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  • Mice  (185)
  • Molecular Sequence Data  (98)
  • American Association for the Advancement of Science (AAAS)  (271)
  • Annual Reviews
  • Society of Exploration Geophysicists (SEG)
  • 2005-2009  (271)
  • 1990-1994
  • 1980-1984
  • 2006  (271)
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Publisher
  • American Association for the Advancement of Science (AAAS)  (271)
  • Annual Reviews
  • Society of Exploration Geophysicists (SEG)
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  • 2005-2009  (271)
  • 1990-1994
  • 1980-1984
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  • 1
    Publication Date: 2006-09-09
    Description: CD8-positive T lymphocytes recognize peptides that are usually derived from the degradation of cellular proteins and are presented by class I molecules of the major histocompatibility complex. Here we describe a human minor histocompatibility antigen created by a polymorphism in the SP110 nuclear phosphoprotein gene. The antigenic peptide comprises two noncontiguous SP110 peptide segments spliced together in reverse order to that in which they occur in the predicted SP110 protein. The antigenic peptide could be produced in vitro by incubation of precursor peptides with highly purified 20S proteasomes. Cutting and splicing probably occur within the proteasome by transpeptidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, Edus H -- Vigneron, Nathalie J -- Gavin, Marc A -- Coulie, Pierre G -- Stroobant, Vincent -- Dalet, Alexandre -- Tykodi, Scott S -- Xuereb, Suzanne M -- Mito, Jeffrey K -- Riddell, Stanley R -- Van den Eynde, Benoit J -- CA106512/CA/NCI NIH HHS/ -- CA18029/CA/NCI NIH HHS/ -- P01 CA018029/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1444-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Immunology, Clinical Research Division, 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/16960008" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Motifs ; Amino Acid Sequence ; Amino Acid Substitution ; *Antigen Presentation ; B-Lymphocytes/immunology ; Cell Line, Transformed ; Cytotoxicity, Immunologic ; Electroporation ; HLA-A Antigens/immunology ; Humans ; Interferon-gamma/metabolism ; Male ; Middle Aged ; Minor Histocompatibility Antigens/genetics/*immunology/*metabolism ; Molecular Sequence Data ; Nuclear Proteins/chemistry/genetics/*immunology/*metabolism ; Peptide Fragments/metabolism ; Polymorphism, Single Nucleotide ; Proteasome Endopeptidase Complex/metabolism ; *Protein Splicing ; T-Lymphocytes, Cytotoxic/*immunology
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  • 2
    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
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  • 3
    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
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  • 4
    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
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  • 5
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    American Association for the Advancement of Science (AAAS)
    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
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  • 6
    Publication Date: 2006-11-18
    Description: Using single-molecule DNA nanomanipulation, we show that abortive initiation involves DNA "scrunching"--in which RNA polymerase (RNAP) remains stationary and unwinds and pulls downstream DNA into itself--and that scrunching requires RNA synthesis and depends on RNA length. We show further that promoter escape involves scrunching, and that scrunching occurs in most or all instances of promoter escape. Our results support the existence of an obligatory stressed intermediate, with approximately one turn of additional DNA unwinding, in escape and are consistent with the proposal that stress in this intermediate provides the driving force to break RNAP-promoter and RNAP-initiation-factor interactions in escape.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754787/" 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/PMC2754787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Revyakin, Andrey -- Liu, Chenyu -- Ebright, Richard H -- Strick, Terence R -- GM41376/GM/NIGMS NIH HHS/ -- R01 GM041376/GM/NIGMS NIH HHS/ -- R01 GM041376-15/GM/NIGMS NIH HHS/ -- R01 GM041376-16/GM/NIGMS NIH HHS/ -- R01 GM041376-17/GM/NIGMS NIH HHS/ -- R01 GM041376-18/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1139-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Waksman Institute, and Department of Chemistry, Rutgers University, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110577" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Biomechanical Phenomena ; DNA/chemistry/*metabolism ; DNA-Directed RNA Polymerases/*metabolism ; Models, Genetic ; Molecular Sequence Data ; Nucleic Acid Conformation ; *Promoter Regions, Genetic ; RNA/biosynthesis ; Transcription Initiation Site/physiology ; Transcription, Genetic/*physiology
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  • 7
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    American Association for the Advancement of Science (AAAS)
    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
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  • 8
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    American Association for the Advancement of Science (AAAS)
    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
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  • 9
    Publication Date: 2006-11-25
