapeutic opportunities for the prevention of CAD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039276/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039276/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teslovich, Tanya M -- Musunuru, Kiran -- Smith, Albert V -- Edmondson, Andrew C -- Stylianou, Ioannis M -- Koseki, Masahiro -- Pirruccello, James P -- Ripatti, Samuli -- Chasman, Daniel I -- Willer, Cristen J -- Johansen, Christopher T -- Fouchier, Sigrid W -- Isaacs, Aaron -- Peloso, Gina M -- Barbalic, Maja -- Ricketts, Sally L -- Bis, Joshua C -- Aulchenko, Yurii S -- Thorleifsson, Gudmar -- Feitosa, Mary F -- Chambers, John -- Orho-Melander, Marju -- Melander, Olle -- Johnson, Toby -- Li, Xiaohui -- Guo, Xiuqing -- Li, Mingyao -- Shin Cho, Yoon -- Jin Go, Min -- Jin Kim, Young -- Lee, Jong-Young -- Park, Taesung -- Kim, Kyunga -- Sim, Xueling -- Twee-Hee Ong, Rick -- Croteau-Chonka, Damien C -- Lange, Leslie A -- Smith, Joshua D -- Song, Kijoung -- Hua Zhao, Jing -- Yuan, Xin -- Luan, Jian'an -- Lamina, Claudia -- Ziegler, Andreas -- Zhang, Weihua -- Zee, Robert Y L -- Wright, Alan F -- Witteman, Jacqueline C M -- Wilson, James F -- Willemsen, Gonneke -- Wichmann, H-Erich -- Whitfield, John B -- Waterworth, Dawn M -- Wareham, Nicholas J -- Waeber, Gerard -- Vollenweider, Peter -- Voight, Benjamin F -- Vitart, Veronique -- Uitterlinden, Andre G -- Uda, Manuela -- Tuomilehto, Jaakko -- Thompson, John R -- Tanaka, Toshiko -- Surakka, Ida -- Stringham, Heather M -- Spector, Tim D -- Soranzo, Nicole -- Smit, Johannes H -- Sinisalo, Juha -- Silander, Kaisa -- Sijbrands, Eric J G -- Scuteri, Angelo -- Scott, James -- Schlessinger, David -- Sanna, Serena -- Salomaa, Veikko -- Saharinen, Juha -- Sabatti, Chiara -- Ruokonen, Aimo -- Rudan, Igor -- Rose, Lynda M -- Roberts, Robert -- Rieder, Mark -- Psaty, Bruce M -- Pramstaller, Peter P -- Pichler, Irene -- Perola, Markus -- Penninx, Brenda W J H -- Pedersen, Nancy L -- Pattaro, Cristian -- Parker, Alex N -- Pare, Guillaume -- Oostra, Ben A -- O'Donnell, Christopher J -- Nieminen, Markku S -- Nickerson, Deborah A -- Montgomery, Grant W -- Meitinger, Thomas -- McPherson, Ruth -- McCarthy, Mark I -- McArdle, Wendy -- Masson, David -- Martin, Nicholas G -- Marroni, Fabio -- Mangino, Massimo -- Magnusson, Patrik K E -- Lucas, Gavin -- Luben, Robert -- Loos, Ruth J F -- Lokki, Marja-Liisa -- Lettre, Guillaume -- Langenberg, Claudia -- Launer, Lenore J -- Lakatta, Edward G -- Laaksonen, Reijo -- Kyvik, Kirsten O -- Kronenberg, Florian -- Konig, Inke R -- Khaw, Kay-Tee -- Kaprio, Jaakko -- Kaplan, Lee M -- Johansson, Asa -- Jarvelin, Marjo-Riitta -- Janssens, A Cecile J W -- Ingelsson, Erik -- Igl, Wilmar -- Kees Hovingh, G -- Hottenga, Jouke-Jan -- Hofman, Albert -- Hicks, Andrew A -- Hengstenberg, Christian -- Heid, Iris M -- Hayward, Caroline -- Havulinna, Aki S -- Hastie, Nicholas D -- Harris, Tamara B -- Haritunians, Talin -- Hall, Alistair S -- Gyllensten, Ulf -- Guiducci, Candace -- Groop, Leif C -- Gonzalez, Elena -- Gieger, Christian -- Freimer, Nelson B -- Ferrucci, Luigi -- Erdmann, Jeanette -- Elliott, Paul -- Ejebe, Kenechi G -- Doring, Angela -- Dominiczak, Anna F -- Demissie, Serkalem -- Deloukas, Panagiotis -- de Geus, Eco J C -- de Faire, Ulf -- Crawford, Gabriel -- Collins, Francis S -- Chen, Yii-der I -- Caulfield, Mark J -- Campbell, Harry -- Burtt, Noel P -- Bonnycastle, Lori L -- Boomsma, Dorret I -- Boekholdt, S Matthijs -- Bergman, Richard N -- Barroso, Ines -- Bandinelli, Stefania -- Ballantyne, Christie M -- Assimes, Themistocles L -- Quertermous, Thomas -- Altshuler, David -- Seielstad, Mark -- Wong, Tien Y -- Tai, E-Shyong -- Feranil, Alan B -- Kuzawa, Christopher W -- Adair, Linda S -- Taylor, Herman A Jr -- Borecki, Ingrid B -- Gabriel, Stacey B -- Wilson, James G -- Holm, Hilma -- Thorsteinsdottir, Unnur -- Gudnason, Vilmundur -- Krauss, Ronald M -- Mohlke, Karen L -- Ordovas, Jose M -- Munroe, Patricia B -- Kooner, Jaspal S -- Tall, Alan R -- Hegele, Robert A -- Kastelein, John J P -- Schadt, Eric E -- Rotter, Jerome I -- Boerwinkle, Eric -- Strachan, David P -- Mooser, Vincent -- Stefansson, Kari -- Reilly, Muredach P -- Samani, Nilesh J -- Schunkert, Heribert -- Cupples, L Adrienne -- Sandhu, Manjinder S -- Ridker, Paul M -- Rader, Daniel J -- van Duijn, Cornelia M -- Peltonen, Leena -- Abecasis, Goncalo R -- Boehnke, Michael -- Kathiresan, Sekar -- 068545/Z/02/Wellcome Trust/United Kingdom -- 076113/B/04/Z/Wellcome Trust/United Kingdom -- 077016/Z/05/Z/Wellcome Trust/United Kingdom -- 079895/Wellcome Trust/United Kingdom -- 1Z01 HG000024/HG/NHGRI NIH HHS/ -- 5R01DK06833603/DK/NIDDK NIH HHS/ -- 5R01DK07568102/DK/NIDDK NIH HHS/ -- 5R01HL087679-02/HL/NHLBI NIH HHS/ -- 5R01HL08770003/HL/NHLBI NIH HHS/ -- 5R01HL08821502/HL/NHLBI NIH HHS/ -- CA 047988/CA/NCI NIH HHS/ -- CZB/4/710/Chief Scientist Office/United Kingdom -- DK062370/DK/NIDDK NIH HHS/ -- DK063491/DK/NIDDK NIH HHS/ -- DK072193/DK/NIDDK NIH HHS/ -- DK078150/DK/NIDDK NIH HHS/ -- DK56350/DK/NIDDK NIH HHS/ -- ES10126/ES/NIEHS NIH HHS/ -- G0000934/Medical Research Council/United Kingdom -- G0401527/Medical Research Council/United Kingdom -- G0601966/Medical Research Council/United Kingdom -- G0700931/Medical Research Council/United Kingdom -- G0701863/Medical Research Council/United Kingdom -- G0801056/Medical Research Council/United Kingdom -- G0801566/Medical Research Council/United Kingdom -- G9521010/Medical Research Council/United Kingdom -- G9521010D/Medical Research Council/United Kingdom -- HHSN268200625226C/PHS HHS/ -- HL 04381/HL/NHLBI NIH HHS/ -- HL 080467/HL/NHLBI NIH HHS/ -- HL-54776/HL/NHLBI NIH HHS/ -- HL085144/HL/NHLBI NIH HHS/ -- K99 HL098364/HL/NHLBI NIH HHS/ -- K99 HL098364-01/HL/NHLBI NIH HHS/ -- K99HL094535/HL/NHLBI NIH HHS/ -- M01-RR00425/RR/NCRR NIH HHS/ -- MC_QA137934/Medical Research Council/United Kingdom -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U106188470/Medical Research Council/United Kingdom -- MC_U127561128/Medical Research Council/United Kingdom -- N01 HC-15103/HC/NHLBI NIH HHS/ -- N01 HC-55222/HC/NHLBI NIH HHS/ -- N01-AG-12100/AG/NIA NIH HHS/ -- N01-HC-25195/HC/NHLBI NIH HHS/ -- N01-HC-35129/HC/NHLBI NIH HHS/ -- N01-HC-45133/HC/NHLBI NIH HHS/ -- N01-HC-55015/HC/NHLBI NIH HHS/ -- N01-HC-55016/HC/NHLBI NIH HHS/ -- N01-HC-55018/HC/NHLBI NIH HHS/ -- N01-HC-55019/HC/NHLBI NIH HHS/ -- N01-HC-55020/HC/NHLBI NIH HHS/ -- N01-HC-55021/HC/NHLBI NIH HHS/ -- N01-HC-55022/HC/NHLBI NIH HHS/ -- N01-HC-75150/HC/NHLBI NIH HHS/ -- N01-HC-85079/HC/NHLBI NIH HHS/ -- N01-HC-85080/HC/NHLBI NIH HHS/ -- N01-HC-85081/HC/NHLBI NIH HHS/ -- N01-HC-85082/HC/NHLBI NIH HHS/ -- N01-HC-85083/HC/NHLBI NIH HHS/ -- N01-HC-85084/HC/NHLBI NIH HHS/ -- N01-HC-85085/HC/NHLBI NIH HHS/ -- N01-HC-85086/HC/NHLBI NIH HHS/ -- N01-HG-65403/HG/NHGRI NIH HHS/ -- N02-HL-6-4278/HL/NHLBI NIH HHS/ -- PG/02/128/British Heart Foundation/United Kingdom -- PG/08/094/British Heart Foundation/United Kingdom -- PG/08/094/26019/British Heart Foundation/United Kingdom -- R01 DK072193/DK/NIDDK NIH HHS/ -- R01 DK078150/DK/NIDDK NIH HHS/ -- R01 HL087647/HL/NHLBI NIH HHS/ -- R01 HL087676/HL/NHLBI NIH HHS/ -- R01 HL089650/HL/NHLBI NIH HHS/ -- R01HL086694/HL/NHLBI NIH HHS/ -- R01HL087641/HL/NHLBI NIH HHS/ -- R01HL087652/HL/NHLBI NIH HHS/ -- R01HL59367/HL/NHLBI NIH HHS/ -- R24 HD050924/HD/NICHD NIH HHS/ -- RC1 HL099634/HL/NHLBI NIH HHS/ -- RC1 HL099634-02/HL/NHLBI NIH HHS/ -- RC1 HL099793/HL/NHLBI NIH HHS/ -- RC2 HL101864,/HL/NHLBI NIH HHS/ -- RC2 HL102419/HL/NHLBI NIH HHS/ -- RG/07/005/23633/British Heart Foundation/United Kingdom -- RR20649/RR/NCRR NIH HHS/ -- SP/08/005/25115/British Heart Foundation/United Kingdom -- T32 GM007092/GM/NIGMS NIH HHS/ -- T32 HG00040/HG/NHGRI NIH HHS/ -- T32HL007208/HL/NHLBI NIH HHS/ -- TW05596/TW/FIC NIH HHS/ -- U01 DK062370/DK/NIDDK NIH HHS/ -- U01 DK062418/DK/NIDDK NIH HHS/ -- U01 HL069757/HL/NHLBI NIH HHS/ -- U01 HL080295/HL/NHLBI NIH HHS/ -- U01HG004402/HG/NHGRI NIH HHS/ -- U54 RR020278/RR/NCRR NIH HHS/ -- UL1RR025005/RR/NCRR NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):707-13. doi: 10.1038/nature09270.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Statistical Genetics, Department of Biostatistics, University of Michigan, Ann Arbor, Michigan 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20686565" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; Animals ; Asian Continental Ancestry Group/genetics ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Coronary Artery Disease/blood/genetics/therapy ; Europe/ethnology ; European Continental Ancestry Group/genetics ; Female ; Genetic Loci/*genetics ; *Genome-Wide Association Study ; Genotype ; Humans ; Lipid Metabolism/*genetics ; Lipids/*blood ; Liver/metabolism ; Male ; Mice ; N-Acetylgalactosaminyltransferases/genetics/metabolism ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Protein Phosphatase 1/genetics/metabolism ; Reproducibility of Results ; Triglycerides/blood
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Targeting Bcr-Abl by combining allosteric with ATP-binding-site inhibitors (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-15
    Description: In an effort to find new pharmacological modalities to overcome resistance to ATP-binding-site inhibitors of Bcr-Abl, we recently reported the discovery of GNF-2, a selective allosteric Bcr-Abl inhibitor. Here, using solution NMR, X-ray crystallography, mutagenesis and hydrogen exchange mass spectrometry, we show that GNF-2 binds to the myristate-binding site of Abl, leading to changes in the structural dynamics of the ATP-binding site. GNF-5, an analogue of GNF-2 with improved pharmacokinetic properties, when used in combination with the ATP-competitive inhibitors imatinib or nilotinib, suppressed the emergence of resistance mutations in vitro, displayed additive inhibitory activity in biochemical and cellular assays against T315I mutant human Bcr-Abl and displayed in vivo efficacy against this recalcitrant mutant in a murine bone-marrow transplantation model. These results show that therapeutically relevant inhibition of Bcr-Abl activity can be achieved with inhibitors that bind to the myristate-binding site and that combining allosteric and ATP-competitive inhibitors can overcome resistance to either agent alone.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2901986/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2901986/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jianming -- Adrian, Francisco J -- Jahnke, Wolfgang -- Cowan-Jacob, Sandra W -- Li, Allen G -- Iacob, Roxana E -- Sim, Taebo -- Powers, John -- Dierks, Christine -- Sun, Fangxian -- Guo, Gui-Rong -- Ding, Qiang -- Okram, Barun -- Choi, Yongmun -- Wojciechowski, Amy -- Deng, Xianming -- Liu, Guoxun -- Fendrich, Gabriele -- Strauss, Andre -- Vajpai, Navratna -- Grzesiek, Stephan -- Tuntland, Tove -- Liu, Yi -- Bursulaya, Badry -- Azam, Mohammad -- Manley, Paul W -- Engen, John R -- Daley, George Q -- Warmuth, Markus -- Gray, Nathanael S -- R01 CA130876/CA/NCI NIH HHS/ -- R01 CA130876-03/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jan 28;463(7280):501-6. doi: 10.1038/nature08675. Epub 2010 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Harvard Medical School, Department of Cancer Biology, Seeley G. Mudd Building 628, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20072125" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*chemistry/metabolism/*pharmacology ; Antineoplastic Combined Chemotherapy Protocols ; Benzamides ; Binding Sites ; Bone Marrow Transplantation ; Cell Line, Tumor ; Crystallization ; Disease Models, Animal ; Drug Resistance, Neoplasm/*drug effects ; Female ; Fusion Proteins, bcr-abl/*chemistry/genetics/metabolism ; Humans ; Imatinib Mesylate ; Inhibitory Concentration 50 ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug ; therapy/enzymology/*metabolism ; Male ; Mass Spectrometry ; Mice ; Models, Molecular ; Mutation/genetics ; Piperazines/chemistry/pharmacology ; Protein Structure, Tertiary ; Pyrimidines/chemistry/metabolism/pharmacology ; Transplantation, Heterologous
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Transfusion independence and HMGA2 activation after gene therapy of human beta-thalassaemia (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-09-17
    Description: The beta-haemoglobinopathies are the most prevalent inherited disorders worldwide. Gene therapy of beta-thalassaemia is particularly challenging given the requirement for massive haemoglobin production in a lineage-specific manner and the lack of selective advantage for corrected haematopoietic stem cells. Compound beta(E)/beta(0)-thalassaemia is the most common form of severe thalassaemia in southeast Asian countries and their diasporas. The beta(E)-globin allele bears a point mutation that causes alternative splicing. The abnormally spliced form is non-coding, whereas the correctly spliced messenger RNA expresses a mutated beta(E)-globin with partial instability. When this is compounded with a non-functional beta(0) allele, a profound decrease in beta-globin synthesis results, and approximately half of beta(E)/beta(0)-thalassaemia patients are transfusion-dependent. The only available curative therapy is allogeneic haematopoietic stem cell transplantation, although most patients do not have a human-leukocyte-antigen-matched, geno-identical donor, and those who do still risk rejection or graft-versus-host disease. Here we show that, 33 months after lentiviral beta-globin gene transfer, an adult patient with severe beta(E)/beta(0)-thalassaemia dependent on monthly transfusions since early childhood has become transfusion independent for the past 21 