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  • Mice  (1,316)
  • American Association for the Advancement of Science (AAAS)  (1,316)
  • International Union of Crystallography
  • Nature Publishing Group
  • 2005-2009  (847)
  • 1980-1984  (469)
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Year
  • 1
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    Molecular biology. Managing associations between different chromosomes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spilianakis, Charalampos G -- Flavell, Richard A -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):207-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16614205" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Nucleus/genetics/metabolism ; Chromosomes, Mammalian/*genetics/metabolism ; DNA Methylation ; DNA-Binding Proteins/*metabolism ; Fluorescent Antibody Technique ; *Gene Expression Regulation ; Genomic Imprinting ; In Situ Hybridization, Fluorescence ; Insulin-Like Growth Factor II/genetics ; Mice ; Neurofibromin 1/genetics ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Regulatory Elements, Transcriptional ; Repressor Proteins/*metabolism ; Transcription, Genetic ; Transcriptional Activation ; Ubiquitin-Protein Ligases/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Characterization of the piRNA complex from rat testes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Small noncoding RNAs regulate processes essential for cell growth and development, including mRNA degradation, translational repression, and transcriptional gene silencing (TGS). During a search for candidate mammalian factors for TGS, we purified a complex that contains small RNAs and Riwi, the rat homolog to human Piwi. The RNAs, frequently 29 to 30 nucleotides in length, are called Piwi-interacting RNAs (piRNAs), 94% of which map to 100 defined (〈 or = 101 kb) genomic regions. Within these regions, the piRNAs generally distribute across only one genomic strand or distribute on two strands but in a divergent, nonoverlapping manner. Preparations of piRNA complex (piRC) contain rRecQ1, which is homologous to qde-3 from Neurospora, a gene implicated in silencing pathways. Piwi has been genetically linked to TGS in flies, and slicer activity cofractionates with the purified complex. These results are consistent with a gene-silencing role for piRC in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lau, Nelson C -- Seto, Anita G -- Kim, Jinkuk -- Kuramochi-Miyagawa, Satomi -- Nakano, Toru -- Bartel, David P -- Kingston, Robert E -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):363-7. Epub 2006 Jun 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778019" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/isolation & purification/metabolism ; Animals ; Chromosomes, Mammalian ; Conserved Sequence ; DNA Helicases/isolation & purification/metabolism ; Gene Library ; Genome ; Male ; Mice ; Proteins/isolation & purification/*metabolism ; *RNA Interference ; RNA, Untranslated/chemistry/genetics/isolation & purification/*metabolism ; Rats ; Rats, Sprague-Dawley ; RecQ Helicases ; Ribonucleoproteins/chemistry/isolation & purification/*metabolism ; Testis/*chemistry ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Cortical 5-HT2A receptor signaling modulates anxiety-like behaviors in mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-29
    Description: Serotonin [5-hydroxytryptamine (5-HT)] neurotransmission in the central nervous system modulates depression and anxiety-related behaviors in humans and rodents, but the responsible downstream receptors remain poorly understood. We demonstrate that global disruption of 5-HT2A receptor (5HT2AR) signaling in mice reduces inhibition in conflict anxiety paradigms without affecting fear-conditioned and depression-related behaviors. Selective restoration of 5HT2AR signaling to the cortex normalized conflict anxiety behaviors. These findings indicate a specific role for cortical 5HT2AR function in the modulation of conflict anxiety, consistent with models of cortical, "top-down" influences on risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisstaub, Noelia V -- Zhou, Mingming -- Lira, Alena -- Lambe, Evelyn -- Gonzalez-Maeso, Javier -- Hornung, Jean-Pierre -- Sibille, Etienne -- Underwood, Mark -- Itohara, Shigeyoshi -- Dauer, William T -- Ansorge, Mark S -- Morelli, Emanuela -- Mann, J John -- Toth, Miklos -- Aghajanian, George -- Sealfon, Stuart C -- Hen, Rene -- Gingrich, Jay A -- KO8 MH01711/MH/NIMH NIH HHS/ -- P01 DA12923/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):536-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Columbia University and the New York State Psychiatric Institute, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/*physiopathology ; Cerebral Cortex/*metabolism ; Conditioning (Psychology) ; Conflict (Psychology) ; Depression/physiopathology ; Exploratory Behavior ; Fear ; Limbic System/metabolism ; Mice ; Mice, Knockout ; Patch-Clamp Techniques ; Periaqueductal Gray/metabolism ; Prosencephalon/metabolism ; Receptor, Serotonin, 5-HT2A/genetics/*metabolism ; Receptor, Serotonin, 5-HT2C/metabolism ; Receptors, Neurotransmitter/metabolism ; Risk-Taking ; Serotonin/physiology ; *Signal Transduction ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    A one-size-fits-all flu vaccine? (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):380-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627732" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic ; Administration, Intranasal ; Animals ; Antibodies, Viral/biosynthesis/immunology ; Antigenic Variation ; Clinical Trials as Topic ; Drug Evaluation, Preclinical ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/immunology ; Humans ; Influenza A virus/*immunology ; *Influenza Vaccines/administration & dosage/immunology ; Influenza, Human/*prevention & control ; Mice ; Nucleoproteins/genetics/immunology ; Orthomyxoviridae Infections/prevention & control ; RNA-Binding Proteins/genetics/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccination ; Vaccines, Attenuated/administration & dosage/immunology ; Vaccines, DNA/administration & dosage/immunology ; Viral Core Proteins/genetics/immunology ; Viral Matrix Proteins/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Lhx2 maintains stem cell character in hair follicles (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: During embryogenesis, stem cells are set aside to fuel the postnatal hair cycle and repair the epidermis after injury. To define how hair follicle stem cells are specified and maintained in an undifferentiated state, we developed a strategy to isolate and transcriptionally profile embryonic hair progenitors in mice. We identified Lhx2 as a transcription factor positioned downstream of signals necessary to specify hair follicle stem cells, but upstream from signals required to drive activated stem cells to terminally differentiate. Using gain- and loss-of-function studies, we uncovered a role for Lhx2 in maintaining the growth and undifferentiated properties of hair follicle progenitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2405918/" 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/PMC2405918/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhee, Horace -- Polak, Lisa -- Fuchs, Elaine -- R01 AR031737/AR/NIAMS NIH HHS/ -- R01 AR031737-24/AR/NIAMS NIH HHS/ -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01 AR050452-04/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Rockefeller University, 1230 York Avenue, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Epidermis/cytology/embryology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Hair/embryology/growth & development ; Hair Follicle/*cytology/embryology/physiology ; Homeodomain Proteins/genetics/*physiology ; LIM-Homeodomain Proteins ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Morphogenesis ; Oligonucleotide Array Sequence Analysis ; Signal Transduction ; Skin Transplantation ; Stem Cells/*physiology ; Transcription Factors/genetics/*physiology ; Up-Regulation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Cell biology. A metabolic push to proliferate (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brasaemle, Dawn L -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1581-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Nutritional Sciences, Rutgers, State University of New Jersey, New Brunswick, NJ 08901, USA. brasaemle@aesop.rutgers.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973864" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Caveolae/metabolism ; Caveolin 1/genetics/*physiology ; Cell Cycle ; Cell Membrane/metabolism ; Cell Proliferation ; Fatty Acids/metabolism ; Glucose/administration & dosage ; Hepatocytes/cytology/*metabolism ; Hydrolysis ; *Lipid Metabolism ; *Liver Regeneration ; Mice ; Models, Biological ; Phospholipids/biosynthesis ; Triglycerides/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Immunology. Restless T cells sniff and go (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mustelin, Tomas -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1902-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program on Inflammatory Disease Research, Infectious and Inflammatory Disease Center, and Program of Signal Transduction, Cancer Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA. tmustelin@burnham.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD ; Antigens, CD28/metabolism ; Antigens, CD80/metabolism ; Antigens, CD86/metabolism ; Antigens, Differentiation/genetics/*physiology ; *Autoimmunity ; CTLA-4 Antigen ; Cell Adhesion ; Cell Movement ; Dendritic Cells/immunology ; Humans ; Integrins/physiology ; Ligands ; Lymph Nodes/*immunology ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Platelet-derived serotonin mediates liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: The liver can regenerate its volume after major tissue loss. In a mouse model of liver regeneration, thrombocytopenia, or impaired platelet activity resulted in the failure to initiate cellular proliferation in the liver. Platelets are major carriers of serotonin in the blood. In thrombocytopenic mice, a serotonin agonist reconstituted liver proliferation. The expression of 5-HT2A and 2B subtype serotonin receptors in the liver increased after hepatectomy. Antagonists of 5-HT2A and 2B receptors inhibited liver regeneration. Liver regeneration was also blunted in mice lacking tryptophan hydroxylase 1, which is the rate-limiting enzyme for the synthesis of peripheral serotonin. This failure of regeneration was rescued by reloading serotonin-free platelets with a serotonin precursor molecule. These results suggest that platelet-derived serotonin is involved in the initiation of liver regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lesurtel, Mickael -- Graf, Rolf -- Aleil, Boris -- Walther, Diego J -- Tian, Yinghua -- Jochum, Wolfram -- Gachet, Christian -- Bader, Michael -- Clavien, Pierre-Alain -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Visceral and Transplantation Surgery, University Hospital of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601191" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Hydroxytryptophan/pharmacology ; Amphetamines/pharmacology ; Animals ; Blood Platelets/metabolism/*physiology ; Busulfan/pharmacology ; Cell Proliferation ; Hepatectomy ; Hepatocytes/cytology ; Liver/metabolism/*physiology ; *Liver Regeneration ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Platelet Count ; Receptor, Serotonin, 5-HT2A/metabolism ; Receptor, Serotonin, 5-HT2B/metabolism ; Serotonin/blood/*physiology ; Serotonin 5-HT2 Receptor Antagonists ; Thrombocytopenia ; Ticlopidine/analogs & derivatives/pharmacology ; Tryptophan Hydroxylase/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Role of iNOS in human host defense (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathan, Carl -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1874-5; author reply 1874-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/enzymology/*immunology ; Cell Culture Techniques ; Cell Differentiation ; Cells, Cultured ; Humans ; Macrophages/cytology/*enzymology ; Mice ; Nitric Oxide Synthase Type II/biosynthesis/*metabolism ; Tuberculosis/enzymology/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Editorial expression of concern (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, Donald -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):592.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ectoderm/*physiology ; *Embryonic Development ; *Gene Expression Regulation, Developmental ; Homeodomain Proteins/*genetics/metabolism ; Mice ; Transcription Factors/*genetics/metabolism ; Trophoblasts/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    alphaE-catenin controls cerebral cortical size by regulating the hedgehog signaling pathway (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: During development, cells monitor and adjust their rates of accumulation to produce organs of predetermined size. We show here that central nervous system-specific deletion of the essential adherens junction gene, alphaE-catenin, causes abnormal activation of the hedgehog pathway, resulting in shortening of the cell cycle, decreased apoptosis, and cortical hyperplasia. We propose that alphaE-catenin connects cell-density-dependent adherens junctions with the developmental hedgehog pathway and that this connection may provide a negative feedback loop controlling the size of developing cerebral cortex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556178/" 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/PMC2556178/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lien, Wen-Hui -- Klezovitch, Olga -- Fernandez, Tania E -- Delrow, Jeff -- Vasioukhin, Valeri -- P41 RR011823/RR/NCRR NIH HHS/ -- P41 RR011823-128171/RR/NCRR NIH HHS/ -- R01 CA098161/CA/NCI NIH HHS/ -- R01 CA098161-01A1/CA/NCI NIH HHS/ -- R01 CA098161-02/CA/NCI NIH HHS/ -- R01 CA098161-03/CA/NCI NIH HHS/ -- R01 CA098161-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1609-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543460" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/*physiology/ultrastructure ; Animals ; Apoptosis ; Cell Adhesion ; Cell Count ; Cell Cycle ; Cell Differentiation ; Cell Polarity ; Central Nervous System/embryology ; Cerebral Cortex/cytology/*embryology/pathology/physiology ; Hedgehog Proteins ; Hyperplasia ; Mice ; Mitosis ; Models, Biological ; Mutation ; Neurons/cytology/*physiology/ultrastructure ; Oligonucleotide Array Sequence Analysis ; *Signal Transduction ; Stem Cells/cytology/ultrastructure ; Trans-Activators/*metabolism ; Up-Regulation ; alpha Catenin/genetics/*physiology
    Print ISSN: 0036-8075
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  • 12
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    Cdx2 gene expression and trophectoderm lineage specification in mouse embryos (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Controversy exists as to whether individual blastomeres from two-cell-stage mouse embryos have identical developmental properties and fate. We show that the transcription factor Cdx2 is expressed in the nuclei of cells derived from the late-dividing but not the first-dividing blastomere of two-cell embryos and, by lineage tracing and RNA interference knock-down experiments, that this lagging cell is the precursor of trophectoderm. Cdx2 mRNA is localized toward the vegetal pole of oocytes, reorients after fertilization, and becomes concentrated in the late-dividing, two-cell-stage blastomere. The asymmetrical distribution of Cdx2 gene products in the oocyte and embryo defines the lineage to trophectoderm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deb, Kaushik -- Sivaguru, Mayandi -- Yong, Hwan Yul -- Roberts, R Michael -- R01 HD21896/HD/NICHD NIH HHS/ -- R01 HD42201/HD/NICHD NIH HHS/ -- R01 RR13438/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):992-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Sciences, Columbia, MO 65211, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; Blastomeres/*physiology ; Cell Nucleus/metabolism ; Cell Polarity ; Ectoderm/*physiology ; *Embryonic Development ; Fertilization ; *Gene Expression Regulation, Developmental ; Homeodomain Proteins/*genetics/*metabolism ; In Situ Hybridization ; Mice ; Morula/physiology ; Oocytes/physiology ; RNA Interference ; RNA, Messenger/genetics/metabolism ; RNA, Small Interfering ; Transcription Factors/*genetics/*metabolism ; Transcription, Genetic ; Trophoblasts/*physiology ; Zygote/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Cell biology. Actin discrimination (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bulinski, J Chloe -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):180-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and the Department of Pathology and Cell Biology, Columbia University, 1212 Amsterdam Avenue, New York, NY 10027-2450, USA. jcb4@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840687" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/chemistry/*metabolism ; Actins/chemistry/genetics/*metabolism ; Aminoacyltransferases/genetics/*metabolism ; Animals ; Arginine/*metabolism ; Cell Movement ; Cytoplasm/chemistry/metabolism ; Evolution, Molecular ; Fibroblasts ; Mice ; Myosins/metabolism ; Profilins/metabolism ; Protein Isoforms/genetics/metabolism ; Pseudopodia/chemistry/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Cell signaling. A new way to burn fat (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neels, Jaap G -- Olefsky, Jerrold M -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1756-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0673, USA. jolefsky@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794069" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyl-CoA Carboxylase/antagonists & inhibitors/*metabolism ; Adipocytes/metabolism ; Adipose Tissue/*metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Energy Intake ; Energy Metabolism ; Enzyme Activation ; Fasting ; Fatty Acids/metabolism ; Hepatocytes/metabolism ; Insulin/physiology ; Insulin Resistance ; *Lipid Metabolism ; Lipogenesis ; Liver/metabolism ; Malonyl Coenzyme A/metabolism ; Mice ; Models, Biological ; Nuclear Proteins/*metabolism ; Obesity/therapy ; Oxidation-Reduction ; Phosphorylation ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/metabolism ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Mouse genetics. NIH knocks out key mouse house (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimm, David -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1863.