    Description: The Dobzhansky-Muller model proposes that hybrid incompatibilities are caused by the interaction between genes that have functionally diverged in the respective hybridizing species. Here, we show that Lethal hybrid rescue (Lhr) has functionally diverged in Drosophila simulans and interacts with Hybrid male rescue (Hmr), which has functionally diverged in D. melanogaster, to cause lethality in F1 hybrid males. LHR localizes to heterochromatic regions of the genome and has diverged extensively in sequence between these species in a manner consistent with positive selection. Rapidly evolving heterochromatic DNA sequences may be driving the evolution of this incompatibility gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brideau, Nicholas J -- Flores, Heather A -- Wang, Jun -- Maheshwari, Shamoni -- Wang, Xu -- Barbash, Daniel A -- R01 GM074737-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1292-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124320" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Mapping ; Crosses, Genetic ; Drosophila/*genetics/physiology ; Drosophila Proteins/chemistry/*genetics/metabolism ; Drosophila melanogaster/*genetics/physiology ; *Evolution, Molecular ; Female ; *Genes, Insect ; Genetic Speciation ; *Hybridization, Genetic ; Male ; Molecular Sequence Data ; Selection, Genetic ; Transformation, Genetic ; Transgenes
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  • 10
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    American Association for the Advancement of Science (AAAS)
    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
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  • 11
    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
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  • 12
    Publication Date: 2006-03-11
    Description: Nisin is a posttranslationally modified antimicrobial peptide that is widely used as a food preservative. It contains five cyclic thioethers of varying sizes that are installed by a single enzyme, NisC. Reported here are the in vitro reconstitution of the cyclization process and the x-ray crystal structure of the NisC enzyme. The structure reveals similarities in fold and substrate activation with mammalian farnesyl transferases, suggesting that human homologs of NisC posttranslationally modify a cysteine of a protein substrate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Bo -- Yu, John Paul J -- Brunzelle, Joseph S -- Moll, Gert N -- van der Donk, Wilfred A -- Nair, Satish K -- GM58822/GM/NIGMS NIH HHS/ -- R01 GM079038/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Illinois at Urbana-Champaign, 600 South Mathews Avenue, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527981" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anti-Bacterial Agents/*biosynthesis/chemistry ; Carbon-Sulfur Lyases/chemistry/genetics/*metabolism ; Crystallography, X-Ray ; Farnesyltranstransferase/chemistry ; Humans ; Lactococcus lactis/*enzymology ; Models, Molecular ; Molecular Sequence Data ; Nisin/*biosynthesis/chemistry ; Protein Conformation ; Protein Processing, Post-Translational ; Sequence Homology, Amino Acid ; Structure-Activity Relationship
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2006-03-11
    Description: Crop domestication frequently began with the selection of plants that did not naturally shed ripe fruits or seeds. The reduction in grain shattering that led to cereal domestication involved genetic loci of large effect. The molecular basis of this key domestication transition, however, remains unknown. Here we show that human selection of an amino acid substitution in the predicted DNA binding domain encoded by a gene of previously unknown function was primarily responsible for the reduction of grain shattering in rice domestication. The substitution undermined the gene function necessary for the normal development of an abscission layer that controls the separation of a grain from the pedicel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Changbao -- Zhou, Ailing -- Sang, Tao -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1936-9. Epub 2006 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Michigan State University, East Lansing, MI 48824, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527928" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Amino Acid Substitution ; Biological Evolution ; Chromosome Mapping ; Computational Biology ; Crops, Agricultural/*genetics/growth & development ; Flowers/growth & development ; Gene Expression ; Genes, Plant ; Genotype ; Molecular Sequence Data ; Mutation ; Oryza/cytology/*genetics/growth & development ; Phenotype ; Plant Proteins/chemistry/*genetics ; Plants, Genetically Modified ; Quantitative Trait Loci ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Analysis, DNA ; Transcription Factors/chemistry/*genetics ; Transformation, Genetic
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  • 14
    Publication Date: 2006-06-17