months. Blood haemoglobin is maintained between 9 and 10 g dl(-1), of which one-third contains vector-encoded beta-globin. Most of the therapeutic benefit results from a dominant, myeloid-biased cell clone, in which the integrated vector causes transcriptional activation of HMGA2 in erythroid cells with further increased expression of a truncated HMGA2 mRNA insensitive to degradation by let-7 microRNAs. The clonal dominance that accompanies therapeutic efficacy may be coincidental and stochastic or result from a hitherto benign cell expansion caused by dysregulation of the HMGA2 gene in stem/progenitor cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355472/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355472/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cavazzana-Calvo, Marina -- Payen, Emmanuel -- Negre, Olivier -- Wang, Gary -- Hehir, Kathleen -- Fusil, Floriane -- Down, Julian -- Denaro, Maria -- Brady, Troy -- Westerman, Karen -- Cavallesco, Resy -- Gillet-Legrand, Beatrix -- Caccavelli, Laure -- Sgarra, Riccardo -- Maouche-Chretien, Leila -- Bernaudin, Francoise -- Girot, Robert -- Dorazio, Ronald -- Mulder, Geert-Jan -- Polack, Axel -- Bank, Arthur -- Soulier, Jean -- Larghero, Jerome -- Kabbara, Nabil -- Dalle, Bruno -- Gourmel, Bernard -- Socie, Gerard -- Chretien, Stany -- Cartier, Nathalie -- Aubourg, Patrick -- Fischer, Alain -- Cornetta, Kenneth -- Galacteros, Frederic -- Beuzard, Yves -- Gluckman, Eliane -- Bushman, Frederick -- Hacein-Bey-Abina, Salima -- Leboulch, Philippe -- AI082020/AI/NIAID NIH HHS/ -- AI52845/AI/NIAID NIH HHS/ -- HL090921/HL/NHLBI NIH HHS/ -- R01 AI052845/AI/NIAID NIH HHS/ -- R01 AI082020/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):318-22. doi: 10.1038/nature09328.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Investigation Center in Biotherapy, Groupe Hospitalier Universitaire Ouest, Inserm/Assistance Publique-Hopitaux de Paris, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20844535" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Blood Cells/cytology/metabolism ; *Blood Transfusion ; Bone Marrow Cells/cytology/metabolism ; Child, Preschool ; Clone Cells/metabolism ; Gene Expression ; *Genetic Therapy ; Genetic Vectors/genetics ; HMGA2 Protein/genetics/*metabolism ; Homeostasis ; Humans ; Lentivirus/genetics ; Male ; MicroRNAs/genetics ; Organ Specificity ; RNA, Messenger/analysis/genetics ; Time Factors ; Transcriptional Activation ; Young Adult ; beta-Globins/*genetics/*metabolism ; beta-Thalassemia/*genetics/metabolism/*therapy
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    The mutation spectrum revealed by paired genome sequences from a lung cancer patient (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-28
    Description: Lung cancer is the leading cause of cancer-related mortality worldwide, with non-small-cell lung carcinomas in smokers being the predominant form of the disease. Although previous studies have identified important common somatic mutations in lung cancers, they have primarily focused on a limited set of genes and have thus provided a constrained view of the mutational spectrum. Recent cancer sequencing efforts have used next-generation sequencing technologies to provide a genome-wide view of mutations in leukaemia, breast cancer and cancer cell lines. Here we present the complete sequences of a primary lung tumour (60x coverage) and adjacent normal tissue (46x). Comparing the two genomes, we identify a wide variety of somatic variations, including 〉50,000 high-confidence single nucleotide variants. We validated 530 somatic single nucleotide variants in this tumour, including one in the KRAS proto-oncogene and 391 others in coding regions, as well as 43 large-scale structural variations. These constitute a large set of new somatic mutations and yield an estimated 17.7 per megabase genome-wide somatic mutation rate. Notably, we observe a distinct pattern of selection against mutations within expressed genes compared to non-expressed genes and in promoter regions up to 5 kilobases upstream of all protein-coding genes. Furthermore, we observe a higher rate of amino acid-changing mutations in kinase genes. We present a comprehensive view of somatic alterations in a single lung tumour, and provide the first evidence, to our knowledge, of distinct selective pressures present within the tumour environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, William -- Jiang, Zhaoshi -- Liu, Jinfeng -- Haverty, Peter M -- Guan, Yinghui -- Stinson, Jeremy -- Yue, Peng -- Zhang, Yan -- Pant, Krishna P -- Bhatt, Deepali -- Ha, Connie -- Johnson, Stephanie -- Kennemer, Michael I -- Mohan, Sankar -- Nazarenko, Igor -- Watanabe, Colin -- Sparks, Andrew B -- Shames, David S -- Gentleman, Robert -- de Sauvage, Frederic J -- Stern, Howard -- Pandita, Ajay -- Ballinger, Dennis G -- Drmanac, Radoje -- Modrusan, Zora -- Seshagiri, Somasekar -- Zhang, Zemin -- England -- Nature. 2010 May 27;465(7297):473-7. doi: 10.1038/nature09004.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioinformatics and Computational Biology, Genentech Inc., South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20505728" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinoma, Non-Small-Cell Lung/*genetics ; DNA Mutational Analysis ; Genome, Human/*genetics ; Humans ; Lung Neoplasms/*genetics ; Male ; Middle Aged ; Models, Biological ; Point Mutation/*genetics ; Selection, Genetic/genetics
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    Conversion of adult pancreatic alpha-cells to beta-cells after extreme beta-cell loss (2010)
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    Publication Date: 2010-04-07
    Description: Pancreatic insulin-producing beta-cells have a long lifespan, such that in healthy conditions they replicate little during a lifetime. Nevertheless, they show increased self-duplication after increased metabolic demand or after injury (that is, beta-cell loss). It is not known whether adult mammals can differentiate (regenerate) new beta-cells after extreme, total beta-cell loss, as in diabetes. This would indicate differentiation from precursors or another heterologous (non-beta-cell) source. Here we show beta-cell regeneration in a transgenic model of diphtheria-toxin-induced acute selective near-total beta-cell ablation. If given insulin, the mice survived and showed beta-cell mass augmentation with time. Lineage-tracing to label the glucagon-producing alpha-cells before beta-cell ablation tracked large fractions of regenerated beta-cells as deriving from alpha-cells, revealing a previously disregarded degree of pancreatic cell plasticity. Such inter-endocrine spontaneous adult cell conversion could be harnessed towards methods of producing beta-cells for diabetes therapies, either in differentiation settings in