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks/economics ; Costs and Cost Analysis ; Embryo, Mammalian/cytology ; Intellectual Property ; Mice ; *Mice, Knockout ; *National Institutes of Health (U.S.) ; *Organizations, Nonprofit/economics ; Stem Cells ; Texas ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Global control of dimorphism and virulence in fungi (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: Microbial pathogens that normally inhabit our environment can adapt to thrive inside mammalian hosts. There are six dimorphic fungi that cause disease worldwide, which switch from nonpathogenic molds in soil to pathogenic yeast after spores are inhaled and exposed to elevated temperature. Mechanisms that regulate this switch remain obscure. We show that a hybrid histidine kinase senses host signals and triggers the transition from mold to yeast. The kinase also regulates cell-wall integrity, sporulation, and expression of virulence genes in vivo. This global regulator shapes how dimorphic fungal pathogens adapt to the mammalian host, which has broad implications for treating and preventing systemic fungal disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemecek, Julie C -- Wuthrich, Marcel -- Klein, Bruce S -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):583-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, University of Wisconsin Hospital and Clinics, Madison, WI 53792, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645097" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastomyces/cytology/enzymology/*genetics/*pathogenicity ; Blastomycosis/microbiology ; Coccidioides/enzymology/genetics/pathogenicity ; Fungal Proteins/genetics/physiology ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Genetic Complementation Test ; Histoplasma/enzymology/genetics/pathogenicity ; Histoplasmosis/microbiology ; Lung Diseases, Fungal/microbiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutagenesis, Insertional ; Open Reading Frames ; Protein Kinases/chemistry/*genetics/*physiology ; RNA Interference ; Saccharomyces cerevisiae/genetics ; Soil Microbiology ; Spores, Fungal/physiology ; Temperature ; Virulence/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Mouse genetics. A mouse for every gene (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimm, David -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1862-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks ; Databases, Factual ; Embryo, Mammalian/cytology ; Financial Support ; Gene Targeting ; *Genes ; Genetic Techniques ; International Cooperation ; Mice ; *Mice, Knockout/genetics ; National Institutes of Health (U.S.) ; Patents as Topic ; Stem Cells ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Ca2+ entry through plasma membrane IP3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-15
    Description: Inositol 1,4,5-trisphosphate receptors (IP3Rs) release calcium ions, Ca2+, from intracellular stores, but their roles in mediating Ca2+ entry are unclear. IP3 stimulated opening of very few (1.9 +/- 0.2 per cell) Ca2+-permeable channels in whole-cell patch-clamp recording of DT40 chicken or mouse B cells. Activation of the B cell receptor (BCR) in perforated-patch recordings evoked the same response. IP3 failed to stimulate intracellular or plasma membrane (PM) channels in cells lacking IP3R. Expression of IP3R restored both responses. Mutations within the pore affected the conductances of IP3-activated PM and intracellular channels similarly. An impermeant pore mutant abolished BCR-evoked Ca2+ signals, and PM IP3Rs were undetectable. After introduction of an alpha-bungarotoxin binding site near the pore, PM IP3Rs were modulated by extracellular alpha-bungarotoxin. IP(3)Rs are unusual among endoplasmic reticulum proteins in being also functionally expressed at the PM, where very few IP3Rs contribute substantially to the Ca2+ entry evoked by the BCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dellis, Olivier -- Dedos, Skarlatos G -- Tovey, Stephen C -- Taufiq-Ur-Rahman -- Dubel, Stefan J -- Taylor, Colin W -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):229-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tennis Court Road, Cambridge, CB2 1PD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Bungarotoxins/metabolism/pharmacology ; Calcium/*metabolism ; Calcium Channels/genetics/*metabolism ; *Calcium Signaling ; Cell Membrane/*metabolism ; Cells, Cultured ; Chickens ; Electric Conductivity ; Endoplasmic Reticulum/metabolism ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; *Ion Channel Gating ; Mice ; Nuclear Envelope/metabolism ; Patch-Clamp Techniques ; Point Mutation ; Rats ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Oligonucleotide-modified gold nanoparticles for intracellular gene regulation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-20
    Description: We describe the use of gold nanoparticle-oligonucleotide complexes as intracellular gene regulation agents for the control of protein expression in cells. These oligonucleotide-modified nanoparticles have affinity constants for complementary nucleic acids that are higher than their unmodified oligonucleotide counterparts, are less susceptible to degradation by nuclease activity, exhibit greater than 99% cellular uptake, can introduce oligonucleotides at a higher effective concentration than conventional transfection agents, and are nontoxic to the cells under the conditions studied. By chemically tailoring the density of DNA bound to the surface of gold nanoparticles, we demonstrated a tunable gene knockdown.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosi, Nathaniel L -- Giljohann, David A -- Thaxton, C Shad -- Lytton-Jean, Abigail K R -- Han, Min Su -- Mirkin, Chad A -- New York, N.Y. -- Science. 2006 May 19;312(5776):1027-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and International Institute for Nanotechnology, Northwestern University, 2145 Sheridan Road, Evanston, IL 60208-3113 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16709779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Deoxyribonucleases/metabolism ; *Gene Expression Regulation ; Glutathione/metabolism ; *Gold ; Green Fluorescent Proteins/genetics ; HeLa Cells ; Humans ; Mice ; *Nanostructures ; *Oligodeoxyribonucleotides, Antisense/metabolism ; RNA, Messenger
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Cell biology. Purinergic chemotaxis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linden, Joel -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1689-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA. jlinden@virginia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170280" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Adenosine Monophosphate/metabolism ; Adenosine Triphosphate/*metabolism ; Animals ; Apyrase/pharmacology ; *Autocrine Communication ; Blood Platelets/metabolism ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Endothelial Cells/metabolism ; Mice ; Models, Biological ; N-Formylmethionine Leucyl-Phenylalanine ; Neutrophils/drug effects/*metabolism/physiology ; Receptor, Adenosine A3/metabolism ; Receptors, Purinergic/*metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2Y2 ; Respiratory Burst/drug effects ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Comment on "Cell type regulates selective segregation of mouse chromosome 7 DNA strands in mitosis" (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: Armakolas and Klar (Reports, 24 February 2006, p. 1146) suggested that segregation of mouse chromosome 7, after induction of a site-specific crossover between homologous chromosomes, is driven by a preferential inheritance of the old Watson and the old Crick DNA strands. However, this interpretation only considered half of the possible outcomes. The conjecture fails when all possible outcomes are examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haber, James E -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1045; author reply 1045.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosenstiel Center and Department of Biology, Brandeis University, Waltham, MA 02454-9110, USA. haber@brandeis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Chromatids/physiology ; *Chromosome Segregation ; Chromosomes, Mammalian/*physiology ; Crossing Over, Genetic ; DNA/metabolism ; Ectoderm/cytology ; Embryo, Mammalian/cytology ; Endoderm/cytology ; G2 Phase ; Mice ; *Mitosis ; Recombination, Genetic ; Stem Cells/cytology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Defective lipolysis and altered energy metabolism in mice lacking adipose triglyceride lipase (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-06
    Description: Fat tissue is the most important energy depot in vertebrates. The release of free fatty acids (FFAs) from stored fat requires the enzymatic activity of lipases. We showed that genetic inactivation of adipose triglyceride lipase (ATGL) in mice increases adipose mass and leads to triacylglycerol deposition in multiple tissues. ATGL-deficient mice accumulated large amounts of lipid in the heart, causing cardiac dysfunction and premature death. Defective cold adaptation indicated that the enzyme provides FFAs to fuel thermogenesis. The reduced availability of ATGL-derived FFAs leads to increased glucose use, increased glucose tolerance, and increased insulin sensitivity. These results indicate that ATGL is rate limiting in the catabolism of cellular fat depots and plays an important role in energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haemmerle, Guenter -- Lass, Achim -- Zimmermann, Robert -- Gorkiewicz, Gregor -- Meyer, Carola -- Rozman, Jan -- Heldmaier, Gerhard -- Maier, Robert -- Theussl, Christian -- Eder, Sandra -- Kratky, Dagmar -- Wagner, Erwin F -- Klingenspor, Martin -- Hoefler, Gerald -- Zechner, Rudolf -- F 3001/Austrian Science Fund FWF/Austria -- F 3002/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 May 5;312(5774):734-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biosciences, University of Graz, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675698" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/metabolism ; Adipose Tissue/anatomy & histology/*enzymology/metabolism ; Adipose Tissue, Brown/enzymology ; Animals ; Blood Glucose/metabolism ; Carboxylic Ester Hydrolases/deficiency/genetics/*metabolism ; Cell Size ; *Energy Metabolism ; Fatty Acids, Nonesterified/blood/metabolism ; Female ; Heart Failure/pathology ; Homeostasis ; Insulin/blood ; Isoproterenol/pharmacology ; Kidney/metabolism ; Lipase/deficiency/genetics/*metabolism ; Lipids/blood ; *Lipolysis/drug effects ; Male ; Mice ; Myocardium/metabolism/pathology ; Myocytes, Cardiac/cytology/metabolism ; Oxygen Consumption ; Testis/metabolism ; Thermogenesis ; Triglycerides/*metabolism ; Ventricular Dysfunction, Left/physiopathology
    Print ISSN: 0036-8075
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  • 23
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    Immunology. Unraveling gut inflammation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strober, Warren -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1052-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Host Defenses, National Institutes of Health. Bethesda, MD 20892-1890. USA. wstrober@niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*biosynthesis/metabolism ; Bacteria/growth & development/*immunology ; Biomarkers, Tumor/*biosynthesis/metabolism ; Crohn Disease/immunology ; Dendritic Cells/immunology/microbiology ; Gastroenteritis/*immunology ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Inflammatory Bowel Diseases/*immunology/metabolism ; Intestinal Mucosa/cytology/immunology/metabolism/microbiology ; Intestines/*microbiology ; Lectins, C-Type/*biosynthesis/metabolism ; Mice ; Paneth Cells/*metabolism ; Peptidoglycan/metabolism ; Proteins/*metabolism ; alpha-Defensins/biosynthesis/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-beta (TGF-beta) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-beta signaling and can be prevented by TGF-beta antagonists such as TGF-beta-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1482474/" 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/PMC1482474/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habashi, Jennifer P -- Judge, Daniel P -- Holm, Tammy M -- Cohn, Ronald D -- Loeys, Bart L -- Cooper, Timothy K -- Myers, Loretha -- Klein, Erin C -- Liu, Guosheng -- Calvi, Carla -- Podowski, Megan -- Neptune, Enid R -- Halushka, Marc K -- Bedja, Djahida -- Gabrielson, Kathleen -- Rifkin, Daniel B -- Carta, Luca -- Ramirez, Francesco -- Huso, David L -- Dietz, Harry C -- K08 HL067056/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601194" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Antagonists/administration & dosage/therapeutic use ; Angiotensin II Type 1 Receptor Blockers/administration & dosage/*therapeutic use ; Animals ; Antibodies/immunology ; Aorta/pathology ; Aortic Aneurysm/etiology/*prevention & control ; *Disease Models, Animal ; Elastic Tissue/pathology ; Female ; Losartan/administration & dosage/*therapeutic use ; Lung/pathology ; Lung Diseases/drug therapy/pathology ; Marfan Syndrome/complications/*drug therapy/metabolism/pathology ; Mice ; Microfilament Proteins/genetics ; Mutation ; Neutralization Tests ; Pregnancy ; Pregnancy Complications/drug therapy ; Propranolol/administration & dosage/therapeutic use ; Pulmonary Alveoli/pathology ; Receptor, Angiotensin, Type 1/metabolism ; Signal Transduction ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*metabolism
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  • 25
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    Receptor activation alters inner surface potential during phagocytosis (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-07-22
    Description: The surface potential of biological membranes varies according to their lipid composition. We devised genetically encoded probes to assess surface potential in intact cells. These probes revealed marked, localized alterations in the charge of the inner surface of the plasma membrane of macrophages during the course of phagocytosis. Hydrolysis of phosphoinositides and displacement of phosphatidylserine accounted for the change in surface potential at the phagosomal cup. Signaling molecules such as K-Ras, Rac1, and c-Src that are targeted to the membrane by electrostatic interactions were rapidly released from membrane subdomains where the surface charge was altered by lipid remodeling during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Terebiznik, Mauricio -- Yu, Liming -- Silvius, John -- Abidi, Wasif M -- Philips, Mark -- Levine, Tim -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):347-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hepatology, and Nutrition Department, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Line ; Cell Membrane/*physiology ; Fluorescent Dyes/metabolism ; Hydrophobic and Hydrophilic Interactions ; Immunoglobulin G/immunology ; Ionomycin/pharmacology ; Lipid Bilayers/metabolism ; Liposomes/metabolism ; Macrophages/*physiology ; Membrane Potentials ; Mice ; Molecular Probes/metabolism ; Neuropeptides/metabolism ; Opsonin Proteins ; Peptides/metabolism ; *Phagocytosis ; Phagosomes/physiology ; Phospholipids/analysis/metabolism ; Receptors, Fc/immunology/metabolism ; Static Electricity ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein ; ras Proteins/metabolism
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  • 26
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    Neuroscience. Neuron, know thy neighbor (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DiCicco-Bloom, Emanuel -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1560-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Cell Biology/Pediatrics (Neurology), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA. diciccem@umdnj.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543446" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/*physiology/ultrastructure ; Animals ; Brain/cytology/*embryology ; *Cell Adhesion ; Cell Count ; Cell Death ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Central Nervous System/cytology/embryology ; Cytoskeleton/physiology ; Hedgehog Proteins ; Hyperplasia ; Mice ; Mutation ; Neurons/cytology/*physiology ; Signal Transduction ; Stem Cells/cytology/physiology ; Trans-Activators/*metabolism ; alpha Catenin/genetics/*physiology
    Print ISSN: 0036-8075
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  • 27