    Description: Vesicular stomatitis virus is a negative-stranded RNA virus. Its nucleoprotein (N) binds the viral genomic RNA and is involved in multiple functions including transcription, replication, and assembly. We have determined a 2.9 angstrom structure of a complex containing 10 molecules of the N protein and 90 bases of RNA. The RNA is tightly sequestered in a cavity at the interface between two lobes of the N protein. This serves to protect the RNA in the absence of polynucleotide synthesis. For the RNA to be accessed, some conformational change in the N protein should be necessary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, Todd J -- Zhang, Xin -- Wertz, Gail W -- Luo, Ming -- AI050066/AI/NIAID NIH HHS/ -- R37 AI012464/AI/NIAID NIH HHS/ -- R37 AI012464-28/AI/NIAID NIH HHS/ -- R37 AI012464-29/AI/NIAID NIH HHS/ -- R37 AI012464-30/AI/NIAID NIH HHS/ -- R37 AI012464-31/AI/NIAID NIH HHS/ -- R37AI012464/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):357-60. Epub 2006 Jun 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, School of Medicine, University of Alabama at Birmingham, 1025 18th Street South, Birmingham, AL 35294, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778022" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Crystallography, X-Ray ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Nucleic Acid Conformation ; Nucleocapsid Proteins/*chemistry/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; RNA, Viral/*chemistry/metabolism ; Ribonucleoproteins/*chemistry ; Sequence Alignment ; Vesicular stomatitis Indiana virus/*chemistry
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  • 15
    Publication Date: 2006-07-01
    Description: The formation of glutaminyl transfer RNA (Gln-tRNA(Gln)) differs among the three domains of life. Most bacteria employ an indirect pathway to produce Gln-tRNA(Gln) by a heterotrimeric glutamine amidotransferase CAB (GatCAB) that acts on the misacylated Glu-tRNA(Gln). Here, we describe a series of crystal structures of intact GatCAB from Staphylococcus aureus in the apo form and in the complexes with glutamine, asparagine, Mn2+, and adenosine triphosphate analog. Two identified catalytic centers for the glutaminase and transamidase reactions are markedly distant but connected by a hydrophilic ammonia channel 30 A in length. Further, we show that the first U-A base pair in the acceptor stem and the D loop of tRNA(Gln) serve as identity elements essential for discrimination by GatCAB and propose a complete model for the overall concerted reactions to synthesize Gln-tRNA(Gln).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, Akiyoshi -- Yao, Min -- Chimnaronk, Sarin -- Sakai, Naoki -- Tanaka, Isao -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Advanced Life Sciences, Hokkaido University, Sapporo 060-0810, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809541" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/metabolism ; Amino Acid Sequence ; Aminoacyltransferases/metabolism ; Ammonia/*metabolism ; Apoenzymes/chemistry/metabolism ; Asparagine/metabolism ; Base Pairing ; Catalytic Domain ; Crystallography, X-Ray ; Glutaminase/metabolism ; Glutamine/*chemistry/metabolism ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Magnesium/metabolism ; Manganese/metabolism ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits ; RNA, Bacterial/chemistry/metabolism ; RNA, Transfer, Amino Acyl/chemistry/*metabolism ; RNA, Transfer, Gln/*chemistry/metabolism ; Staphylococcus aureus/*enzymology/genetics/metabolism
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  • 16
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    American Association for the Advancement of Science (AAAS)
    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
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  • 17
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    American Association for the Advancement of Science (AAAS)
    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
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  • 18
    Publication Date: 2006-11-11
    Description: The molecular mechanisms controlling human hair growth and scalp hair loss are poorly understood. By screening about 350,000 individuals in two populations from the Volga-Ural region of Russia, we identified a gene mutation in families who show an inherited form of hair loss and a hair growth defect. Affected individuals were homozygous for a deletion in the LIPH gene on chromosome 3q27, caused by short interspersed nuclear element-retrotransposon-mediated recombination. The LIPH gene is expressed in hair follicles and encodes a phospholipase called lipase H (alternatively known as membrane-associated phosphatidic acid-selective phospholipase A1alpha), an enzyme that regulates the production of bioactive lipids. These results suggest that lipase H participates in hair growth and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kazantseva, Anastasiya -- Goltsov, Andrey -- Zinchenko, Rena -- Grigorenko, Anastasia P -- Abrukova, Anna V -- Moliaka, Yuri K -- Kirillov, Alexander G -- Guo, Zhiru -- Lyle, Stephen -- Ginter, Evgeny K -- Rogaev, Evgeny I -- K08-AR02179/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):982-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brudnick Neuropsychiatric Research Institute, Department of Psychiatry, University of Massachusetts Medical School, 303 Belmont Street, Worcester, MA 01604, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095700" target="_blank"〉PubMed〈/a〉
    Keywords: Alu Elements ; Amino Acid Sequence ; Base Sequence ; Chromosomes, Human, Pair 3/genetics ; Exons ; Female ; Gene Deletion ; Gene Expression ; Genetic Markers ; Hair/*growth & development ; Hair Follicle/enzymology ; Heterozygote ; Homozygote ; Humans ; Hypotrichosis/*genetics ; Lipase/chemistry/*genetics/metabolism ; Lipid Metabolism ; Lod Score ; Male ; Molecular Sequence Data ; Pedigree ; Protein Structure, Tertiary ; Recombination, Genetic ; Retroelements ; Russia ; Tandem Repeat Sequences
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  • 19
    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
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  • 20
    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
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  • 21
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    American Association for the Advancement of Science (AAAS)