vitro or in induced regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877635/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877635/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thorel, Fabrizio -- Nepote, Virginie -- Avril, Isabelle -- Kohno, Kenji -- Desgraz, Renaud -- Chera, Simona -- Herrera, Pedro L -- U01 DK072522/DK/NIDDK NIH HHS/ -- U01 DK072522-01/DK/NIDDK NIH HHS/ -- U01 DK072522-02/DK/NIDDK NIH HHS/ -- U01 DK072522-03/DK/NIDDK NIH HHS/ -- U01 DK072522-04/DK/NIDDK NIH HHS/ -- U01 DK072522-05/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Apr 22;464(7292):1149-54. doi: 10.1038/nature08894. Epub 2010 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Physiology & Metabolism, University of Geneva Faculty of Medicine, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20364121" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/metabolism ; Cell Count ; Cell Death/drug effects ; Cell Differentiation/*physiology ; Cell Lineage ; Cell Proliferation ; Cell Transdifferentiation/*physiology ; Cellular Reprogramming ; Diphtheria Toxin/pharmacology/toxicity ; Female ; Glucagon/biosynthesis/genetics/secretion ; Glucagon-Secreting Cells/*cytology/metabolism/secretion ; Humans ; Insulin/biosynthesis/pharmacology/secretion ; Insulin-Secreting Cells/*cytology/drug effects/metabolism/secretion ; Male ; Mice ; Mice, Transgenic ; Rats ; Regeneration/physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Ecology: A world without mosquitoes (2010)
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    Publication Date: 2010-07-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fang, Janet -- England -- Nature. 2010 Jul 22;466(7305):432-4. doi: 10.1038/466432a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651669" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arctic Regions ; *Biodiversity ; Biomass ; Birds/physiology ; Culicidae/classification/growth & development/parasitology/*physiology ; Female ; *Food Chain ; Forecasting ; Humans ; Insect Vectors/parasitology/*physiology ; Larva/physiology ; Male ; *Models, Biological ; Plants/metabolism ; Pollination/physiology ; Population Density
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    Circulating mitochondrial DAMPs cause inflammatory responses to injury (2010)
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    Publication Date: 2010-03-06
    Description: Injury causes a systemic inflammatory response syndrome (SIRS) that is clinically much like sepsis. Microbial pathogen-associated molecular patterns (PAMPs) activate innate immunocytes through pattern recognition receptors. Similarly, cellular injury can release endogenous 'damage'-associated molecular patterns (DAMPs) that activate innate immunity. Mitochondria are evolutionary endosymbionts that were derived from bacteria and so might bear bacterial molecular motifs. Here we show that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally important immune consequences. MTDs include formyl peptides and mitochondrial DNA. These activate human polymorphonuclear neutrophils (PMNs) through formyl peptide receptor-1 and Toll-like receptor (TLR) 9, respectively. MTDs promote PMN Ca(2+) flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo. Circulating MTDs can elicit neutrophil-mediated organ injury. Cellular disruption by trauma releases mitochondrial DAMPs with evolutionarily conserved similarities to bacterial PAMPs into the circulation. These signal through innate immune pathways identical to those activated in sepsis to create a sepsis-like state. The release of such mitochondrial 'enemies within' by cellular injury is a key link between trauma, inflammation and SIRS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2843437/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2843437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qin -- Raoof, Mustafa -- Chen, Yu -- Sumi, Yuka -- Sursal, Tolga -- Junger, Wolfgang -- Brohi, Karim -- Itagaki, Kiyoshi -- Hauser, Carl J -- R01 GM059179/GM/NIGMS NIH HHS/ -- R01 GM059179-08/GM/NIGMS NIH HHS/ -- R01 GM059179-09/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Mar 4;464(7285):104-7. doi: 10.1038/nature08780.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Division of Trauma, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203610" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Lung Injury/immunology/pathology ; Animals ; Calcium Signaling ; Cells, Cultured ; CpG Islands/immunology ; DNA, Mitochondrial/blood/immunology ; Femur/injuries ; Fractures, Bone/immunology/pathology ; Humans ; Immunity, Innate/immunology ; Liver/immunology/injuries/pathology ; Male ; Mitochondria/*immunology/*secretion ; Mitogen-Activated Protein Kinases/metabolism ; Muscle, Skeletal/immunology/pathology ; N-Formylmethionine Leucyl-Phenylalanine/immunology/metabolism ; Neutrophils/enzymology/immunology/metabolism ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, Formyl Peptide/metabolism ; Sepsis/immunology/metabolism/microbiology ; Systemic Inflammatory Response ; Syndrome/blood/*complications/*immunology/pathology ; Toll-Like Receptor 9/metabolism ; Wounds and Injuries/blood/*complications/*immunology/pathology
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    Ground truth is the test that counts (2010)
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    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nonacs, Peter -- England -- Nature. 2010 Oct 7;467(7316):661. doi: 10.1038/467661c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20930828" target="_blank"〉PubMed〈/a〉
    Keywords: *Altruism ; Animals ; *Biological Evolution ; Cooperative Behavior ; Female ; Male ; Mathematics ; *Models, Biological ; Selection, Genetic
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    Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes (2010)
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    Publication Date: 2010-11-12