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    Sequential interplay of nicotinic and GABAergic signaling guides neuronal development (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-13
    Description: GABA (gamma-aminobutyric acid), the major inhibitory transmitter in the brain, goes through a transitory phase of excitation during development. The excitatory phase promotes neuronal growth and integration into circuits. We show here that spontaneous nicotinic cholinergic activity is responsible for terminating GABAergic excitation and initiating inhibition. It does so by changing chloride transporter levels, shifting the driving force on GABA-induced currents. The timing of the transition is critical, because the two phases of GABAergic signaling provide contrasting developmental instructions. Synergistic with nicotinic excitation, GABAergic inhibition constrains neuronal morphology and innervation. The results reveal a multitiered activity-dependent strategy controlling neuronal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Zhaoping -- Neff, Robert A -- Berg, Darwin K -- NS012601/NS/NINDS NIH HHS/ -- NS035469/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 8;314(5805):1610-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17158331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadmium/pharmacology ; Calcium/metabolism ; Chick Embryo ; Chlorides/metabolism ; Ganglia, Parasympathetic/cytology/embryology ; Hippocampus/cytology/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/cytology/*physiology ; Nicotine/metabolism/pharmacology ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Receptors, Nicotinic/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Sodium-Potassium-Chloride Symporters/metabolism ; Solute Carrier Family 12, Member 2 ; Symporters/genetics/metabolism ; Synaptic Transmission ; Transfection ; alpha7 Nicotinic Acetylcholine Receptor ; gamma-Aminobutyric Acid/*metabolism
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    ATP release guides neutrophil chemotaxis via P2Y2 and A3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: Cells must amplify external signals to orient and migrate in chemotactic gradient fields. We find that human neutrophils release adenosine triphosphate (ATP) from the leading edge of the cell surface to amplify chemotactic signals and direct cell orientation by feedback through P2Y2 nucleotide receptors. Neutrophils rapidly hydrolyze released ATP to adenosine that then acts via A3-type adenosine receptors, which are recruited to the leading edge, to promote cell migration. Thus, ATP release and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling gradient sensing and migration of neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Yu -- Corriden, Ross -- Inoue, Yoshiaki -- Yip, Linda -- Hashiguchi, Naoyuki -- Zinkernagel, Annelies -- Nizet, Victor -- Insel, Paul A -- Junger, Wolfgang G -- GM-60475/GM/NIGMS NIH HHS/ -- GM-66232/GM/NIGMS NIH HHS/ -- PR043034/PR/OCPHP CDC HHS/ -- R01 GM-51477/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of California San Diego, San Diego, CA 92103, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170310" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism/pharmacology ; Adenosine A3 Receptor Agonists ; Adenosine A3 Receptor Antagonists ; Adenosine Triphosphate/analogs & derivatives/*metabolism/pharmacology ; Animals ; *Autocrine Communication ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Cytoplasmic Granules/metabolism ; HL-60 Cells ; Humans ; Hydrolysis ; Mice ; Mice, Knockout ; Neutrophils/drug effects/metabolism/*physiology ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A3/*metabolism ; Receptors, Purinergic P2/*metabolism ; Receptors, Purinergic P2Y2 ; Signal Transduction ; Suramin/pharmacology
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    Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: A common single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations in brain anatomy and memory, but its relevance to clinical disorders is unclear. We generated a variant BDNF mouse (BDNF(Met/Met)) that reproduces the phenotypic hallmarks in humans with the variant allele. BDNF(Met) was expressed in brain at normal levels, but its secretion from neurons was defective. When placed in stressful settings, BDNF(Met/Met) mice exhibited increased anxiety-related behaviors that were not normalized by the antidepressant, fluoxetine. A variant BDNF may thus play a key role in genetic predispositions to anxiety and depressive disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1880880/" 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/PMC1880880/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhe-Yu -- Jing, Deqiang -- Bath, Kevin G -- Ieraci, Alessandro -- Khan, Tanvir -- Siao, Chia-Jen -- Herrera, Daniel G -- Toth, Miklos -- Yang, Chingwen -- McEwen, Bruce S -- Hempstead, Barbara L -- Lee, Francis S -- MH060478/MH/NIMH NIH HHS/ -- MH068850/MH/NIMH NIH HHS/ -- NS052819/NS/NINDS NIH HHS/ -- NS30687/NS/NINDS NIH HHS/ -- R01 NS052819/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10021, USA. zheyuchen@sdu.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023662" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anxiety/drug therapy/*genetics ; Behavior, Animal ; Brain-Derived Neurotrophic Factor/*genetics/*physiology ; Conditioning (Psychology) ; Dendrites/ultrastructure ; Dentate Gyrus/cytology ; Fear ; Fluoxetine/administration & dosage/pharmacology ; Hippocampus/anatomy & histology/metabolism ; Memory ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Neurons/cytology/metabolism ; Organ Size ; *Polymorphism, Single Nucleotide ; Rats ; Rats, Sprague-Dawley ; Serotonin Uptake Inhibitors/administration & dosage/pharmacology
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    A bacterial protein enhances the release and efficacy of liposomal cancer drugs (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-25
    Description: Clostridium novyi-NT is an anaerobic bacterium that can infect hypoxic regions within experimental tumors. Because C. novyi-NT lyses red blood cells, we hypothesized that its membrane-disrupting properties could be exploited to enhance the release of liposome-encapsulated drugs within tumors. Here, we show that treatment of mice bearing large, established tumors with C. novyi-NT plus a single dose of liposomal doxorubicin often led to eradication of the tumors. The bacterial factor responsible for the enhanced drug release was identified as a previously unrecognized protein termed liposomase. This protein could potentially be incorporated into diverse experimental approaches for the specific delivery of chemotherapeutic agents to tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheong, Ian -- Huang, Xin -- Bettegowda, Chetan -- Diaz, Luis A Jr -- Kinzler, Kenneth W -- Zhou, Shibin -- Vogelstein, Bert -- CA062924/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and the Ludwig Center for Cancer Genetics and Therapeutics, Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antineoplastic Agents/*administration & dosage/pharmacokinetics/therapeutic use ; Bacterial Proteins/chemistry/genetics/*metabolism ; Base Sequence ; Camptothecin/administration & dosage/analogs & ; derivatives/pharmacokinetics/therapeutic use ; Cell Line, Tumor ; Cloning, Molecular ; Clostridium/*chemistry/genetics ; Colorectal Neoplasms/*drug therapy ; Doxorubicin/*administration & dosage/pharmacokinetics/therapeutic use ; Drug Carriers ; Humans ; Lipase/chemistry/genetics/*metabolism ; Lipid Bilayers/chemistry ; Liposomes/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Protein Structure, Tertiary
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    Neuroscience. Neurons find strength through synchrony in the brain (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alonso, Jose-Manuel -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1604-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, State University of New York College of Optometry, New York, NY 10036, USA. jalonso@sunyopt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Excitatory Postsynaptic Potentials ; Mice ; Neural Pathways ; Neurons/*physiology ; Rats ; Somatosensory Cortex/*physiology ; Synapses/*physiology ; *Synaptic Transmission ; Thalamus/*physiology
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    A critical role for the innate immune signaling molecule IRAK-4 in T cell activation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-01
    Description: IRAK-4 is a protein kinase that is pivotal in mediating signals for innate immune responses. Here, we report that IRAK-4 signaling is also essential for eliciting adaptive immune responses. Thus, in the absence of IRAK-4, in vivo T cell responses were significantly impaired. Upon T cell receptor stimulation, IRAK-4 is recruited to T cell lipid rafts, where it induces downstream signals, including protein kinase C activation through the association with Zap70. This signaling pathway was found to be required for optimal activation of nuclear factor kappaB. Our findings suggest that T cells use this critical regulator of innate immunity for the development of acquired immunity, suggesting that IRAK-4 may be involved in direct signal cross talk between the two systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Nobutaka -- Suzuki, Shinobu -- Millar, Douglas G -- Unno, Midori -- Hara, Hiromitsu -- Calzascia, Thomas -- Yamasaki, Sho -- Yokosuka, Tadashi -- Chen, Nien-Jung -- Elford, Alisha R -- Suzuki, Jun-Ichiro -- Takeuchi, Arata -- Mirtsos, Christine -- Bouchard, Denis -- Ohashi, Pamela S -- Yeh, Wen-Chen -- Saito, Takashi -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1927-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama City, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574867" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Activation ; Immunity, Innate ; Interleukin-1 Receptor-Associated Kinases ; Isoenzymes/metabolism ; *Lymphocyte Activation ; Membrane Microdomains/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; NF-kappa B/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism ; Protein Kinase C/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; ZAP-70 Protein-Tyrosine Kinase/metabolism
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    Evidence for a functional second thymus in mice (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-03-04
    Description: The thymus organ supports the development of T cells and is located in the thorax. Here, we report the existence of a second thymus in the mouse neck, which develops after birth and grows to the size of a small lymph node. The cervical thymus had a typical medulla-cortex structure, was found to support T cell development, and could correct T cell deficiency in athymic nude mice upon transplantation. The identification of a regular second thymus in the mouse may provide evolutionary links to thymus organogenesis in other vertebrates and suggests a need to reconsider the effect of thoracic thymectomy on de novo T cell production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Terszowski, Grzegorz -- Muller, Susanna M -- Bleul, Conrad C -- Blum, Carmen -- Schirmbeck, Reinhold -- Reimann, Jorg -- Pasquier, Louis Du -- Amagai, Takashi -- Boehm, Thomas -- Rodewald, Hans-Reimer -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):284-7. Epub 2006 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Ulm, D-89081 Ulm, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513945" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Choristoma ; Forkhead Transcription Factors/genetics/physiology ; Hematopoietic Stem Cells/cytology ; Hepatitis B Antibodies/biosynthesis ; Hepatitis B Surface Antigens/immunology ; Histocompatibility Antigens Class II ; Immunocompetence ; Lymphopoiesis ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; *Neck ; Receptors, Antigen, T-Cell/analysis ; Self Tolerance ; T-Lymphocytes/*immunology ; Thymectomy ; Thymus Gland/anatomy & histology/growth & development/*immunology/transplantation
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    Alterations in 5-HT1B receptor function by p11 in depression-like states (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-10
    Description: The pathophysiology of depression remains enigmatic, although abnormalities in serotonin signaling have been implicated. We have found that the serotonin 1B receptor [5-hydroxytryptamine (5-HT1B) receptor] interacts with p11. p11 increases localization of 5-HT1B receptors at the cell surface. p11 is increased in rodent brains by antidepressants or electroconvulsive therapy, but decreased in an animal model of depression and in brain tissue from depressed patients. Overexpression of p11 increases 5-HT1B receptor function in cells and recapitulates certain behaviors seen after antidepressant treatment in mice. p11 knockout mice exhibit a depression-like phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reactions to an antidepressant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Chergui, Karima -- Rachleff, Ilan -- Flajolet, Marc -- Zhang, Xiaoqun -- El Yacoubi, Malika -- Vaugeois, Jean-Marie -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):77-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400147" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Animals ; Annexin A2/genetics/*metabolism ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Brain/drug effects/metabolism ; Cell Membrane/metabolism ; Depression/genetics/*metabolism ; Electroconvulsive Therapy ; Female ; Humans ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Neurons/metabolism ; Rats ; Receptor, Serotonin, 5-HT1B/*metabolism ; S100 Proteins/genetics/*metabolism ; Serotonin/metabolism/physiology ; Signal Transduction ; Two-Hybrid System Techniques
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    Biomedicine. Life, the universe, and body temperature (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saper, Clifford B -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):773-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Division of Sleep Medicine, and Program in Neuroscience, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. csaper@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Body Temperature ; Body Temperature Regulation ; Body Weight ; Humans ; Hypothalamus/physiology ; Ion Channels/genetics/physiology ; *Longevity ; Mice ; Mice, Transgenic ; Mitochondrial Proteins/genetics/physiology ; Preoptic Area/*physiology
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    Role of noradrenergic signaling by the nucleus tractus solitarius in mediating opiate reward (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Norepinephrine (NE) is widely implicated in opiate withdrawal, but much less is known about its role in opiate-induced locomotion and reward. In mice lacking dopamine beta-hydroxylase (DBH), an enzyme critical for NE synthesis, we found that NE was necessary for morphine-induced conditioned place preference (CPP; a measure of reward) and locomotion. These deficits were rescued by systemic NE restoration. Viral restoration of DBH expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored CPP for morphine. Morphine-induced locomotion was partially restored by DBH expression in either brain region. These data suggest that NE signaling by the nucleus tractus solitarius is necessary for morphine reward.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Valerie G -- Heusner, Carrie L -- Bland, Ross J -- During, Matthew J -- Weinshenker, David -- Palmiter, Richard D -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1017-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Conditioning (Psychology) ; Dopamine beta-Hydroxylase/genetics/metabolism ; Droxidopa/pharmacology ; Locomotion/drug effects ; Locus Coeruleus/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Morphine/*pharmacology ; Motor Activity/drug effects ; Norepinephrine/*physiology ; *Reward ; Signal Transduction ; Solitary Nucleus/*physiology ; *Synaptic Transmission
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    Combinatorial effects of odorant mixes in olfactory cortex (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-03-11
    Description: In mammals, each odorant is detected by a combination of different odorant receptors. Signals from different types of receptors are segregated in the nose and the olfactory bulb, but appear to be combined in individual neurons in the olfactory cortex. Here, we report that binary odorant mixes stimulate cortical neurons that are not stimulated by their individual component odorants. We propose that cortical neurons require combinations of receptor inputs for activation and that merging the receptor codes of two odorants provides novel combinations of receptor inputs that stimulate neurons beyond those activated by the single odorants. These findings may explain why odorant mixtures can elicit novel odor percepts in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, Zhihua -- Buck, Linda B -- R03 DC008700-01/DC/NIDCD NIH HHS/ -- R21 DC008628-01/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1477-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Complex Mixtures ; Cytoskeletal Proteins/metabolism ; Humans ; In Situ Hybridization, Fluorescence/methods ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/metabolism ; Neurons/physiology ; *Odors ; Olfactory Pathways/cytology/*physiology ; Olfactory Receptor Neurons/physiology ; RNA, Messenger/metabolism ; Receptors, Odorant/*physiology ; Smell/*physiology
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    Developmental biology. The Turing model comes of molecular age (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-02