    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
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  • 22
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    American Association for the Advancement of Science (AAAS)
    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
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  • 23
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    American Association for the Advancement of Science (AAAS)
    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
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  • 24
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    American Association for the Advancement of Science (AAAS)
    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
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  • 25
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    American Association for the Advancement of Science (AAAS)
    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
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  • 26
    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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  • 27
    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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  • 28
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    American Association for the Advancement of Science (AAAS)
    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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  • 29
    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 30
    Publication Date: 2006-11-25
    Description: For microbial pathogens, phylogeographic differentiation seems to be relatively common. However, the neutral population structure of Salmonella enterica serovar Typhi reflects the continued existence of ubiquitous haplotypes over millennia. In contrast, clinical use of fluoroquinolones has yielded at least 15 independent gyrA mutations within a decade and stimulated clonal expansion of haplotype H58 in Asia and Africa. Yet, antibiotic-sensitive strains and haplotypes other than H58 still persist despite selection for antibiotic resistance. Neutral evolution in Typhi appears to reflect the asymptomatic carrier state, and adaptive evolution depends on the rapid transmission of phenotypic changes through acute infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652035/" 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/PMC2652035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roumagnac, Philippe -- Weill, Francois-Xavier -- Dolecek, Christiane -- Baker, Stephen -- Brisse, Sylvain -- Chinh, Nguyen Tran -- Le, Thi Anh Hong -- Acosta, Camilo J -- Farrar, Jeremy -- Dougan, Gordon -- Achtman, Mark -- 076962/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1301-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Infektionsbiologie, Department of Molecular Biology, Chariteplatz 1, 10117 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124322" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Africa ; Alleles ; Anti-Bacterial Agents/pharmacology/therapeutic use ; Asia ; *Biological Evolution ; Carrier State/*microbiology ; DNA Gyrase/genetics ; Drug Resistance, Bacterial ; Drug Resistance, Multiple, Bacterial ; Fluoroquinolones/pharmacology/therapeutic use ; *Genes, Bacterial ; Genetic Variation ; Haplotypes ; Humans ; Molecular Sequence Data ; Mutation ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Salmonella typhi/drug effects/*genetics ; Selection, Genetic ; Typhoid Fever/drug therapy/*microbiology
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  • 31
    Publication Date: 2006-08-12
    Description: Mutations in the human neurotrypsin gene are associated with autosomal recessive mental retardation. To further understand the pathophysiological consequences of the lack of this serine protease, we studied Tequila (Teq), the Drosophila neurotrypsin ortholog, using associative memory as a behavioral readout. We found that teq inactivation resulted in a long-term memory (LTM)-specific defect. After LTM conditioning of wild-type flies, teq expression transiently increased in the mushroom bodies. Moreover, specific inhibition of teq expression in adult mushroom bodies resulted in a reversible LTM defect. Hence, the Teq pathway is essential for information processing in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Didelot, Gerard -- Molinari, Florence -- Tchenio, Paul -- Comas, Daniel -- Milhiet, Elodie -- Munnich, Arnold -- Colleaux, Laurence -- Preat, Thomas -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):851-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genes et Dynamique des Systemes de Memoire, UMR CNRS 7637, Ecole Superieure de Physique et de Chimie Industrielles, 10 Rue Vauquelin 75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902143" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Conditioning, Classical ; Drosophila Proteins/chemistry/genetics/*physiology ; Drosophila melanogaster/genetics/*physiology ; Gene Expression ; Gene Expression Regulation ; Humans ; Learning ; *Memory ; Mifepristone/pharmacology ; Models, Animal ; Molecular Sequence Data ; Mushroom Bodies/anatomy & histology/physiology ; Mutation ; Odors ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Serine Endopeptidases/chemistry/genetics/*physiology
    Print ISSN: 0036-8075
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  • 32
    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
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  • 33
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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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  • 34