    Description: Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality. Rett syndrome is characterized by apparently normal early development followed by regression, motor abnormalities, seizures and features of autism, especially stereotyped behaviours. The mechanisms mediating these features are poorly understood. Here we show that mice lacking Mecp2 from GABA (gamma-aminobutyric acid)-releasing neurons recapitulate numerous Rett syndrome and autistic features, including repetitive behaviours. Loss of MeCP2 from a subset of forebrain GABAergic neurons also recapitulates many features of Rett syndrome. MeCP2-deficient GABAergic neurons show reduced inhibitory quantal size, consistent with a presynaptic reduction in glutamic acid decarboxylase 1 (Gad1) and glutamic acid decarboxylase 2 (Gad2) levels, and GABA immunoreactivity. These data demonstrate that MeCP2 is critical for normal function of GABA-releasing neurons and that subtle dysfunction of GABAergic neurons contributes to numerous neuropsychiatric phenotypes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057962/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chao, Hsiao-Tuan -- Chen, Hongmei -- Samaco, Rodney C -- Xue, Mingshan -- Chahrour, Maria -- Yoo, Jong -- Neul, Jeffrey L -- Gong, Shiaoching -- Lu, Hui-Chen -- Heintz, Nathaniel -- Ekker, Marc -- Rubenstein, John L R -- Noebels, Jeffrey L -- Rosenmund, Christian -- Zoghbi, Huda Y -- 29709/PHS HHS/ -- F31MH078678/MH/NIMH NIH HHS/ -- HD024064/HD/NICHD NIH HHS/ -- HD053862/HD/NICHD NIH HHS/ -- K08 NS052240/NS/NINDS NIH HHS/ -- K08 NS052240-01/NS/NINDS NIH HHS/ -- K08 NS052240-02/NS/NINDS NIH HHS/ -- K08 NS052240-03/NS/NINDS NIH HHS/ -- K08 NS052240-04/NS/NINDS NIH HHS/ -- K08 NS052240-05/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- R01 HD062553/HD/NICHD NIH HHS/ -- R01 NS048884/NS/NINDS NIH HHS/ -- R01 NS057819/NS/NINDS NIH HHS/ -- R01 NS057819-04/NS/NINDS NIH HHS/ -- R01 NS057819-05/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 11;468(7321):263-9. doi: 10.1038/nature09582.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉]Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/complications/genetics/pathology/*physiopathology ; Brain/cytology ; Compulsive Behavior/complications/genetics/physiopathology ; Disease Models, Animal ; Electroencephalography ; Genotype ; Glutamate Decarboxylase/metabolism ; Hippocampus/pathology/physiopathology ; Homeodomain Proteins/genetics ; Inhibitory Postsynaptic Potentials ; Long-Term Potentiation ; Male ; Methyl-CpG-Binding Protein 2/*deficiency/genetics/*metabolism ; Mice ; Mice, Transgenic ; Neural Inhibition ; Neuronal Plasticity ; Neurons/metabolism ; Phenotype ; Presynaptic Terminals/metabolism ; Psychomotor Disorders/complications/genetics/physiopathology ; Reflex, Startle/genetics ; Respiration ; Rett Syndrome/complications/genetics/pathology/*physiopathology ; Self-Injurious Behavior/complications/genetics/physiopathology ; *Signal Transduction ; Stereotypic Movement Disorder/complications/genetics/pathology/*physiopathology ; Survival Rate ; Synaptic Transmission ; Vesicular Inhibitory Amino Acid Transport Proteins/genetics ; gamma-Aminobutyric Acid/*metabolism
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    Somatic sex identity is cell autonomous in the chicken (2010)
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    Publication Date: 2010-03-12
    Description: In the mammalian model of sex determination, embryos are considered to be sexually indifferent until the transient action of a sex-determining gene initiates gonadal differentiation. Although this model is thought to apply to all vertebrates, this has yet to be established. Here we have examined three lateral gynandromorph chickens (a rare, naturally occurring phenomenon in which one side of the animal appears male and the other female) to investigate the sex-determining mechanism in birds. These studies demonstrated that gynandromorph birds are genuine male:female chimaeras, and indicated that male and female avian somatic cells may have an inherent sex identity. To test this hypothesis, we transplanted presumptive mesoderm between embryos of reciprocal sexes to generate embryos containing male:female chimaeric gonads. In contrast to the outcome for mammalian mixed-sex chimaeras, in chicken mixed-sex chimaeras the donor cells were excluded from the functional structures of the host gonad. In an example where female tissue was transplanted into a male host, donor cells contributing to the developing testis retained a female identity and expressed a marker of female function. Our study demonstrates that avian somatic cells possess an inherent sex identity and that, in birds, sexual differentiation is substantively cell autonomous.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925877/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925877/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, D -- McBride, D -- Nandi, S -- McQueen, H A -- McGrew, M J -- Hocking, P M -- Lewis, P D -- Sang, H M -- Clinton, M -- BB/E011276/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E015425/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H012486/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBE0154251/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2010 Mar 11;464(7286):237-42. doi: 10.1038/nature08852.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Developmental Biology, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, Midlothian EH25 9PS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220842" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Physiological Phenomena ; Chick Embryo ; Chickens/genetics/*physiology ; Chimera/genetics/physiology ; Female ; Gonadal Hormones/metabolism ; Male ; Sex Characteristics ; Sex Differentiation/genetics/*physiology
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    Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content (2010)
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    Publication Date: 2010-01-15
    Description: The human Y chromosome began to evolve from an autosome hundreds of millions of years ago, acquiring a sex-determining function and undergoing a series of inversions that suppressed crossing over with the X chromosome. Little is known about the recent evolution of the Y chromosome because only the human Y chromosome has been fully sequenced. Prevailing theories hold that Y chromosomes evolve by gene loss, the pace of which slows over time, eventually leading to a paucity of genes, and stasis. These theories have been buttressed by partial sequence data from newly emergent plant and animal Y chromosomes, but they have not been tested in older, highly evolved Y chromosomes such as that of humans. Here we finished sequencing of the male-specific region of the Y chromosome (MSY) in our closest living relative, the chimpanzee, achieving levels of accuracy and completion previously reached for the human MSY. By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content, indicating rapid evolution during the past 6 million years. The chimpanzee MSY contains twice as many massive palindromes as the human MSY, yet it has lost large fractions of the MSY protein-coding genes and gene families present in the last common ancestor. We suggest that the extraordinary divergence of the chimpanzee and human MSYs was driven by four synergistic factors: the prominent role of the MSY in sperm production, 'genetic hitchhiking' effects in the absence of meiotic crossing over, frequent ectopic recombination within the MSY, and species differences in mating behaviour. Although genetic decay may be the principal dynamic in the evolution of newly emergent Y chromosomes, wholesale