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383235/" 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/PMC4383235/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maini, Philip K -- Baker, Ruth E -- Chuong, Cheng-Ming -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR042177-11/AR/NIAMS NIH HHS/ -- R01 AR042177-12/AR/NIAMS NIH HHS/ -- R01 AR047364/AR/NIAMS NIH HHS/ -- R01 AR047364-04/AR/NIAMS NIH HHS/ -- R01 AR047364-05/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1397-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Mathematical Biology, University of Oxford, Oxford OX1 3LB, UK. maini@maths.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17138885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Diffusion ; Hair Follicle/*growth & development/metabolism ; Intercellular Signaling Peptides and Proteins/*metabolism ; Mathematics ; Mice ; *Models, Biological ; Signal Transduction ; Wnt Proteins/*metabolism
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    Immunology. When F-actin becomes too much of a good thing (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dustin, Michael L -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):767-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Progam in Molecular Pathogenesis, Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA. dustin@saturn.med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902113" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/antagonists & inhibitors/metabolism ; Actins/*metabolism ; Animals ; Apoptosis ; Binding Sites ; Cell Death ; Cell Movement ; *Chemotaxis, Leukocyte ; Homeostasis ; Intracellular Membranes/physiology ; Membrane Potentials ; Mice ; Microfilament Proteins/chemistry/*physiology ; Mitochondria/*physiology ; Protein Structure, Tertiary ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology/*physiology ; Voltage-Dependent Anion Channels/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Prions in skeletal muscles of deer with chronic wasting disease (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-28
    Description: The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Angers, Rachel C -- Browning, Shawn R -- Seward, Tanya S -- Sigurdson, Christina J -- Miller, Michael W -- Hoover, Edward A -- Telling, Glenn C -- 2RO1 NS040334-04/NS/NINDS NIH HHS/ -- N01-AI-25491/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1117. Epub 2006 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY 40536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Chemistry ; *Deer ; Humans ; Mice ; Mice, Transgenic ; Muscle, Skeletal/*chemistry ; PrPSc Proteins/*analysis ; Prions/*analysis ; Tissue Extracts/administration & dosage ; Wasting Disease, Chronic/*metabolism/*transmission
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    New neurons follow the flow of cerebrospinal fluid in the adult brain (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-18
    Description: In the adult brain, neuroblasts born in the subventricular zone migrate from the walls of the lateral ventricles to the olfactory bulb. How do these cells orient over such a long distance and through complex territories? Here we show that neuroblast migration parallels cerebrospinal fluid (CSF) flow. Beating of ependymal cilia is required for normal CSF flow, concentration gradient formation of CSF guidance molecules, and directional migration of neuroblasts. Results suggest that polarized epithelial cells contribute important vectorial information for guidance of young, migrating neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawamoto, Kazunobu -- Wichterle, Hynek -- Gonzalez-Perez, Oscar -- Cholfin, Jeremy A -- Yamada, Masayuki -- Spassky, Nathalie -- Murcia, Noel S -- Garcia-Verdugo, Jose Manuel -- Marin, Oscar -- Rubenstein, John L R -- Tessier-Lavigne, Marc -- Okano, Hideyuki -- Alvarez-Buylla, Arturo -- HD 32116/HD/NICHD NIH HHS/ -- NS 28478/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):629-32. Epub 2006 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and Developmental and Stem Cell Biology Program, University of California San Francisco, San Francisco, CA 94143, USA. sawamoto@sc.itc.keio.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Tissue Transplantation ; Cell Movement ; Cell Polarity ; Cerebral Ventricles/cytology/physiology ; Cerebrospinal Fluid/*physiology ; Choroid Plexus/secretion ; Cilia/physiology ; Ependyma/cytology/*physiology ; Epithelial Cells/physiology ; Intercellular Signaling Peptides and Proteins ; Mice ; Nerve Tissue Proteins/cerebrospinal fluid ; Neurons/cytology/*physiology ; Olfactory Bulb/cytology/physiology ; Recombinant Fusion Proteins/cerebrospinal fluid
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Dendritic cell apoptosis in the maintenance of immune tolerance (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: Apoptosis in the immune system is critical for maintaining self-tolerance and preventing autoimmunity. Nevertheless, inhibiting apoptosis in lymphocytes is not alone sufficient to break self-tolerance, suggesting the involvement of other cell types. We investigated whether apoptosis in dendritic cells (DCs) helps regulate self-tolerance by generating transgenic mice expressing the baculoviral caspase inhibitor, p35, in DCs (DC-p35). DC-p35 mice displayed defective DC apoptosis, resulting in their accumulation and, in turn, chronic lymphocyte activation and systemic autoimmune manifestations. The observation that a defect in DC apoptosis can independently lead to autoimmunity is consistent with a central role for these cells in maintaining immune self-tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Min -- Wang, Yui-Hsi -- Wang, Yihong -- Huang, Li -- Sandoval, Hector -- Liu, Yong-Jun -- Wang, Jin -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1160-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA. minc@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497935" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Aging ; Animals ; Antibodies, Antinuclear/analysis ; *Apoptosis ; *Autoimmunity ; B-Lymphocytes/immunology ; Caspase Inhibitors ; Cell Survival ; Dendritic Cells/*immunology/*physiology ; Kidney/immunology ; Lung/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; *Self Tolerance ; Spleen/immunology ; T-Lymphocytes/immunology ; Viral Proteins/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genetic polymorphism of Fc (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandey, Janardan P -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1376-7; author reply 1376-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527951" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Immunoglobulin G/immunology ; Mice ; *Polymorphism, Genetic ; Receptors, IgG/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hoxa2- and rhombomere-dependent development of the mouse facial somatosensory map (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: In the mouse trigeminal pathway, sensory inputs from distinct facial structures, such as whiskers or lower jaw and lip, are topographically mapped onto the somatosensory cortex through relay stations in the thalamus and hindbrain. In the developing hindbrain, the mechanisms generating such maps remain elusive. We found that in the principal sensory nucleus, the whisker-related map is contributed by rhombomere 3-derived neurons, whereas the rhombomere 2-derived progeny supply the lower jaw and lip representation. Moreover, early Hoxa2 expression in neuroepithelium prevents the trigeminal nerve from ectopically projecting to the cerebellum, whereas late expression in the principal sensory nucleus promotes selective arborization of whisker-related afferents and topographic connectivity to the thalamus. Hoxa2 inactivation further results in the absence of whisker-related maps in the postnatal brain. Thus, Hoxa2- and rhombomere 3-dependent cues determine the whisker area map and are required for the assembly of the whisker-to-barrel somatosensory circuit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oury, Franck -- Murakami, Yasunori -- Renaud, Jean-Sebastien -- Pasqualetti, Massimo -- Charnay, Patrick -- Ren, Shu-Yue -- Rijli, Filippo M -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1408-13. Epub 2006 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/Universite Louis Pasteur, UMR 7104, BP 10142, Communaute Urbaine de Strasbourg, 67404 Illkirch Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902088" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; Axons/ultrastructure ; Face/innervation ; Homeodomain Proteins/genetics/*physiology ; Lip/innervation ; Mandible/embryology/innervation ; Mice ; Mice, Transgenic ; Mutation ; Neurons, Afferent/cytology ; Receptor, EphA4/metabolism ; Receptor, EphA7/metabolism ; Rhombencephalon/cytology/*embryology/metabolism ; Somatosensory Cortex/*anatomy & histology/embryology ; Thalamus/embryology/metabolism ; Trigeminal Ganglion/embryology/metabolism ; Trigeminal Nerve/*embryology/physiology ; Ventral Thalamic Nuclei/embryology ; Vibrissae/*innervation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Development. Gene-suppressing proteins reveal secrets of stem cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):349.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627706" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*metabolism ; Cell Differentiation ; Chromatin/*physiology ; Embryo, Mammalian/cytology ; Gene Expression Regulation, Developmental ; *Gene Silencing ; *Genes, Regulator ; Genome, Human ; Humans ; Mice ; Nuclear Proteins ; Pluripotent Stem Cells/cytology/*physiology ; Polycomb Repressive Complex 2 ; Polycomb-Group Proteins ; Repressor Proteins/*metabolism
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    Prion-induced amyloid heart disease with high blood infectivity in transgenic mice (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-11
    Description: We investigated extraneural manifestations in scrapie-infected transgenic mice expressing prion protein lacking the glycophosphatydylinositol membrane anchor. In the brain, blood, and heart, both abnormal protease-resistant prion protein (PrPres) and prion infectivity were readily detected by immunoblot and by inoculation into nontransgenic recipients. The titer of infectious scrapie in blood plasma exceeded 10(7) 50% infectious doses per milliliter. The hearts of these transgenic mice contained PrPres-positive amyloid deposits that led to myocardial stiffness and cardiac disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820586/" 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/PMC1820586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trifilo, Matthew J -- Yajima, Toshitaka -- Gu, Yusu -- Dalton, Nancy -- Peterson, Kirk L -- Race, Richard E -- Meade-White, Kimberly -- Portis, John L -- Masliah, Eliezer -- Knowlton, Kirk U -- Chesebro, Bruce -- Oldstone, Michael B A -- 5R01HL66424-04/HL/NHLBI NIH HHS/ -- AGO4342/PHS HHS/ -- NS041219-05/NS/NINDS NIH HHS/ -- P01 AG004342/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Viral-Immunobiology Laboratory, Departments of Molecular and Integrative Neurosciences and Infectology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825571" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/*analysis ; Amyloidosis/blood/etiology/*pathology/physiopathology ; Animals ; Blotting, Western ; Cardiac Catheterization ; Coronary Vessels/chemistry/pathology ; Disease Models, Animal ; Glycosylphosphatidylinositols ; Heart Diseases/blood/etiology/*pathology/physiopathology ; Heart Function Tests ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microcirculation/chemistry/pathology ; Myocardial Contraction ; Myocardium/*chemistry/*pathology ; PrPC Proteins/chemistry ; PrPSc Proteins/*analysis/blood ; Scrapie/blood/*pathology/physiopathology ; Staining and Labeling ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    p53 regulates mitochondrial respiration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: The energy that sustains cancer cells is derived preferentially from glycolysis. This metabolic change, the Warburg effect, was one of the first alterations in cancer cells recognized as conferring a survival advantage. Here, we show that p53, one of the most frequently mutated genes in cancers, modulates the balance between the utilization of respiratory and glycolytic pathways. We identify Synthesis of Cytochrome c Oxidase 2 (SCO2) as the downstream mediator of this effect in mice and human cancer cell lines. SCO2 is critical for regulating the cytochrome c oxidase (COX) complex, the major site of oxygen utilization in the eukaryotic cell. Disruption of the SCO2 gene in human cancer cells with wild-type p53 recapitulated the metabolic switch toward glycolysis that is exhibited by p53-deficient cells. That SCO2 couples p53 to mitochondrial respiration provides a possible explanation for the Warburg effect and offers new clues as to how p53 might affect aging and metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matoba, Satoaki -- Kang, Ju-Gyeong -- Patino, Willmar D -- Wragg, Andrew -- Boehm, Manfred -- Gavrilova, Oksana -- Hurley, Paula J -- Bunz, Fred -- Hwang, Paul M -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1650-3. Epub 2006 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728594" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Carrier Proteins ; Cell Line, Tumor ; *Cell Respiration ; Cell Survival ; Electron Transport Complex IV/*genetics/metabolism/physiology ; Gene Expression Regulation, Neoplastic ; *Genes, p53 ; Glycolysis ; Humans ; Membrane Proteins/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria/*metabolism ; Mitochondria, Liver/*metabolism ; Mitochondrial Proteins ; Mutation ; Oxygen Consumption ; Proteins/*genetics/physiology ; RNA, Small Interfering ; Recombination, Genetic ; Transcription, Genetic ; Transcriptional Activation ; Tumor Suppressor Protein p53/*physiology
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    Stem cells. Scientists create human stem cell line from 'dead' embryos (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1869.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*cytology/physiology ; Cell Differentiation ; *Cell Line ; Cell Proliferation ; *Embryo Loss ; Embryo Research/economics ; Humans ; Mice ; *Pluripotent Stem Cells/cytology ; Research Support as Topic
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    Reversal of diabetes in non-obese diabetic mice without spleen cell-derived beta cell regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-25
    Description: Autoimmune destruction of beta cells is the predominant cause of type 1 diabetes mellitus (T1DM) in humans and is modeled in non-obese diabetic (NOD) mice. Many therapeutic interventions prevent the development of T1DM in NOD mice, but few can induce its reversal once established. Intervention with Freund's complete adjuvant, semi-allogeneic splenocytes, and temporary islet transplantation has been reported to cure NOD mice of established T1DM. Using the same approach, we report here that this treatment cured 32% of NOD mice of established diabetes (〉340 milligrams per deciliter blood glucose), although beta cells in these mice were not derived from donor splenocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chong, Anita S -- Shen, Jikun -- Tao, Jing -- Yin, Dengping -- Kuznetsov, Andrey -- Hara, Manami -- Philipson, Louis H -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1774-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Transplantation, Department of Surgery, University of Chicago, Chicago, IL 60637, USA. achong@uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556844" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; Blood Glucose/analysis ; Cell Differentiation ; *Cell Transplantation ; Combined Modality Therapy ; Diabetes Mellitus, Type 1/immunology/pathology/*therapy ; Female ; Freund's Adjuvant/*therapeutic use ; Green Fluorescent Proteins/analysis ; Insulin-Secreting Cells/*cytology/physiology ; *Islets of Langerhans Transplantation ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Regeneration ; Spleen/*cytology ; Stem Cells/cytology/physiology
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    Immunology. Foiled dendritic cell suicide may lead to autoimmunity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1086.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497897" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Autoimmune Diseases/immunology ; *Autoimmunity ; Caspase 10 ; Caspase Inhibitors ; Caspases/genetics/metabolism ; Dendritic Cells/*immunology/*physiology ; Humans ; Lymphocyte Activation ; Mice ; Mutation ; Viral Proteins/genetics/metabolism
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    Cell biology. Balancing life-or-death decisions (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bartek, Jiri -- Lukas, Jiri -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):261-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark. jb@cancer.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; BRCA2 Protein/metabolism ; Cell Cycle ; Cell Nucleus/metabolism ; Cell Survival ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/*metabolism ; *DNA Damage ; DNA Repair ; DNA Replication ; Forkhead Transcription Factors/*metabolism ; Gene Expression Regulation ; Humans ; Mice ; Models, Biological ; Phosphorylation ; RNA, Small Interfering ; Transcription, Genetic ; cdc25 Phosphatases/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Caveolin-1 is essential for liver regeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-16