    Publication Date: 2006-11-18
    Description: Our knowledge of Neanderthals is based on a limited number of remains and artifacts from which we must make inferences about their biology, behavior, and relationship to ourselves. Here, we describe the characterization of these extinct hominids from a new perspective, based on the development of a Neanderthal metagenomic library and its high-throughput sequencing and analysis. Several lines of evidence indicate that the 65,250 base pairs of hominid sequence so far identified in the library are of Neanderthal origin, the strongest being the ascertainment of sequence identities between Neanderthal and chimpanzee at sites where the human genomic sequence is different. These results enabled us to calculate the human-Neanderthal divergence time based on multiple randomly distributed autosomal loci. Our analyses suggest that on average the Neanderthal genomic sequence we obtained and the reference human genome sequence share a most recent common ancestor approximately 706,000 years ago, and that the human and Neanderthal ancestral populations split approximately 370,000 years ago, before the emergence of anatomically modern humans. Our finding that the Neanderthal and human genomes are at least 99.5% identical led us to develop and successfully implement a targeted method for recovering specific ancient DNA sequences from metagenomic libraries. This initial analysis of the Neanderthal genome advances our understanding of the evolutionary relationship of Homo sapiens and Homo neanderthalensis and signifies the dawn of Neanderthal genomics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583069/" 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/PMC2583069/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noonan, James P -- Coop, Graham -- Kudaravalli, Sridhar -- Smith, Doug -- Krause, Johannes -- Alessi, Joe -- Chen, Feng -- Platt, Darren -- Paabo, Svante -- Pritchard, Jonathan K -- Rubin, Edward M -- 1-F32-GM074367/GM/NIGMS NIH HHS/ -- HL066681/HL/NHLBI NIH HHS/ -- R01 HG002772/HG/NHGRI NIH HHS/ -- R01 HG002772-01/HG/NHGRI NIH HHS/ -- R01 HG002772-1/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1113-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Energy Joint Genome Institute, 2800 Mitchell Drive, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones ; Cell Nucleus ; DNA/*genetics/isolation & purification ; DNA, Mitochondrial ; *Fossils ; Gene Pool ; Genome ; Genome, Human ; Genomic Library ; History, Ancient ; Hominidae/*genetics ; Humans ; Male ; Molecular Sequence Data ; Pan troglodytes/genetics ; Polymerase Chain Reaction ; Sequence Alignment ; *Sequence Analysis, DNA/methods ; Time
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  • 35
    Publication Date: 2006-03-11
    Description: A biosynthetic approach was developed to control and probe cooperativity in multiunit biomotor assemblies by linking molecular motors to artificial protein scaffolds. This approach provides precise control over spatial and elastic coupling between motors. Cooperative interactions between monomeric kinesin-1 motors attached to protein scaffolds enhance hydrolysis activity and microtubule gliding velocity. However, these interactions are not influenced by changes in the elastic properties of the scaffold, distinguishing multimotor transport from that powered by unorganized monomeric motors. These results highlight the role of supramolecular architecture in determining mechanisms of collective transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diehl, Michael R -- Zhang, Kechun -- Lee, Heun Jin -- Tirrell, David A -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125, USA. diehl@rice.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16527982" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/chemistry ; Amino Acid Sequence ; Elasticity ; Elastin/chemistry ; Hydrolysis ; Kinesin/chemistry ; Microtubules/physiology ; Models, Biological ; Molecular Motor Proteins/*physiology ; Molecular Sequence Data ; Protein Engineering ; Protein Structure, Tertiary ; Proteins/chemistry/*physiology ; Recombinant Proteins/chemistry ; Structure-Activity Relationship
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  • 36
    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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  • 37
    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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  • 38
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    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
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  • 39
    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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  • 40
    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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  • 41
    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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  • 42
    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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  • 43
    Publication Date: 2006-01-28