renovation is the paramount theme in the continuing evolution of chimpanzee, human and perhaps other older MSYs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653425/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653425/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Jennifer F -- Skaletsky, Helen -- Pyntikova, Tatyana -- Graves, Tina A -- van Daalen, Saskia K M -- Minx, Patrick J -- Fulton, Robert S -- McGrath, Sean D -- Locke, Devin P -- Friedman, Cynthia -- Trask, Barbara J -- Mardis, Elaine R -- Warren, Wesley C -- Repping, Sjoerd -- Rozen, Steve -- Wilson, Richard K -- Page, David C -- R01 HG000257/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jan 28;463(7280):536-9. doi: 10.1038/nature08700. Epub 2010 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20072128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Human, Y/*genetics ; DNA/chemistry/genetics ; Genes/*genetics ; Humans ; Male ; Molecular Sequence Data ; *Nucleic Acid Conformation ; Pan troglodytes/*genetics ; Sequence Homology, Nucleic Acid ; Y Chromosome/*genetics
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    S-glutathionylation uncouples eNOS and regulates its cellular and vascular function (2010)
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    Publication Date: 2010-12-24
    Description: Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)(*-)), which are key mediators of cellular signalling. In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. In the absence of BH(4), NO synthesis is abrogated and instead O(2)(*-) is generated. While NOS dysfunction occurs in diseases with redox stress, BH(4) repletion only partly restores NOS activity and NOS-dependent vasodilation. This suggests that there is an as yet unidentified redox-regulated mechanism controlling NOS function. Protein thiols can undergo S-glutathionylation, a reversible protein modification involved in cellular signalling and adaptation. Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchange with oxidized glutathione or reaction of oxidant-induced protein thiyl radicals with reduced glutathione. Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation. Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)(*-) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function. We show that eNOS S-glutathionylation in endothelial cells, with loss of NO and gain of O(2)(*-) generation, is associated with impaired endothelium-dependent vasodilation. In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation. Thus, S-glutathionylation of eNOS is a pivotal switch providing redox regulation of cellular signalling, endothelial function and vascular tone.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chun-An -- Wang, Tse-Yao -- Varadharaj, Saradhadevi -- Reyes, Levy A -- Hemann, Craig -- Talukder, M A Hassan -- Chen, Yeong-Renn -- Druhan, Lawrence J -- Zweier, Jay L -- K99 HL103846/HL/NHLBI NIH HHS/ -- K99 HL103846-02/HL/NHLBI NIH HHS/ -- R01 HL038324/HL/NHLBI NIH HHS/ -- R01 HL038324-20/HL/NHLBI NIH HHS/ -- R01 HL063744/HL/NHLBI NIH HHS/ -- R01 HL063744-09/HL/NHLBI NIH HHS/ -- R01HL103846/HL/NHLBI NIH HHS/ -- R01HL38324/HL/NHLBI NIH HHS/ -- R01HL63744/HL/NHLBI NIH HHS/ -- R01HL65608/HL/NHLBI NIH HHS/ -- R01HL83237/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1115-8. doi: 10.1038/nature09599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Dithiothreitol/pharmacology ; Endothelial Cells/metabolism ; Endothelium, Vascular/*metabolism ; Glutathione/*metabolism ; Humans ; Male ; Mercaptoethanol/pharmacology ; Mutation ; Nitric Oxide Synthase Type III/genetics/*metabolism ; Oxidation-Reduction ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Sprague-Dawley ; Reducing Agents/pharmacology ; Signal Transduction ; Vasodilation/physiology
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    Neural evidence for inequality-averse social preferences (2010)
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    Publication Date: 2010-02-26
    Description: A popular hypothesis in the social sciences is that humans have social preferences to reduce inequality in outcome distributions because it has a negative impact on their experienced reward. Although there is a large body of behavioural and anthropological evidence consistent with the predictions of these theories, there is no direct neural evidence for the existence of inequality-averse preferences. Such evidence would be especially useful because some behaviours that are consistent with a dislike for unequal outcomes could also be explained by concerns for social image or reciprocity, which do not require a direct aversion towards inequality. Here we use functional MRI to test directly for the existence of inequality-averse social preferences in the human brain. Inequality was created by recruiting pairs of subjects and giving one of them a large monetary endowment. While both subjects evaluated further monetary transfers from the experimenter to themselves and to the other participant, we measured neural responses in the ventral striatum and ventromedial prefrontal cortex, two areas that have been shown to be involved in the valuation of monetary and primary rewards in both social and non-social contexts. Consistent with inequality-averse models of social preferences, we find that activity in these areas was more responsive to transfers to others than to self in the 'high-pay' subject, whereas the activity of the 'low-pay' subject showed the opposite pattern. These results provide direct evidence for the validity of this class of models, and also show that the brain's reward circuitry is sensitive to both advantageous and disadvantageous inequality.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tricomi, Elizabeth -- Rangel, Antonio -- Camerer, Colin F -- O'Doherty, John P -- England -- Nature. 2010 Feb 25;463(7284):1089-91. doi: 10.1038/nature08785.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Psychology Department, Rutgers University, Newark, New Jersey 07102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20182511" target="_blank"〉PubMed〈/a〉
    Keywords: Basal Ganglia/physiology ; Beneficence ; Humans ; Magnetic Resonance Imaging ; Male ; *Models, Neurological ; Prefrontal Cortex/anatomy & histology/physiology ; Reproducibility of Results ; *Reward ; Role Playing ; *Social Behavior ; Social Justice/*economics/*psychology ; Young Adult
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    A role for the elongator complex in zygotic paternal genome demethylation (2010)
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    Publication Date: 2010-01-08