    Description: Liver regeneration is an orchestrated cellular response that coordinates cell activation, lipid metabolism, and cell division. We found that caveolin-1 gene-disrupted mice (cav1-/- mice) exhibited impaired liver regeneration and low survival after a partial hepatectomy. Hepatocytes showed dramatically reduced lipid droplet accumulation and did not advance through the cell division cycle. Treatment of cav1-/- mice with glucose (which is a predominant energy substrate when compared to lipids) drastically increased survival and reestablished progression of the cell cycle. Thus, caveolin-1 plays a crucial role in the mechanisms that coordinate lipid metabolism with the proliferative response occurring in the liver after cellular injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, Manuel A -- Albor, Cecilia -- Ingelmo-Torres, Mercedes -- Nixon, Susan J -- Ferguson, Charles -- Kurzchalia, Teymuras -- Tebar, Francesc -- Enrich, Carlos -- Parton, Robert G -- Pol, Albert -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1628-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Biologia Cellular, Facultat de Medicina, Institut d'Investigacions Biomediques August Pi i Sunyer, Universitat de Barcelona, Casanova 143, 08036 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caveolae/metabolism ; Caveolin 1/genetics/*physiology ; Cell Cycle ; Cell Division ; Fatty Acids/blood/metabolism ; Glucose/administration & dosage ; Hepatectomy ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/cytology/*metabolism ; *Lipid Metabolism ; Lipids/blood ; Liver/metabolism/ultrastructure ; *Liver Regeneration ; Male ; Mice ; Phosphorylation ; RNA, Small Interfering ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Triglycerides/blood/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Positive regulation of Itk PH domain function by soluble IP4 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-07
    Description: Pleckstrin homology (PH) domain-mediated protein recruitment to cellular membranes is of paramount importance for signal transduction. The recruitment of many PH domains is controlled through production and turnover of their membrane ligand, phosphatidylinositol 3,4,5-trisphosphate (PIP3). We show that phosphorylation of the second messenger inositol 1,4,5-trisphosphate (IP3) into inositol 1,3,4,5-tetrakisphosphate (IP4) establishes another mode of PH domain regulation through a soluble ligand. At physiological concentrations, IP4 promoted PH domain binding to PIP3. In primary mouse CD4+CD8+ thymocytes, this was required for full activation of the protein tyrosine kinase Itk after T cell receptor engagement. Our data suggest that IP4 establishes a feedback loop of phospholipase C-gamma1 activation through Itk that is essential for T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Yina H -- Grasis, Juris A -- Miller, Andrew T -- Xu, Ruo -- Soonthornvacharin, Stephen -- Andreotti, Amy H -- Tsoukas, Constantine D -- Cooke, Michael P -- Sauer, Karsten -- AR048848/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):886-9. Epub 2007 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412921" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; *Amino Acid Motifs ; Animals ; Diglycerides/metabolism ; Feedback, Physiological ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol Phosphates/*metabolism/pharmacology ; Lymphopoiesis ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Organ Culture Techniques ; Phosphatidylinositol Phosphates/metabolism ; Phospholipase C gamma/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/chemistry/*metabolism ; Receptors, Antigen, T-Cell/immunology ; Second Messenger Systems ; Signal Transduction ; Solubility ; T-Lymphocytes/cytology/immunology/*metabolism
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    CDK2-dependent phosphorylation of FOXO1 as an apoptotic response to DNA damage (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: The function of cyclin-dependent kinase 2 (CDK2) is often abolished after DNA damage. The inhibition of CDK2 plays a central role in DNA damage-induced cell cycle arrest and DNA repair. However, whether CDK2 also influences the survival of cells under genotoxic stress is unknown. Forkhead box O (FOXO) transcription factors are emerging as key regulators of cell survival. CDK2 specifically phosphorylated FOXO1 at serine-249 (Ser249) in vitro and in vivo. Phosphorylation of Ser249 resulted in cytoplasmic localization and inhibition of FOXO1. This phosphorylation was abrogated upon DNA damage through the cell cycle checkpoint pathway that is dependent on the protein kinases Chk1 and Chk2. Moreover, silencing of FOXO1 by small interfering RNA diminished DNA damage-induced death in both p53-deficient and p53-proficient cells. This effect was reversed by restored expression of FOXO1 in a manner depending on phosphorylation of Ser249. Functional interaction between CDK2 and FOXO1 provides a mechanism that regulates apoptotic cell death after DNA strand breakage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Haojie -- Regan, Kevin M -- Lou, Zhenkun -- Chen, Junjie -- Tindall, Donald J -- CA91956/CA/NCI NIH HHS/ -- DK60920/DK/NIDDK NIH HHS/ -- DK65236/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Camptothecin/pharmacology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Checkpoint Kinase 2 ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/genetics/*metabolism ; Cytoplasm/metabolism ; *DNA Damage ; Forkhead Transcription Factors/antagonists & inhibitors/*metabolism ; Humans ; Mice ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription, Genetic ; Transfection ; Tumor Suppressor Protein p53/metabolism
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    A positive feedback loop promotes transcription surge that jump-starts Salmonella virulence circuit (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-13
    Description: The PhoP/PhoQ two-component system is a master regulator of Salmonella pathogenicity. Here we report that induction of the PhoP/PhoQ system results in an initial surge of PhoP phosphorylation; the occupancy of target promoters by the PhoP protein; and the transcription of PhoP-activated genes, which then subsides to reach new steady-state levels. This surge in PhoP activity is due to PhoP positively activating its own transcription, because a strain constitutively expressing the PhoP protein attained steady-state levels of activation asymptotically, without the surge. The strain constitutively expressing the PhoP protein was attenuated for virulence in mice, demonstrating that the surge conferred by PhoP's positive feedback loop is necessary to jump-start Salmonella's virulence program.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, Dongwoo -- Lee, Eun-Jin -- Huang, Henry -- Groisman, Eduardo A -- AI49561/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 8;314(5805):1607-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Howard Hughes Medical Institute, Washington University School of Medicine, Campus Box 8230, 660 South Euclid Avenue, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17158330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/*genetics/*metabolism ; *Feedback, Physiological ; Gene Expression Regulation, Bacterial ; Magnesium/metabolism ; Mice ; Phosphorylation ; Promoter Regions, Genetic ; RNA, Bacterial/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/*genetics/metabolism/*pathogenicity ; *Transcription, Genetic ; Virulence
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    Structural insight into pre-B cell receptor function (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-14
    Description: The pre-B cell receptor (pre-BCR) serves as a checkpoint in B cell development. In the 2.7 angstrom structure of a human pre-BCR Fab-like fragment, consisting of an antibody heavy chain (HC) paired with the surrogate light chain, the "unique regions" of VpreB and lambda5 replace the complementarity-determining region 3 (CDR3) loop of an antibody light chain and appear to "probe" the HC CDR3, potentially influencing the selection of the antibody repertoire. Biochemical analysis indicates that the pre-BCR is impaired in its ability to recognize antigen, which, together with electron microscopic visualization of a pre-BCR dimer, suggests ligand-independent oligomerization as the likely signaling mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bankovich, Alexander J -- Raunser, Stefan -- Juo, Z Sean -- Walz, Thomas -- Davis, Mark M -- Garcia, K Christopher -- T32 AI007290/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 13;316(5822):291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17431183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Complementarity Determining Regions/chemistry/physiology ; Crystallography, X-Ray ; Humans ; Immunoglobulin Heavy Chains/chemistry/physiology ; Immunoglobulin Light Chains/chemistry/physiology ; Immunoglobulin Light Chains, Surrogate ; Membrane Glycoproteins/*chemistry/physiology/ultrastructure ; Mice ; Models, Molecular ; Pre-B Cell Receptors ; Protein Conformation ; Receptors, Antigen, B-Cell/*chemistry/physiology/ultrastructure ; Recombinant Proteins ; Structure-Activity Relationship
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    B cell ligand discrimination through a spreading and contraction response (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-06
    Description: B cells recognize foreign antigens by virtue of cell surface immunoglobulin receptors and are most effectively activated by membrane-bound ligands. Here, we show that in the early stages of this process, B cells exhibit a two-phase response in which they first spread over the antigen-bearing membrane and then contract, thereby collecting bound antigen into a central aggregate. The extent of this response, which is both signaling- and actin-dependent, determines the quantity of antigen accumulated and hence the degree of B cell activation. Brownian dynamic simulations reproduce essential features of the antigen collection process and suggest a possible basis for affinity discrimination. We propose that dynamic spreading is an important step of the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fleire, S J -- Goldman, J P -- Carrasco, Y R -- Weber, M -- Bray, D -- Batista, F D -- G64713/PHS HHS/ -- New York, N.Y. -- Science. 2006 May 5;312(5774):738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675699" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Algorithms ; Animals ; Antibody Affinity ; Antigen Presentation ; Antigens, Surface/*immunology ; B-Lymphocytes/*immunology/*physiology ; Cell Shape ; Computer Simulation ; Flow Cytometry ; Ligands ; Lipid Bilayers ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence ; Models, Immunological ; Muramidase/immunology ; Receptors, Antigen, B-Cell/*immunology/metabolism ; Recombinant Fusion Proteins/immunology ; Signal Transduction ; Stochastic Processes ; T-Lymphocytes/immunology
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    Protrudin induces neurite formation by directional membrane trafficking (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-11-04
    Description: Guanosine triphosphatases of the Rab family are key regulators of membrane trafficking, with Rab11 playing a specific role in membrane recycling. We identified a mammalian protein, protrudin, that promoted neurite formation through interaction with the guanosine diphosphate (GDP)-bound form of Rab11. Phosphorylation of protrudin by extracellular signal-regulated kinase (ERK) in response to nerve growth factor promoted protrudin association with Rab11-GDP. Down-regulation of protrudin by RNA interference induced membrane extension in all directions and inhibited neurite formation. Thus, protrudin regulates Rab11-dependent membrane recycling to promote the directional membrane trafficking required for neurite formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirane, Michiko -- Nakayama, Keiichi I -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082457" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Guanosine Diphosphate/metabolism ; HeLa Cells ; Humans ; MAP Kinase Kinase 1/metabolism ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Growth Factor/pharmacology/physiology ; Neurites/*physiology ; PC12 Cells ; Phosphorylation ; RNA Interference ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Vesicular Transport Proteins ; rab GTP-Binding Proteins/metabolism
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    A clonogenic bone marrow progenitor specific for macrophages and dendritic cells (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-12-03
    Description: Macrophages and dendritic cells (DCs) are crucial for immune and inflammatory responses and belong to a network of cells that has been termed the mononuclear phagocyte system (MPS). However, the origin and lineage of these cells remain poorly understood. Here, we describe the isolation and clonal analysis of a mouse bone marrow progenitor that is specific for monocytes, several macrophage subsets, and resident spleen DCs in vivo. It was also possible to recapitulate this differentiation in vitro by using treatment with the cytokines macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. Thus, macrophages and DCs appear to renew from a common progenitor, providing a cellular and molecular basis for the concept of the MPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fogg, Darin K -- Sibon, Claire -- Miled, Chaouki -- Jung, Steffen -- Aucouturier, Pierre -- Littman, Dan R -- Cumano, Ana -- Geissmann, Frederic -- A133856/PHS HHS/ -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):83-7. Epub 2005 Dec 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Laboratory of Mononuclear Phagocyte Biology, Avenir Team, Necker Enfants Malades Institute, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322423" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Separation ; Clone Cells ; Colony-Stimulating Factors/pharmacology ; Dendritic Cells/*cytology ; Flow Cytometry ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Transplantation ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/*cytology ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/immunology ; Proto-Oncogene Proteins c-kit/analysis ; Receptors, Cytokine/analysis ; Receptors, HIV/analysis ; Recombinant Proteins ; Spleen/cytology
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    Regulation of hepatic stellate cell differentiation by the neurotrophin receptor p75NTR (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-31
    Description: Differentiation of hepatic stellate cells (HSCs) to extracellular matrix- and growth factor-producing cells supports liver regeneration through promotion of hepatocyte proliferation. We show that the neurotrophin receptor p75NTR, a tumor necrosis factor receptor superfamily member expressed in HSCs after fibrotic and cirrhotic liver injury in humans, is a regulator of liver repair. In mice, depletion of p75NTR exacerbated liver pathology and inhibited hepatocyte proliferation in vivo. p75NTR-/- HSCs failed to differentiate to myofibroblasts and did not support hepatocyte proliferation. Moreover, inhibition of p75NTR signaling to the small guanosine triphosphatase Rho resulted in impaired HSC differentiation. Our results identify signaling from p75NTR to Rho as a mechanism for the regulation of HSC differentiation to regeneration-promoting cells that support hepatocyte proliferation in the diseased liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Passino, Melissa A -- Adams, Ryan A -- Sikorski, Shoana L -- Akassoglou, Katerina -- 5T32-GM07752/GM/NIGMS NIH HHS/ -- NS051470/NS/NINDS NIH HHS/ -- P30-NS047101/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 30;315(5820):1853-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Diego (UCSD), La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17395831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Disease Progression ; Extracellular Matrix/metabolism ; Fibroblasts/*cytology ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/*cytology ; Liver/*cytology/metabolism/pathology/physiology ; Liver Diseases/metabolism/*pathology ; *Liver Regeneration ; Mice ; Nerve Growth Factor/pharmacology ; Receptors, Nerve Growth Factor/genetics/*metabolism ; Signal Transduction ; rho GTP-Binding Proteins/metabolism
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    Cell signaling. The art of the soluble (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Irvine, Robin -- New York, N.Y. -- Science. 2007 May 11;316(5826):845-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, UK. rfi20@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17495162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol Phosphates/*metabolism ; Lymphocytes/physiology ; Mice ; Phosphatidylinositol Diacylglycerol-Lyase/genetics/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphorylation ; Phosphotransferases (Phosphate Group Acceptor)/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/chemistry/*metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Repressor Proteins/metabolism ; Saccharomyces cerevisiae/genetics/growth & development/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Schizosaccharomyces/genetics/metabolism ; Second Messenger Systems ; *Signal Transduction ; Solubility