    Description: The spread of H5N1 avian influenza viruses (AIVs) from China to Europe has raised global concern about their potential to infect humans and cause a pandemic. In spite of their substantial threat to human health, remarkably little AIV whole-genome information is available. We report here a preliminary analysis of the first large-scale sequencing of AIVs, including 2196 AIV genes and 169 complete genomes. We combine this new information with public AIV data to identify new gene alleles, persistent genotypes, compensatory mutations, and a potential virulence determinant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Obenauer, John C -- Denson, Jackie -- Mehta, Perdeep K -- Su, Xiaoping -- Mukatira, Suraj -- Finkelstein, David B -- Xu, Xiequn -- Wang, Jinhua -- Ma, Jing -- Fan, Yiping -- Rakestraw, Karen M -- Webster, Robert G -- Hoffmann, Erich -- Krauss, Scott -- Zheng, Jie -- Zhang, Ziwei -- Naeve, Clayton W -- AI95357/AI/NIAID NIH HHS/ -- CA 21765/CA/NCI NIH HHS/ -- R01 GM061739/GM/NIGMS NIH HHS/ -- R01 GM069916/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1576-80. Epub 2006 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hartwell Center for Bioinformatics and Biotechnology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/virology ; Computational Biology ; *Genes, Viral ; Genome, Viral ; Humans ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H2N2 Subtype/genetics ; Influenza A Virus, H3N2 Subtype/genetics ; Influenza A Virus, H3N8 Subtype/genetics ; Influenza A Virus, H5N1 Subtype/chemistry/*genetics/pathogenicity ; Influenza A Virus, H5N2 Subtype/genetics ; Influenza A Virus, H7N7 Subtype/genetics ; Influenza A Virus, H9N2 Subtype/genetics ; Influenza A virus/chemistry/*genetics/isolation & purification/pathogenicity ; Influenza in Birds/virology ; Influenza, Human/virology ; Molecular Sequence Data ; Mutation ; Phylogeny ; RNA, Viral/genetics ; Reassortant Viruses/genetics ; Sequence Analysis, DNA ; Viral Nonstructural Proteins/*chemistry/genetics ; Viral Proteins/chemistry/genetics ; Virulence Factors/*chemistry/genetics
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  • 44
    Publication Date: 2006-10-28
    Description: The social amoebas (Dictyostelia) display conditional multicellularity in a wide variety of forms. Despite widespread interest in Dictyostelium discoideum as a model system, almost no molecular data exist from the rest of the group. We constructed the first molecular phylogeny of the Dictyostelia with parallel small subunit ribosomal RNA and a-tubulin data sets, and we found that dictyostelid taxonomy requires complete revision. A mapping of characters onto the phylogeny shows that the dominant trend in dictyostelid evolution is increased size and cell type specialization of fruiting structures, with some complex morphologies evolving several times independently. Thus, the latter may be controlled by only a few genes, making their underlying mechanisms relatively easy to unravel.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2173941/" 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/PMC2173941/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaap, Pauline -- Winckler, Thomas -- Nelson, Michaela -- Alvarez-Curto, Elisa -- Elgie, Barrie -- Hagiwara, Hiromitsu -- Cavender, James -- Milano-Curto, Alicia -- Rozen, Daniel E -- Dingermann, Theodor -- Mutzel, Rupert -- Baldauf, Sandra L -- 057137/Wellcome Trust/United Kingdom -- 076618/Wellcome Trust/United Kingdom -- BB/D013453/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- COD16760/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):661-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Life Sciences, University of Dundee, DD15EH Dundee, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068267" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; DNA, Protozoan/genetics ; DNA, Ribosomal/genetics ; Dictyosteliida/*classification/*cytology/genetics/growth & development ; Dictyostelium/classification/cytology/genetics/growth & development ; Genes, Protozoan ; Molecular Sequence Data ; *Phylogeny ; RNA, Ribosomal/genetics ; Spores, Protozoan/cytology ; Tubulin/genetics
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  • 45
    Publication Date: 2006-09-02
    Description: Glycosyltransferases (GTs), an essential class of ubiquitous enzymes, are generally perceived as unidirectional catalysts. In contrast, we report that four glycosyltransferases from two distinct natural product biosynthetic pathways-calicheamicin and vancomycin-readily catalyze reversible reactions, allowing sugars and aglycons to be exchanged with ease. As proof of the broader applicability of these new reactions, more than 70 differentially glycosylated calicheamicin and vancomycin variants are reported. This study suggests the reversibility of GT-catalyzed reactions may be general and useful for generating exotic nucleotide sugars, establishing in vitro GT activity in complex systems, and enhancing natural product diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Changsheng -- Griffith, Byron R -- Fu, Qiang -- Albermann, Christoph -- Fu, Xun -- Lee, In-Kyoung -- Li, Lingjun -- Thorson, Jon S -- AI52218/AI/NIAID NIH HHS/ -- CA84374/CA/NCI NIH HHS/ -- GM70637/GM/NIGMS NIH HHS/ -- U19 CA113297/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Biosynthetic Chemistry, Pharmaceutical Sciences Division, School of Pharmacy, National Cooperative Drug Discovery Group Program, University of Wisconsin (UW)-Madison, 777 Highland Avenue, Madison, WI 53705-2222, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946071" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoglycosides/biosynthesis/chemistry/*metabolism ; Carbohydrate Sequence ; Catalysis ; Enediynes ; Glucosyltransferases/*metabolism ; Glycosylation ; Glycosyltransferases/genetics/*metabolism ; Micromonospora/enzymology/genetics ; Molecular Sequence Data ; Molecular Structure ; Nucleoside Diphosphate Sugars/metabolism ; Pentoses/metabolism ; Thymine Nucleotides/metabolism ; Vancomycin/*analogs & derivatives/biosynthesis/chemistry/metabolism
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  • 46