    Description: The life cycle of mammals begins when a sperm enters an egg. Immediately after fertilization, both the maternal and paternal genomes undergo dramatic reprogramming to prepare for the transition from germ cell to somatic cell transcription programs. One of the molecular events that takes place during this transition is the demethylation of the paternal genome. Despite extensive efforts, the factors responsible for paternal DNA demethylation have not been identified. To search for such factors, we developed a live cell imaging system that allows us to monitor the paternal DNA methylation state in zygotes. Through short-interfering-RNA-mediated knockdown in mouse zygotes, we identified Elp3 (also called KAT9), a component of the elongator complex, to be important for paternal DNA demethylation. We demonstrate that knockdown of Elp3 impairs paternal DNA demethylation as indicated by reporter binding, immunostaining and bisulphite sequencing. Similar results were also obtained when other elongator components, Elp1 and Elp4, were knocked down. Importantly, injection of messenger RNA encoding the Elp3 radical SAM domain mutant, but not the HAT domain mutant, into MII oocytes before fertilization also impaired paternal DNA demethylation, indicating that the SAM radical domain is involved in the demethylation process. Our study not only establishes a critical role for the elongator complex in zygotic paternal genome demethylation, but also indicates that the demethylation process may be mediated through a reaction that requires an intact radical SAM domain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834414/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834414/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Yuki -- Yamagata, Kazuo -- Hong, Kwonho -- Wakayama, Teruhiko -- Zhang, Yi -- R01 GM068804/GM/NIGMS NIH HHS/ -- R01 GM068804-07/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jan 28;463(7280):554-8. doi: 10.1038/nature08732. Epub 2010 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Chapel Hill, North Carolina 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20054296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; *DNA Methylation ; Embryonic Development/*genetics ; Female ; Gene Knockdown Techniques ; Genome/*genetics ; Histone Acetyltransferases/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mutation/genetics ; Protein Structure, Tertiary/genetics ; Zygote/*metabolism
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    Science in court: DNA's identity crisis (2010)
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    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, Natasha -- England -- Nature. 2010 Mar 18;464(7287):347-8. doi: 10.1038/464347a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237538" target="_blank"〉PubMed〈/a〉
    Keywords: Artifacts ; Bias (Epidemiology) ; Confidentiality ; DNA Fingerprinting/*methods/*standards ; Forensic Genetics/*methods/*standards ; Great Britain ; Humans ; Male ; Microsatellite Repeats/genetics ; Polymerase Chain Reaction ; Reproducibility of Results
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    Calcium-dependent protein kinase 1 is an essential regulator of exocytosis in Toxoplasma (2010)
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    Publication Date: 2010-05-21
    Description: Calcium-regulated exocytosis is a ubiquitous process in eukaryotes, whereby secretory vesicles fuse with the plasma membrane and release their contents in response to an intracellular calcium surge. This process regulates various cellular functions such as plasma membrane repair in plants and animals, the discharge of defensive spikes in Paramecium, and the secretion of insulin from pancreatic cells, immune modulators from lymphocytes, and chemical transmitters from neurons. In animal cells, serine/threonine kinases including cAMP-dependent protein kinase, protein kinase C and calmodulin kinases have been implicated in calcium-signal transduction leading to regulated secretion. Although plants and protozoa also regulate secretion by means of intracellular calcium, the method by which these signals are relayed has not been explained. Here we show that the Toxoplasma gondii calcium-dependent protein kinase 1 (TgCDPK1) is an essential regulator of calcium-dependent exocytosis in this opportunistic human pathogen. Conditional suppression of TgCDPK1 revealed that it controls calcium-dependent secretion of specialized organelles called micronemes, resulting in a block of essential phenotypes including parasite motility, host-cell invasion, and egress. These phenotypes were recapitulated by using a chemical biology approach in which pyrazolopyrimidine-derived compounds specifically inhibited TgCDPK1 and disrupted the parasite's life cycle at stages dependent on microneme secretion. Inhibition was specific to TgCDPK1, because expression of a resistant mutant kinase reversed sensitivity to the inhibitor. TgCDPK1 is conserved among apicomplexans and belongs to a family of kinases shared with plants and ciliates, suggesting that related CDPKs may have a function in calcium-regulated secretion in other organisms. Because this kinase family is absent from mammalian hosts, it represents a validated target that may be exploitable for chemotherapy against T. gondii and related apicomplexans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874977/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874977/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lourido, Sebastian -- Shuman, Joel -- Zhang, Chao -- Shokat, Kevan M -- Hui, Raymond -- Sibley, L David -- R01 AI034036/AI/NIAID NIH HHS/ -- R01 AI034036-17/AI/NIAID NIH HHS/ -- England -- Nature. 2010 May 20;465(7296):359-62. doi: 10.1038/nature09022.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Avenue, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485436" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cells, Cultured ; *Exocytosis ; Fibroblasts/parasitology ; Foreskin ; Gene Knockout Techniques ; Host-Pathogen Interactions/physiology ; Humans ; Male ; Molecular Sequence Data ; Organelles/metabolism ; Phenotype ; Protein Kinases/deficiency/genetics/*metabolism ; Protein Phosphatase 1/chemistry/metabolism ; Toxoplasma/*cytology/*enzymology/pathogenicity/physiology
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    Skp2 targeting suppresses tumorigenesis by Arf-p53-independent cellular senescence (2010)
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    Publication Date: 2010-03-20