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    Cell signaling. A ciliary signaling switch (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christensen, Soren Tvorup -- Ott, Carolyn Marie -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):330-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Copenhagen, Copenhagen DK-2100, Denmark. stchristensen@aki.ku.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism ; Cilia/*physiology ; Hedgehog Proteins/*metabolism ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Receptors, Cell Surface/*metabolism ; Receptors, G-Protein-Coupled/metabolism ; *Signal Transduction ; Sterols/metabolism ; Transcription, Genetic
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    Immunology. The sources of a lipid conundrum (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chun, Jerold -- New York, N.Y. -- Science. 2007 Apr 13;316(5822):208-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. jchun@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17431159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endothelium, Vascular/physiology ; Fingolimod Hydrochloride ; Humans ; Immunosuppressive Agents/pharmacology ; Lymphocytes/*physiology ; Lysophospholipids/isolation & purification/*physiology ; Mice ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Propylene Glycols/pharmacology ; Receptors, Lysosphingolipid/metabolism ; Sphingosine/*analogs & derivatives/isolation & ; purification/pharmacology/physiology
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    Biomedicine. Every joint has a silver lining (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Firestein, Gary S -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):952-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Allergy and Immunology, University of California, San Diego, School of Medicine, 9500 Gilman Drive, MC 0656, La Jolla, CA 92093-0656, USA. gfirestein@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17303744" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/immunology/pathology/*therapy ; Cadherins/*antagonists & inhibitors/genetics/physiology ; Disease Models, Animal ; Humans ; Mice ; Synovial Membrane/*cytology/pathology
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    Emergence of novel color vision in mice engineered to express a human cone photopigment (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-24
    Description: Changes in the genes encoding sensory receptor proteins are an essential step in the evolution of new sensory capacities. In primates, trichromatic color vision evolved after changes in X chromosome-linked photopigment genes. To model this process, we studied knock-in mice that expressed a human long-wavelength-sensitive (L) cone photopigment in the form of an X-linked polymorphism. Behavioral tests demonstrated that heterozygous females, whose retinas contained both native mouse pigments and human L pigment, showed enhanced long-wavelength sensitivity and acquired a new capacity for chromatic discrimination. An inherent plasticity in the mammalian visual system thus permits the emergence of a new dimension of sensory experience based solely on gene-driven changes in receptor organization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacobs, Gerald H -- Williams, Gary A -- Cahill, Hugh -- Nathans, Jeremy -- EY002052/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 23;315(5819):1723-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Research Institute and Department of Psychology, University of California, Santa Barbara, CA 93106, USA. jacobs@psych.ucsb.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17379811" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Color Perception/*genetics ; Discrimination (Psychology) ; Electroretinography ; Female ; Genetic Engineering ; Heterozygote ; Humans ; Light ; Male ; Mice ; Neuronal Plasticity ; Primates/genetics/physiology ; Retinal Cone Photoreceptor Cells/*physiology ; Retinal Pigments/*genetics/*physiology ; X Chromosome/genetics ; X Chromosome Inactivation
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    Immunology. The shape of things to come (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fitzgerald, Katherine A -- Golenbock, Douglas T -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1574-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA. kate.fitzgerald@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569850" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Vesicular Transport/metabolism ; *Adjuvants, Immunologic ; Animals ; Crystallography, X-Ray ; Glycolipids/chemistry/metabolism ; Humans ; Hydrophobic and Hydrophilic Interactions ; Ligands ; Lipid A/*analogs & derivatives/chemistry/immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Antigen 96/*chemistry/metabolism ; Mice ; Phosphates/metabolism ; Protein Conformation ; Receptors, Interleukin/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; Toll-Like Receptor 4/chemistry/*immunology/metabolism
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    Mosaic organization of neural stem cells in the adult brain (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: The in vivo potential of neural stem cells in the postnatal mouse brain is not known, but because they produce many different types of neurons, they must be either very versatile or very diverse. By specifically targeting stem cells and following their progeny in vivo, we showed that postnatal stem cells in different regions produce different types of neurons, even when heterotopically grafted or grown in culture. This suggests that rather than being plastic and homogeneous, neural stem cells are a restricted and diverse population of progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merkle, Florian T -- Mirzadeh, Zaman -- Alvarez-Buylla, Arturo -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):381-4. Epub 2007 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery and Developmental and Stem Cell Biology Program, University of California, San Francisco, San Francisco, CA 94143-0525, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615304" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology ; Animals ; Animals, Newborn ; Astrocytes/cytology ; Brain/*cytology ; Cell Differentiation ; Cells, Cultured ; Interneurons/cytology ; Lateral Ventricles/cytology ; Mice ; Neuroglia/cytology ; Neurons/*cytology ; Olfactory Bulb/cytology ; Stem Cell Transplantation ; Transplantation, Heterotopic
    Print ISSN: 0036-8075
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    Molecular basis for the nerve dependence of limb regeneration in an adult vertebrate (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-03
    Description: The limb blastemal cells of an adult salamander regenerate the structures distal to the level of amputation, and the surface protein Prod 1 is a critical determinant of their proximodistal identity. The anterior gradient protein family member nAG is a secreted ligand for Prod 1 and a growth factor for cultured newt blastemal cells. nAG is sequentially expressed after amputation in the regenerating nerve and the wound epidermis-the key tissues of the stem cell niche-and its expression in both locations is abrogated by denervation. The local expression of nAG after electroporation is sufficient to rescue a denervated blastema and regenerate the distal structures. Our analysis brings together the positional identity of the blastema and the classical nerve dependence of limb regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696928/" 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/PMC2696928/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Anoop -- Godwin, James W -- Gates, Phillip B -- Garza-Garcia, A Acely -- Brockes, Jeremy P -- G0600229/Medical Research Council/United Kingdom -- G0600229(77696)/Medical Research Council/United Kingdom -- G9537983/Medical Research Council/United Kingdom -- G9537983(56733)/Medical Research Council/United Kingdom -- MC_U117574559/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):772-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD59/*physiology ; COS Cells ; Cells, Cultured ; Cercopithecus aethiops ; Denervation ; Extremities/innervation ; Glycosylphosphatidylinositols/physiology ; Growth Substances ; Intercellular Signaling Peptides and Proteins/isolation & ; purification/*physiology/secretion ; Ligands ; Mice ; Notophthalmus viridescens ; Peripheral Nerves/*physiology ; Regeneration/*physiology ; Stem Cells/*cytology ; Two-Hybrid System Techniques
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    Protein kinase C beta and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66Shc (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: The 66-kilodalton isoform of the growth factor adapter Shc (p66Shc) translates oxidative damage into cell death by acting as reactive oxygen species (ROS) producer within mitochondria. However, the signaling link between cellular stress and mitochondrial proapoptotic activity of p66Shc was not known. We demonstrate that protein kinase C beta, activated by oxidative conditions in the cell, induces phosphorylation of p66Shc and triggers mitochondrial accumulation of the protein after it is recognized by the prolyl isomerase Pin1. Once imported, p66Shc causes alterations of mitochondrial Ca2+ responses and three-dimensional structure, thus inducing apoptosis. These data identify a signaling route that activates an apoptotic inducer shortening the life span and could be a potential target of pharmacological approaches to inhibit aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinton, Paolo -- Rimessi, Alessandro -- Marchi, Saverio -- Orsini, Francesca -- Migliaccio, Enrica -- Giorgio, Marco -- Contursi, Cristina -- Minucci, Saverio -- Mantovani, Fiamma -- Wieckowski, Mariusz R -- Del Sal, Giannino -- Pelicci, Pier Giuseppe -- Rizzuto, Rosario -- GGP05284/Telethon/Italy -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):659-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental and Diagnostic Medicine, Section of General Pathology and Interdisciplinary Center for the Study of Inflammation (ICSI), University of Ferrara, Ferrera, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272725" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*metabolism ; Adenosine Triphosphate/metabolism/pharmacology ; Animals ; *Apoptosis ; Calcium/metabolism ; Calcium Signaling ; *Cell Aging ; Cell Survival ; Cells, Cultured ; Cyclosporine/pharmacology ; Hydrogen Peroxide/metabolism/pharmacology ; Mice ; Mitochondria/*metabolism/ultrastructure ; Mutation ; Oxidative Stress ; Peptidylprolyl Isomerase/*metabolism ; Permeability ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/genetics/*metabolism ; Protein Kinase C beta ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/metabolism ; Shc Signaling Adaptor Proteins ; *Signal Transduction
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    Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-10
    Description: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/metabolism
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    Hardwiring the brain: endocannabinoids shape neuronal connectivity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: The roles of endocannabinoid signaling during central nervous system development are unknown. We report that CB(1) cannabinoid receptors (CB(1)Rs) are enriched in the axonal growth cones of gamma-aminobutyric acid-containing (GABAergic) interneurons in the rodent cortex during late gestation. Endocannabinoids trigger CB(1)R internalization and elimination from filopodia and induce chemorepulsion and collapse of axonal growth cones of these GABAergic interneurons by activating RhoA. Similarly, endocannabinoids diminish the galvanotropism of Xenopus laevis spinal neurons. These findings, together with the impaired target selection of cortical GABAergic interneurons lacking CB(1)Rs, identify endocannabinoids as axon guidance cues and demonstrate that endocannabinoid signaling regulates synaptogenesis and target selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berghuis, Paul -- Rajnicek, Ann M -- Morozov, Yury M -- Ross, Ruth A -- Mulder, Jan -- Urban, Gabriella M -- Monory, Krisztina -- Marsicano, Giovanni -- Matteoli, Michela -- Canty, Alison -- Irving, Andrew J -- Katona, Istvan -- Yanagawa, Yuchio -- Rakic, Pasko -- Lutz, Beat -- Mackie, Ken -- Harkany, Tibor -- DA00286/DA/NIDA NIH HHS/ -- DA015916/DA/NIDA NIH HHS/ -- DA11322/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-17177 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cannabinoid Receptor Modulators/metabolism/*physiology ; Cell Movement ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/ultrastructure ; *Endocannabinoids ; Growth Cones/physiology/ultrasonography ; In Situ Hybridization ; Interneurons/metabolism/*physiology/ultrasonography ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/agonists/*physiology ; Signal Transduction ; Stem Cells/metabolism ; Synapses/physiology/ultrasonography ; Xenopus Proteins/physiology ; Xenopus laevis ; gamma-Aminobutyric Acid/metabolism
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    Blastocyst axis is specified independently of early cell lineage but aligns with the ZP shape (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-21
    Description: The mechanisms controlling the establishment of the embryonic-abembryonic (E-Ab) axis of the mammalian blastocyst are controversial. We used in vitro time-lapse imaging and in vivo lineage labeling to provide evidence that the E-Ab axis of the mouse blastocyst is generated independently of early cell lineage. Rather, both the boundary between two-cell blastomeres and the E-Ab axis of the blastocyst align relative to the ellipsoidal shape of the zona pellucida (ZP), an extraembryonic structure. Lack of correlation between cell lineage and the E-Ab axis can be explained by the rotation of the embryo within the ZP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurotaki, Yoko -- Hatta, Kohei -- Nakao, Kazuki -- Nabeshima, Yo-Ichi -- Fujimori, Toshihiko -- New York, N.Y. -- Science. 2007 May 4;316(5825):719-23. Epub 2007 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446354" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*cytology/physiology ; Blastocyst Inner Cell Mass ; Blastomeres/*physiology ; Body Patterning ; Cell Lineage ; Cell Movement ; Cell Nucleus/physiology ; *Embryonic Development ; Green Fluorescent Proteins ; Image Processing, Computer-Assisted ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Fluorescence ; Motion Pictures as Topic ; Rotation ; Zona Pellucida/physiology/*ultrastructure
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    Staphylococcus aureus Panton-Valentine leukocidin causes necrotizing pneumonia (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-01-20
    Description: The Staphylococcus aureus Panton-Valentine leukocidin (PVL) is a pore-forming toxin secreted by strains epidemiologically associated with the current outbreak of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and with the often-lethal necrotizing pneumonia. To investigate the role of PVL in pulmonary disease, we tested the pathogenicity of clinical isolates, isogenic PVL-negative and PVL-positive S. aureus strains, as well as purified PVL, in a mouse acute pneumonia model. Here we show that PVL is sufficient to cause pneumonia and that the expression of this leukotoxin induces global changes in transcriptional levels of genes encoding secreted and cell wall-anchored staphylococcal proteins, including the lung inflammatory factor staphylococcal protein A (Spa).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Labandeira-Rey, Maria -- Couzon, Florence -- Boisset, Sandrine -- Brown, Eric L -- Bes, Michele -- Benito, Yvonne -- Barbu, Elena M -- Vazquez, Vanessa -- Hook, Magnus -- Etienne, Jerome -- Vandenesch, Francois -- Bowden, M Gabriela -- AI020624/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 23;315(5815):1130-3. Epub 2007 Jan 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Extracellular Matrix Biology, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17234914" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/metabolism ; Bacterial Toxins/genetics ; Calcium-Binding Proteins/genetics/metabolism ; Disease Models, Animal ; Exotoxins/genetics/*physiology ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; Hemorrhage ; Leukocidins/genetics/*physiology ; Lung/microbiology/*pathology ; Methicillin Resistance ; Mice ; Mice, Inbred BALB C ; Necrosis ; Oligonucleotide Array Sequence Analysis ; Pneumonia, Staphylococcal/*microbiology/*pathology ; Staphylococcal Protein A/genetics/*metabolism ; Staphylococcus aureus/genetics/growth & development/metabolism/*pathogenicity ; Transcription, Genetic ; Virulence ; Virulence Factors/genetics/*physiology
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    RAP80 targets BRCA1 to specific ubiquitin structures at DNA damage sites (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-26