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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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  • 47
    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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  • 48
    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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  • 49
    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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  • 50
    Publication Date: 2006-01-18
    Description: The specialized ribonuclease Dicer initiates RNA interference by cleaving double-stranded RNA (dsRNA) substrates into small fragments about 25 nucleotides in length. In the crystal structure of an intact Dicer enzyme, the PAZ domain, a module that binds the end of dsRNA, is separated from the two catalytic ribonuclease III (RNase III) domains by a flat, positively charged surface. The 65 angstrom distance between the PAZ and RNase III domains matches the length spanned by 25 base pairs of RNA. Thus, Dicer itself is a molecular ruler that recognizes dsRNA and cleaves a specified distance from the helical end.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macrae, Ian J -- Zhou, Kaihong -- Li, Fei -- Repic, Adrian -- Brooks, Angela N -- Cande, W Zacheus -- Adams, Paul D -- Doudna, Jennifer A -- New York, N.Y. -- Science. 2006 Jan 13;311(5758):195-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410517" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Conserved Sequence ; Crystallography, X-Ray ; Giardia lamblia/enzymology ; Humans ; Lanthanoid Series Elements/metabolism ; Models, Molecular ; Molecular Sequence Data ; Protein Structure, Tertiary ; RNA Interference ; RNA, Double-Stranded/*metabolism ; RNA, Protozoan/metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Ribonuclease III/*chemistry/metabolism ; Schizosaccharomyces/genetics ; Structure-Activity Relationship
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  • 51
    Publication Date: 2006-03-25
    Description: Tracheal cytotoxin (TCT), a naturally occurring fragment of Gram-negative peptidoglycan, is a potent elicitor of innate immune responses in Drosophila. It induces the heterodimerization of its recognition receptors, the peptidoglycan recognition proteins (PGRPs) LCa and LCx, which activates the immune deficiency pathway. The crystal structure at 2.1 angstrom resolution of TCT in complex with the ectodomains of PGRP-LCa and PGRP-LCx shows that TCT is bound to and presented by the LCx ectodomain for recognition by the LCa ectodomain; the latter lacks a canonical peptidoglycan-docking groove conserved in other PGRPs. The interface, revealed in atomic detail, between TCT and the receptor complex highlights the importance of the anhydro-containing disaccharide in bridging the two ectodomains together and the critical role of diaminopimelic acid as the specificity determinant for PGRP interaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Chung-I -- Chelliah, Yogarany -- Borek, Dominika -- Mengin-Lecreulx, Dominique -- Deisenhofer, Johann -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1761-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Texas Southwestern Medical Center at Dallas, 6001 Forest Park Road, Dallas, TX 75390-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556841" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/*chemistry/metabolism ; Crystallization ; Crystallography, X-Ray ; Cytotoxins/*chemistry/metabolism ; Drosophila melanogaster ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Peptidoglycan/*chemistry/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
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  • 52
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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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  • 53
    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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  • 54
    Publication Date: 2006-06-17
    Description: The Xist noncoding RNA is the key initiator of the process of X chromosome inactivation in eutherian mammals, but its precise function and origin remain unknown. Although Xist is well conserved among eutherians, until now, no homolog has been identified in other mammals. We show here that Xist evolved, at least partly, from a protein-coding gene and that the loss of protein-coding function of the proto-Xist coincides with the four flanking protein genes becoming pseudogenes. This event occurred after the divergence between eutherians and marsupials, which suggests that mechanisms of dosage compensation have evolved independently in both lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duret, Laurent -- Chureau, Corinne -- Samain, Sylvie -- Weissenbach, Jean -- Avner, Philip -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1653-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biometrie et Biologie Evolutive (UMR 5558), CNRS and Universite Lyon 1, 16 rue Raphael Dubois, 69622 Villeurbanne Cedex, France. duret@biomserv.univ-lyon1.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle/genetics ; Chickens/genetics ; Dogs/genetics ; *Evolution, Molecular ; Exons ; Female ; Humans ; Male ; Mammals/*genetics ; Mice/genetics ; Molecular Sequence Data ; Opossums/genetics ; Phylogeny ; *Pseudogenes ; RNA, Long Noncoding ; RNA, Untranslated/*genetics ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Vertebrates/*genetics ; X Chromosome Inactivation ; Xenopus/genetics
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  • 55