    Description: Cellular senescence has been recently shown to have an important role in opposing tumour initiation and promotion. Senescence induced by oncogenes or by loss of tumour suppressor genes is thought to critically depend on induction of the p19(Arf)-p53 pathway. The Skp2 E3-ubiquitin ligase can act as a proto-oncogene and its aberrant overexpression is frequently observed in human cancers. Here we show that although Skp2 inactivation on its own does not induce cellular senescence, aberrant proto-oncogenic signals as well as inactivation of tumour suppressor genes do trigger a potent, tumour-suppressive senescence response in mice and cells devoid of Skp2. Notably, Skp2 inactivation and oncogenic-stress-driven senescence neither elicit activation of the p19(Arf)-p53 pathway nor DNA damage, but instead depend on Atf4, p27 and p21. We further demonstrate that genetic Skp2 inactivation evokes cellular senescence even in oncogenic conditions in which the p19(Arf)-p53 response is impaired, whereas a Skp2-SCF complex inhibitor can trigger cellular senescence in p53/Pten-deficient cells and tumour regression in preclinical studies. Our findings therefore provide proof-of-principle evidence that pharmacological inhibition of Skp2 may represent a general approach for cancer prevention and therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928066/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Hui-Kuan -- Chen, Zhenbang -- Wang, Guocan -- Nardella, Caterina -- Lee, Szu-Wei -- Chan, Chia-Hsin -- Yang, Wei-Lei -- Wang, Jing -- Egia, Ainara -- Nakayama, Keiichi I -- Cordon-Cardo, Carlos -- Teruya-Feldstein, Julie -- Pandolfi, Pier Paolo -- R01 CA082328/CA/NCI NIH HHS/ -- R01 CA082328-13/CA/NCI NIH HHS/ -- R01 MD004038/MD/NIMHD NIH HHS/ -- England -- Nature. 2010 Mar 18;464(7287):374-9. doi: 10.1038/nature08815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237562" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 4/metabolism ; Adenovirus E1A Proteins/genetics/metabolism ; Animals ; *Cell Aging/drug effects ; *Cell Transformation, Neoplastic/drug effects ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Fibroblasts ; Male ; Mice ; PTEN Phosphohydrolase/deficiency/genetics/metabolism ; Prostate/cytology/metabolism ; Prostatic Neoplasms/drug therapy/pathology/prevention & control ; Proto-Oncogene Proteins p21(ras)/genetics/metabolism ; S-Phase Kinase-Associated Proteins/antagonists & inhibitors/genetics/*metabolism ; SKP Cullin F-Box Protein Ligases/metabolism ; Tumor Suppressor Protein p53/deficiency/metabolism
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    Developmental genetics: Time for teeth (2010)
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    Publication Date: 2010-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shadan, Sadaf -- England -- Nature. 2010 Mar 4;464(7285):43. doi: 10.1038/464043a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203600" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child, Preschool ; Female ; Finland ; Genome-Wide Association Study ; Great Britain ; Humans ; Infant ; Male ; Polymorphism, Single Nucleotide/*genetics ; Time Factors ; *Tooth, Deciduous/*growth & development
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    Reproductive ageing: Of worms and women (2010)
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    Publication Date: 2010-11-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flurkey, Kevin -- Harrison, David E -- P30 AG025707/AG/NIA NIH HHS/ -- R01 AG026074/AG/NIA NIH HHS/ -- England -- Nature. 2010 Nov 18;468(7322):386-7. doi: 10.1038/468386a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21085171" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/*physiology ; Animals ; Caenorhabditis elegans/cytology/embryology/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/metabolism ; Embryo, Nonmammalian/cytology/embryology ; Female ; Fertility/genetics/*physiology ; Humans ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Longevity/genetics/*physiology ; Male ; Maternal Age ; Models, Animal ; Models, Biological ; Oocytes/growth & development/*physiology ; Receptor, Insulin/genetics/metabolism ; Signal Transduction/genetics/physiology ; Transforming Growth Factor beta/metabolism
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    Genome-wide erasure of DNA methylation in mouse primordial germ cells is affected by AID deficiency (2010)
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    Publication Date: 2010-01-26
    Description: Epigenetic reprogramming including demethylation of DNA occurs in mammalian primordial germ cells (PGCs) and in early embryos, and is important for the erasure of imprints and epimutations, and the return to pluripotency. The extent of this reprogramming and its molecular mechanisms are poorly understood. We previously showed that the cytidine deaminases AID and APOBEC1 can deaminate 5-methylcytosine in vitro and in Escherichia coli, and in the mouse are expressed in tissues in which demethylation occurs. Here we profiled DNA methylation throughout the genome by unbiased bisulphite next generation sequencing in wild-type and AID-deficient mouse PGCs at embryonic day (E)13.5. Wild-type PGCs revealed marked genome-wide erasure of methylation to a level below that of methylation deficient (Np95(-/-), also called Uhrf1(-/-)) embryonic stem cells, with female PGCs being less methylated than male ones. By contrast, AID-deficient PGCs were up to three times more methylated than wild-type ones; this substantial difference occurred throughout the genome, with introns, intergenic regions and transposons being relatively more methylated than exons. Relative hypermethylation in AID-deficient PGCs was confirmed by analysis of individual loci in the genome. Our results reveal that erasure of DNA methylation in the germ line is a global process, hence limiting the potential for transgenerational epigenetic inheritance. AID deficiency interferes with genome-wide erasure of DNA methylation patterns, indicating that AID has a critical function in epigenetic reprogramming and potentially in restricting the inheritance of epimutations in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965733/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965733/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popp, Christian -- Dean, Wendy -- Feng, Suhua -- Cokus, Shawn J -- Andrews, Simon -- Pellegrini, Matteo -- Jacobsen, Steven E -- Reik, Wolf -- G0700098/Medical Research Council/United Kingdom -- R37 GM060398/GM/NIGMS NIH HHS/ -- R37 GM060398-11/GM/NIGMS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- England -- Nature. 2010 Feb 25;463(7284):1101-5. doi: 10.1038/nature08829.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20098412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytidine Deaminase/*deficiency/genetics/*metabolism ; *DNA Methylation ; DNA Transposable Elements/genetics ; Embryo, Mammalian/cytology/embryology/metabolism ; Epigenesis, Genetic/genetics ; Exons/genetics ; Female ; *Genome/genetics ; Germ Cells/enzymology/*metabolism ; Introns/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/deficiency/genetics ; Octamer Transcription Factor-3/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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