    Description: Mutations affecting the BRCT domains of the breast cancer-associated tumor suppressor BRCA1 disrupt the recruitment of this protein to DNA double-strand breaks (DSBs). The molecular structures at DSBs recognized by BRCA1 are presently unknown. We report the interaction of the BRCA1 BRCT domain with RAP80, a ubiquitin-binding protein. RAP80 targets a complex containing the BRCA1-BARD1 (BRCA1-associated ring domain protein 1) E3 ligase and the deubiquitinating enzyme (DUB) BRCC36 to MDC1-gammaH2AX-dependent lysine(6)- and lysine(63)-linked ubiquitin polymers at DSBs. These events are required for cell cycle checkpoint and repair responses to ionizing radiation, implicating ubiquitin chain recognition and turnover in the BRCA1-mediated repair of DSBs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706583/" 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/PMC2706583/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sobhian, Bijan -- Shao, Genze -- Lilli, Dana R -- Culhane, Aedin C -- Moreau, Lisa A -- Xia, Bing -- Livingston, David M -- Greenberg, Roger A -- K08 CA106597/CA/NCI NIH HHS/ -- K08 CA106597-01A2/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1198-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Genetics and Department of Medicine, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525341" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; BRCA1 Protein/*metabolism ; Binding Sites ; Carrier Proteins/*metabolism ; Cell Line ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair/physiology ; HeLa Cells ; Humans ; Mice ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Nucleic Acid Conformation ; Protein Structure, Tertiary ; Tumor Suppressor Proteins/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligases/metabolism
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    The genomic landscapes of human breast and colorectal cancers (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Laura D -- Parsons, D Williams -- Jones, Sian -- Lin, Jimmy -- Sjoblom, Tobias -- Leary, Rebecca J -- Shen, Dong -- Boca, Simina M -- Barber, Thomas -- Ptak, Janine -- Silliman, Natalie -- Szabo, Steve -- Dezso, Zoltan -- Ustyanksky, Vadim -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Karchin, Rachel -- Wilson, Paul A -- Kaminker, Joshua S -- Zhang, Zemin -- Croshaw, Randal -- Willis, Joseph -- Dawson, Dawn -- Shipitsin, Michail -- Willson, James K V -- Sukumar, Saraswati -- Polyak, Kornelia -- Park, Ben Ho -- Pethiyagoda, Charit L -- Pant, P V Krishna -- Ballinger, Dennis G -- Sparks, Andrew B -- Hartigan, James -- Smith, Douglas R -- Suh, Erick -- Papadopoulos, Nickolas -- Buckhaults, Phillip -- Markowitz, Sanford D -- Parmigiani, Giovanni -- Kinzler, Kenneth W -- Velculescu, Victor E -- Vogelstein, Bert -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA109274/CA/NCI NIH HHS/ -- CA112828/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM070219/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- P30-CA43703/CA/NCI NIH HHS/ -- RR017698/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1108-13. Epub 2007 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics/metabolism ; Cell Line ; Chromosome Mapping ; Colorectal Neoplasms/*genetics/metabolism ; Computational Biology ; DNA, Neoplasm ; Databases, Genetic ; Genes, Neoplasm ; Genome, Human ; Humans ; Metabolic Networks and Pathways/genetics ; Mice ; Mutation ; Neoplasm Proteins/genetics/metabolism ; Sequence Analysis, DNA
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    Biomedicine. HIV drug shows promise as potential cancer treatment (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17823319" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*therapeutic use ; Clinical Trials as Topic ; HIV Protease Inhibitors/*therapeutic use ; Humans ; Mice ; Nelfinavir/therapeutic use
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    Polymerizing actin fibers position integrins primed to probe for adhesion sites (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-17
    Description: Migrating cells extend protrusions, probing the surrounding matrix in search of permissive sites to form adhesions. We found that actin fibers polymerizing along the leading edge directed local protrusions and drove synchronous sideways movement of beta1 integrin adhesion receptors. These movements lead to the clustering and positioning of conformationally activated, but unligated, beta1 integrins along the leading edge of fibroblast lamellae and growth cone filopodia. Thus, rapid actin-based movement of primed integrins along the leading edge suggests a "sticky fingers" mechanism to probe for new adhesion sites and to direct migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galbraith, Catherine G -- Yamada, Kenneth M -- Galbraith, James A -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):992-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17303755" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*physiology ; Animals ; Antigens, CD29/*physiology ; Cell Adhesion/*physiology ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Movement/*physiology ; Extracellular Matrix/metabolism ; Fibroblasts/physiology ; Fibronectins/metabolism ; Green Fluorescent Proteins/metabolism ; Mice ; Microfilament Proteins/metabolism ; NIH 3T3 Cells ; Phosphoproteins/metabolism ; Protein Binding ; Pseudopodia/metabolism
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    Dynamic visualization of thrombopoiesis within bone marrow (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-22
    Description: Platelets are generated from megakaryocytes (MKs) in mammalian bone marrow (BM) by mechanisms that remain poorly understood. Here we describe the use of multiphoton intravital microscopy in intact BM to visualize platelet generation in mice. MKs were observed as sessile cells that extended dynamic proplatelet-like protrusions into microvessels. These intravascular extensions appeared to be sheared from their transendothelial stems by flowing blood, resulting in the appearance of proplatelets in peripheral blood. In vitro, proplatelet production from differentiating MKs was enhanced by fluid shear. These results confirm the concept of proplatelet formation in vivo and are consistent with the possibility that blood flow-induced hydrodynamic shear stress is a biophysical determinant of thrombopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Junt, Tobias -- Schulze, Harald -- Chen, Zhao -- Massberg, Steffen -- Goerge, Tobias -- Krueger, Andreas -- Wagner, Denisa D -- Graf, Thomas -- Italiano, Joseph E Jr -- Shivdasani, Ramesh A -- von Andrian, Ulrich H -- HL068130/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL63143/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1767-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17885137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins ; Blood Platelets/*cytology ; Bone Marrow/*physiology ; Cells, Cultured ; Luminescent Proteins ; Megakaryocytes/*cytology ; Mice ; Microscopy, Fluorescence, Multiphoton ; Platelet Membrane Glycoprotein IIb ; Shear Strength ; Thrombopoiesis/*physiology
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    Building an HIV-proof immune system (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):612-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; CD4-Positive T-Lymphocytes/immunology/virology ; Clinical Trials as Topic ; *Genetic Therapy ; Genetic Vectors ; HIV/genetics/immunology ; HIV Antibodies/genetics/immunology ; HIV Infections/*immunology/*therapy ; Hematopoietic Stem Cells/immunology ; Humans ; *Immunotherapy ; Mice ; Transduction, Genetic
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    Microbiology. Mayhem in the lung (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kahl, Barbara C -- Peters, Georg -- New York, N.Y. -- Science. 2007 Feb 23;315(5815):1082-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Microbiology, University of Munster, Domagkstrasse 10, D-49149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17322047" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/genetics/metabolism ; Animals ; Bacterial Toxins/analysis ; Exotoxins/analysis/*physiology ; Gene Expression Regulation, Bacterial ; Hemorrhage ; Leukocidins/analysis/*physiology ; Lung/chemistry/microbiology/*pathology ; Methicillin Resistance ; Mice ; Models, Biological ; Necrosis ; Phagocytosis ; Pneumonia, Staphylococcal/*microbiology/*pathology ; Respiratory Mucosa/microbiology ; Staphylococcal Protein A/genetics/*metabolism ; Staphylococcus aureus/genetics/growth & development/metabolism/*pathogenicity ; Virulence Factors/analysis/*physiology
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    PKA type IIalpha holoenzyme reveals a combinatorial strategy for isoform diversity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: The catalytic (C) subunit of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) is inhibited by two classes of regulatory subunits, RI and RII. The RII subunits are substrates as well as inhibitors and do not require adenosine triphosphate (ATP) to form holoenzyme, which distinguishes them from RI subunits. To understand the molecular basis for isoform diversity, we solved the crystal structure of an RIIalpha holoenzyme and compared it to the RIalpha holoenzyme. Unphosphorylated RIIalpha(90-400), a deletion mutant, undergoes major conformational changes as both of the cAMP-binding domains wrap around the C subunit's large lobe. The hallmark of this conformational reorganization is the helix switch in domain A. The C subunit is in an open conformation, and its carboxyl-terminal tail is disordered. This structure demonstrates the conserved and isoform-specific features of RI and RII and the importance of ATP, and also provides a new paradigm for designing isoform-specific activators or antagonists for PKA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036697/" 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/PMC4036697/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Jian -- Brown, Simon H J -- von Daake, Sventja -- Taylor, Susan S -- GM34921/GM/NIGMS NIH HHS/ -- R01 GM034921/GM/NIGMS NIH HHS/ -- R01 GM034921-23/GM/NIGMS NIH HHS/ -- T32-CA009524/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):274-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932298" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Motifs ; Animals ; Binding Sites ; Catalytic Domain ; Crystallography, X-Ray ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinase RIIalpha Subunit ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit ; Cyclic AMP-Dependent Protein Kinases/*chemistry/genetics/metabolism ; Holoenzymes/chemistry ; Hydrophobic and Hydrophilic Interactions ; Isoenzymes/chemistry ; Mice ; Models, Molecular ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
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    Cell signaling. Nuclear actin as choreographer of cell morphology and transcription (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Jiang I -- Crabtree, Gerald R -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1710-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howared Hughes Medical Institute and Stanford University School of Medicine, Stanford, CA 94305-5323, USA. crabtree@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588921" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*physiology ; Animals ; Cell Nucleus/*physiology ; Cell Shape/physiology ; Gene Expression Regulation ; Mice ; Protein Transport ; Serum Response Factor/physiology ; Signal Transduction/*physiology ; Trans-Activators/*physiology ; Transcription, Genetic/physiology
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    A plasminogen-activating protease specifically controls the development of primary pneumonic plague (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-27
    Description: Primary pneumonic plague is transmitted easily, progresses rapidly, and causes high mortality, but the mechanisms by which Yersinia pestis overwhelms the lungs are largely unknown. We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination during pneumonic plague than during bubonic plague. Experiments manipulating its temporal expression showed that Pla allows Y. pestis to replicate rapidly in the airways, causing a lethal fulminant pneumonia; if unexpressed, inflammation is aborted, and lung repair is activated. Inhibition of Pla expression prolonged the survival of animals with the disease, offering a therapeutic option to extend the period during which antibiotics are effective.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lathem, Wyndham W -- Price, Paul A -- Miller, Virginia L -- Goldman, William E -- AI53298/AI/NIAID NIH HHS/ -- DK52574/DK/NIDDK NIH HHS/ -- F32 AI069688-01/AI/NIAID NIH HHS/ -- NRSA T32 GM07067/GM/NIGMS NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):509-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17255510" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Colony Count, Microbial ; Cytokines/genetics/metabolism ; Female ; Fibrinogen/metabolism ; Gene Expression Regulation ; Gene Expression Regulation, Bacterial ; Lung/immunology/*microbiology/pathology ; Mice ; Mice, Inbred C57BL ; Mutation ; Plague/immunology/*microbiology/pathology ; Plasminogen/metabolism ; Plasminogen Activators/genetics/*metabolism ; Pneumonia, Bacterial/immunology/*microbiology/pathology ; Spleen/microbiology ; Tetracyclines/pharmacology ; Virulence Factors/genetics/metabolism ; Yersinia pestis/enzymology/genetics/growth & development/*pathogenicity
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    Physiology. Proteasomes keep the circadian clock ticking (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gatfield, David -- Schibler, Ueli -- New York, N.Y. -- Science. 2007 May 25;316(5828):1135-6. Epub 2007 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and NCCR Frontiers in Genetics, Sciences III, University of Geneva, CH-1211 Geneva-4, Switzerland. david.gatfield@molbio.unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17495136" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle Proteins/physiology ; Circadian Rhythm/genetics/*physiology ; Cryptochromes ; F-Box Proteins/physiology ; Flavoproteins/physiology ; Mice ; Nuclear Proteins/physiology ; Period Circadian Proteins ; Phenotype ; Proteasome Endopeptidase Complex/*physiology ; Transcription Factors/physiology
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    Immunology. The root of platelet production (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geddis, Amy E -- Kaushansky, Kenneth -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1689-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pediatrics and Medicine, University of California, San Diego, CA 92103-8811, USA. kkaushansky@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17885117" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Blood Platelets/*cytology ; Humans ; Megakaryocytes/*cytology ; Mice ; Thrombopoiesis/*physiology
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    Endocrine disrupters. Controversy continues after panel rules on bisphenol A (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):884-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702917" target="_blank"〉PubMed〈/a〉
    Keywords: *Advisory Committees ; Animals ; Benzhydryl Compounds ; Child ; Endocrine Disruptors/administration & dosage/*toxicity ; Female ; Humans ; Male ; Mice ; Phenols/administration & dosage/*toxicity ; Pregnancy ; United States
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    Antibody class switching mediated by yeast endonuclease-generated DNA breaks (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: Antibody class switching in activated B cells uses class switch recombination (CSR), which joins activation-induced cytidine deaminase (AID)-dependent double-strand breaks (DSBs) within two large immunoglobulin heavy chain (IgH) locus switch (S) regions that lie up to 200 kilobases apart. To test postulated roles of S regions and AID in CSR, we generated mutant B cells in which donor Smu and accepter Sgamma1 regions were replaced with yeast I-SceI endonuclease sites. We found that site-specific I-SceI DSBs mediate recombinational IgH locus class switching from IgM to IgG1 without S regions or AID. We propose that CSR evolved to exploit a general DNA repair process that promotes joining of widely separated DSBs within a chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zarrin, Ali A -- Del Vecchio, Catherine -- Tseng, Eva -- Gleason, Megan -- Zarin, Payam -- Tian, Ming -- Alt, Frederick W -- 2P01AI031541-15/AI/NIAID NIH HHS/ -- P01CA092625-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):377-81. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Children's Hospital, CBR Institute for Biomedical Research, and Department of Genetics, Harvard University Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Cell Line ; Cytidine Deaminase/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair ; Deoxyribonucleases, Type II Site-Specific/genetics/*metabolism ; Embryonic Stem Cells ; Gene Targeting ; Genes, Immunoglobulin Heavy Chain ; Hybridomas ; *Immunoglobulin Class Switching ; Immunoglobulin G/biosynthesis/genetics ; Immunoglobulin M/biosynthesis/genetics ; *Immunoglobulin Switch Region ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae Proteins
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    Menin controls growth of pancreatic beta-cells in pregnant mice and promotes gestational diabetes mellitus (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-03
    Description: During pregnancy, maternal pancreatic islets grow to match dynamic physiological demands, but the mechanisms regulating adaptive islet growth in this setting are poorly understood. Here we show that menin, a protein previously characterized as an endocrine tumor suppressor and transcriptional regulator, controls islet growth in pregnant mice. Pregnancy stimulated proliferation of maternal pancreatic islet beta-cells that was accompanied by reduced islet levels of menin and its targets. Transgenic expression of menin in maternal beta-cells prevented islet expansion and led to hyperglycemia and impaired glucose tolerance, hallmark features of gestational diabetes. Prolactin, a hormonal regulator of pregnancy, repressed islet menin levels and stimulated beta-cell proliferation. These results expand our understanding of mechanisms underlying diabetes pathogenesis and reveal potential targets for therapy in diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karnik, Satyajit K -- Chen, Hainan -- McLean, Graeme W -- Heit, Jeremy J -- Gu, Xueying -- Zhang, Andrew Y -- Fontaine, Magali -- Yen, Michael H -- Kim, Seung K -- T32DK007217-32/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975067" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Diabetes, Gestational/*etiology/metabolism ; Female ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Obesity/metabolism ; Pregnancy ; Prolactin/metabolism ; Proto-Oncogene Proteins/*physiology ; Tumor Cells, Cultured
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    Medicine. Tumor suppressor may also affect gestational diabetes (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):729.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes, Gestational/*metabolism ; Female ; Humans ; Insulin-Secreting Cells/cytology ; Mice ; Pregnancy ; Prolactin/physiology ; Proto-Oncogene Proteins/genetics/*physiology ; Tumor Suppressor Proteins/*physiology
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    Of aging mice and men (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Richard -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):390; author reply 390.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947563" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Glucuronidase/deficiency/*genetics ; Humans ; Mice ; *Models, Animal ; Signal Transduction ; Vitamin D/*administration & dosage/metabolism ; Wnt Proteins/metabolism
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    Engineering entropy-driven reactions and networks catalyzed by DNA (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-17
    Description: Artificial biochemical circuits are likely to play as large a role in biological engineering as electrical circuits have played in the engineering of electromechanical devices. Toward that end, nucleic acids provide a designable substrate for the regulation of biochemical reactions. However, it has been difficult to incorporate signal amplification components. We introduce a design strategy that allows a specified input oligonucleotide to catalyze the release of a specified output oligonucleotide, which in turn can serve as a catalyst for other reactions. This reaction, which is driven forward by the configurational entropy of the released molecule, provides an amplifying circuit element that is simple, fast, modular, composable, and robust. We have constructed and characterized several circuits that amplify nucleic acid signals, including a feedforward cascade with quadratic kinetics and a positive feedback circuit with exponential growth kinetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, David Yu -- Turberfield, Andrew J -- Yurke, Bernard -- Winfree, Erik -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1121-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computation and Neural Systems, California Institute of Technology, MC 136-93, 1200 East California Boulevard, Pasadena, CA91125, USA. dzhang@dna.caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalysis ; Chemical Engineering ; *Computers, Molecular ; DNA/*chemistry ; Entropy ; Equipment Design ; Feedback, Physiological ; Mice ; Nanotechnology ; Nucleic Acid Hybridization ; Rabbits
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    Cadherin-11 in synovial lining formation and pathology in arthritis (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-01-27
    Description: The normal synovium forms a membrane at the edges of joints and provides lubrication and nutrients for the cartilage. In rheumatoid arthritis, the synovium is the site of inflammation, and it participates in an organized tissue response that damages cartilage and bone. We identified cadherin-11 as essential for the development of the synovium. Cadherin-11-deficient mice have a hypoplastic synovial lining, display a disorganized synovial reaction to inflammation, and are resistant to inflammatory arthritis. Cadherin-11 therapeutics prevent and reduce arthritis in mouse models. Thus, synovial cadherin-11 determines the behavior of synovial cells in their proinflammatory and destructive tissue response in inflammatory arthritis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, David M -- Kiener, Hans P -- Agarwal, Sandeep K -- Noss, Erika H -- Watts, Gerald F M -- Chisaka, Osamu -- Takeichi, Masatoshi -- Brenner, Michael B -- K08 AR2214/AR/NIAMS NIH HHS/ -- R01 AR48114/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):1006-10. Epub 2007 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, 1 Jimmy Fund Way, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17255475" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/therapeutic use ; Arthritis, Experimental ; Arthritis, Rheumatoid/metabolism/*pathology/therapy ; Cadherins/*antagonists & inhibitors/biosynthesis/deficiency/*physiology ; Cell Adhesion/physiology ; Disease Models, Animal ; Extracellular Matrix/metabolism ; Fibroblasts/metabolism ; L Cells (Cell Line) ; Male ; Mice ; Mice, Inbred C57BL ; Organ Culture Techniques ; Synovial Membrane/*cytology/*pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neuroscience. Spying on new neurons in the human brain (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):899-900.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991833" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Adult Stem Cells/chemistry/*cytology ; Animals ; Biomarkers/*analysis ; Brain/cytology/embryology ; Brain Chemistry ; Child ; Fatty Acids/analysis ; Hippocampus/chemistry/*cytology ; Humans ; Magnetic Resonance Spectroscopy/*methods ; Mice ; Rats ; Stem Cells/chemistry/*cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    PDZ domain binding selectivity is optimized across the mouse proteome (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-21
    Description: PDZ domains have long been thought to cluster into discrete functional classes defined by their peptide-binding preferences. We used protein microarrays and quantitative fluorescence polarization to characterize the binding selectivity of 157 mouse PDZ domains with respect to 217 genome-encoded peptides. We then trained a multidomain selectivity model to predict PDZ domain-peptide interactions across the mouse proteome with an accuracy that exceeds many large-scale, experimental investigations of protein-protein interactions. Contrary to the current paradigm, PDZ domains do not fall into discrete classes; instead, they are evenly distributed throughout selectivity space, which suggests that they have been optimized across the proteome to minimize cross-reactivity. We predict that focusing on families of interaction domains, which facilitates the integration of experimentation and modeling, will play an increasingly important role in future investigations of protein function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674608/" 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/PMC2674608/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stiffler, Michael A -- Chen, Jiunn R -- Grantcharova, Viara P -- Lei, Ying -- Fuchs, Daniel -- Allen, John E -- Zaslavskaia, Lioudmila A -- MacBeath, Gavin -- 1 RO1 GM072872-01/GM/NIGMS NIH HHS/ -- 5 T32 GM07598-25/GM/NIGMS NIH HHS/ -- R01 GM072872/GM/NIGMS NIH HHS/ -- R01 GM072872-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):364-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641200" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Amino Acid Sequence ; Animals ; Computational Biology ; Computer Simulation ; Fluorescence Polarization ; Mice ; Peptides/*metabolism ; Protein Array Analysis ; Protein Binding ; *Protein Structure, Tertiary ; Proteome/chemistry/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    Autophagy-dependent viral recognition by plasmacytoid dendritic cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: Plasmacytoid dendritic cells (pDCs) detect viruses in the acidified endosomes by means of Toll-like receptors (TLRs). Yet, pDC responses to certain single-stranded RNA (ssRNA) viruses occur only after live viral infection. We present evidence here that the recognition of such viruses by TLR7 requires transport of cytosolic viral replication intermediates into the lysosome by the process of autophagy. In addition, autophagy was found to be required for the production of interferon-alpha by pDCs. These results support a key role for autophagy in mediating ssRNA virus detection and interferon-alpha secretion by pDCs and suggest that cytosolic replication intermediates of viruses serve as pathogen signatures recognized by TLR7.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Heung Kyu -- Lund, Jennifer M -- Ramanathan, Balaji -- Mizushima, Noboru -- Iwasaki, Akiko -- AI054359/AI/NIAID NIH HHS/ -- AI064705/AI/NIAID NIH HHS/ -- AI07019/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1398-401. Epub 2007 Feb 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Dendritic Cells/*immunology/physiology/*virology ; Endosomes/immunology/virology ; Female ; Immunity, Innate ; Interferon-alpha/metabolism ; Interleukin-12/metabolism ; Lysosomes/virology ; Male ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Transgenic ; Phagosomes/physiology/ultrastructure ; RNA, Viral/*immunology/metabolism ; Rhabdoviridae Infections/*immunology ; Toll-Like Receptor 7/*immunology ; Vesicular stomatitis Indiana virus/*immunology/physiology ; Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of spontaneous intestinal tumorigenesis through the adaptor protein MyD88 (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-07
    Description: Inflammation is increasingly recognized as an important component of tumorigenesis, although the mechanisms and pathways involved are not well understood. Tumor development is regulated by products of several modifier genes, but instructions for their tumor-specific expression are currently unknown. We show that the signaling through the adaptor protein MyD88 has a critical role in spontaneous tumor development in mice with heterozygous mutation in the adenomatous polyposis coli (APC) gene. We found that MyD88-dependent signaling controls the expression of several key modifier genes of intestinal tumorigenesis and has a critical role in both spontaneous and carcinogen-induced tumor development. This study thus reveals the important role of an innate immune signaling pathway in intestinal tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rakoff-Nahoum, Seth -- Medzhitov, Ruslan -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):124-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615359" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Proliferation ; Colonic Neoplasms/genetics/immunology/pathology/physiopathology ; Disease Models, Animal ; Female ; Gene Expression Regulation, Neoplastic ; Genes, APC ; Immunity, Innate ; Intestinal Neoplasms/genetics/immunology/pathology/*physiopathology ; Intestine, Large/pathology ; Intestine, Small/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/genetics/*physiology ; *Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immunology. Eating in to avoid infection (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1376-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. caetano@cancer.org.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17347432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cytokines/metabolism ; Dendritic Cells/*immunology/physiology/*virology ; Endosomes/immunology/virology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Membrane Glycoproteins/immunology/physiology ; Mice ; Mice, Transgenic ; RNA, Viral/*immunology/metabolism ; Rhabdoviridae Infections/*immunology ; Signal Transduction ; Toll-Like Receptor 7/immunology/physiology ; Toll-Like Receptor 9/immunology/physiology ; Toll-Like Receptors/immunology/*physiology ; Vesicular stomatitis Indiana virus/*immunology/physiology ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    RNA maps reveal new RNA classes and a possible function for pervasive transcription (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: Significant fractions of eukaryotic genomes give rise to RNA, much of which is unannotated and has reduced protein-coding potential. The genomic origins and the associations of human nuclear and cytosolic polyadenylated RNAs longer than 200 nucleotides (nt) and whole-cell RNAs less than 200 nt were investigated in this genome-wide study. Subcellular addresses for nucleotides present in detected RNAs were assigned, and their potential processing into short RNAs was investigated. Taken together, these observations suggest a novel role for some unannotated RNAs as primary transcripts for the production of short RNAs. Three potentially functional classes of RNAs have been identified, two of which are syntenically conserved and correlate with the expression state of protein-coding genes. These data support a highly interleaved organization of the human transcriptome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapranov, Philipp -- Cheng, Jill -- Dike, Sujit -- Nix, David A -- Duttagupta, Radharani -- Willingham, Aarron T -- Stadler, Peter F -- Hertel, Jana -- Hackermuller, Jorg -- Hofacker, Ivo L -- Bell, Ian -- Cheung, Evelyn -- Drenkow, Jorg -- Dumais, Erica -- Patel, Sandeep -- Helt, Gregg -- Ganesh, Madhavan -- Ghosh, Srinka -- Piccolboni, Antonio -- Sementchenko, Victor -- Tammana, Hari -- Gingeras, Thomas R -- N01-CO-12400/CO/NCI NIH HHS/ -- U01HG003147/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 8;316(5830):1484-8. Epub 2007 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Affymetrix Laboratory, Affymetrix, Inc., 3420 Central Expressway, Santa Clara, CA, 95051, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytosol/metabolism ; Exons ; Gene Expression ; Genome ; *Genome, Human ; HeLa Cells ; Humans ; Mice ; Promoter Regions, Genetic ; RNA/*genetics/metabolism ; RNA Precursors/*genetics/metabolism ; RNA, Messenger/*genetics/*metabolism ; Synteny ; Terminator Regions, Genetic ; *Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Specialized inhibitory synaptic actions between nearby neocortical pyramidal neurons (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-05
    Description: We found that, in the mouse visual cortex, action potentials generated in a single layer-2/3 pyramidal (excitatory) neuron can reliably evoke large, constant-latency inhibitory postsynaptic currents in other nearby pyramidal cells. This effect is mediated by axo-axonic ionotropic glutamate receptor-mediated excitation of the nerve terminals of inhibitory interneurons, which connect to the target pyramidal cells. Therefore, individual cortical excitatory neurons can generate inhibition independently from the somatic firing of inhibitory interneurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, Ming -- Yoshimura, Yumiko -- Takada, Naoki -- Horibe, Shoko -- Komatsu, Yukio -- New York, N.Y. -- Science. 2007 May 4;316(5825):758-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17478724" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism/pharmacology ; *Inhibitory Postsynaptic Potentials ; Interneurons/physiology ; Mice ; Mice, Inbred C57BL ; Neural Inhibition ; Patch-Clamp Techniques ; Presynaptic Terminals/physiology ; Pyramidal Cells/*physiology ; Receptors, AMPA/physiology ; Receptors, Kainic Acid/physiology ; Synapses/*physiology ; Synaptic Transmission ; Visual Cortex/cytology/*physiology ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The after-hours mutant reveals a role for Fbxl3 in determining mammalian circadian period (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: By screening N-ethyl-N-nitrosourea-mutagenized animals for alterations in rhythms of wheel-running activity, we identified a mouse mutation, after hours (Afh). The mutation, a Cys(358)Ser substitution in Fbxl3, an F-box protein with leucine-rich repeats, results in long free-running rhythms of about 27 hours in homozygotes. Circadian transcriptional and translational oscillations are attenuated in Afh mice. The Afh allele significantly affected Per2 expression and delayed the rate of Cry protein degradation in Per2::Luciferase tissue slices. Our in vivo and in vitro studies reveal a central role for Fbxl3 in mammalian circadian timekeeping.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godinho, Sofia I H -- Maywood, Elizabeth S -- Shaw, Linda -- Tucci, Valter -- Barnard, Alun R -- Busino, Luca -- Pagano, Michele -- Kendall, Rachel -- Quwailid, Mohamed M -- Romero, M Rosario -- O'neill, John -- Chesham, Johanna E -- Brooker, Debra -- Lalanne, Zuzanna -- Hastings, Michael H -- Nolan, Patrick M -- MC_U105170643/Medical Research Council/United Kingdom -- MC_U142684172/Medical Research Council/United Kingdom -- MC_U142684173/Medical Research Council/United Kingdom -- MC_U142684175/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 May 11;316(5826):897-900. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Mammalian Genetics Unit, Harwell, Oxfordshire OX11 0RD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463252" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; CLOCK Proteins ; COS Cells ; Cell Cycle Proteins/genetics/metabolism ; Cercopithecus aethiops ; *Circadian Rhythm/genetics ; Crosses, Genetic ; Cryptochromes ; F-Box Proteins/*genetics/*physiology ; Female ; Flavoproteins/genetics/metabolism ; Gene Expression Regulation ; Liver/metabolism ; Lung/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; *Point Mutation ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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