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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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  • 56
    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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  • 57
    Publication Date: 2006-08-12
    Description: Transient infection of eukaryotic cells with commensal and extraintestinal pathogenic Escherichia coli of phylogenetic group B2 blocks mitosis and induces megalocytosis. This trait is linked to a widely spread genomic island that encodes giant modular nonribosomal peptide and polyketide synthases. Contact with E. coli expressing this gene cluster causes DNA double-strand breaks and activation of the DNA damage checkpoint pathway, leading to cell cycle arrest and eventually to cell death. Discovery of hybrid peptide-polyketide genotoxins in E. coli will change our view on pathogenesis and commensalism and open new biotechnological applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nougayrede, Jean-Philippe -- Homburg, Stefan -- Taieb, Frederic -- Boury, Michele -- Brzuszkiewicz, Elzbieta -- Gottschalk, Gerhard -- Buchrieser, Carmen -- Hacker, Jorg -- Dobrindt, Ulrich -- Oswald, Eric -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INRA, UMR1225, Ecole Nationale Veterinaire de Toulouse, Toulouse F-31076, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Death ; Cell Line ; Cell Nucleus/chemistry ; Cytotoxins/*metabolism ; DNA/analysis ; *DNA Damage ; DNA-Binding Proteins/metabolism ; Escherichia coli/genetics/*pathogenicity/*physiology ; G2 Phase ; *Genomic Islands ; HeLa Cells ; Histones/metabolism ; Humans ; Intestinal Mucosa/cytology/microbiology ; Molecular Sequence Data ; Mutagenesis ; Mutagens/*metabolism ; Peptides/*metabolism ; Phosphorylation ; Polyketide Synthases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Signal Transduction ; Tumor Suppressor Proteins/metabolism
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  • 58
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    American Association for the Advancement of Science (AAAS)
    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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  • 59
    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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  • 60
    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
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  • 61
    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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  • 62
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    American Association for the Advancement of Science (AAAS)
    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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  • 63
    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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  • 64
    Publication Date: 2006-07-22
    Description: Rice fields are a global source of the greenhouse gas methane, which is produced by methanogenic archaea, and by methanogens of Rice Cluster I (RC-I) in particular. RC-I methanogens are not yet available in pure culture, and the mechanistic reasons for their prevalence in rice fields are unknown. We reconstructed a complete RC-I genome (3.18 megabases) using a metagenomic approach. Sequence analysis demonstrated an aerotolerant, H2/CO2-dependent lifestyle and enzymatic capacities for carbohydrate metabolism and assimilatory sulfate reduction, hitherto unknown among methanogens. These capacities and a unique set of antioxidant enzymes and DNA repair mechanisms as well as oxygen-insensitive enzymes provide RC-I with a selective advantage over other methanogens in its habitats, thereby explaining the prevalence of RC-I methanogens in the rice rhizosphere.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erkel, Christoph -- Kube, Michael -- Reinhardt, Richard -- Liesack, Werner -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):370-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute for Terrestrial Microbiology, Karl-von-Frisch-Strasse, 35043 Marburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857943" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/biosynthesis/metabolism ; Carbohydrate Metabolism ; DNA Repair ; Euryarchaeota/classification/*genetics/metabolism/physiology ; *Genome, Archaeal ; Genomics ; Glycolysis ; Methane/*biosynthesis ; Methanomicrobiales/classification/genetics/metabolism/physiology ; Methanosarcinales/classification/genetics/metabolism/physiology ; Molecular Sequence Data ; Oryza/*microbiology ; Oxidative Stress ; Pyruvic Acid/metabolism ; Sequence Alignment ; Sequence Analysis, DNA ; *Soil Microbiology ; Sulfates/metabolism ; Sulfur/metabolism
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  • 65
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    American Association for the Advancement of Science (AAAS)
    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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  • 66
    Publication Date: 2006-07-22
    Description: CorA family members are ubiquitously distributed transporters of divalent metal cations and are considered to be the primary Mg2+ transporter of Bacteria and Archaea. We have determined a 2.9 angstrom resolution structure of CorA from Thermotoga maritima that reveals a pentameric cone-shaped protein. Two potential regulatory metal binding sites are found in the N-terminal domain that bind both Mg2+ and Co2+. The structure of CorA supports an efflux system involving dehydration and rehydration of divalent metal ions potentially mediated by a ring of conserved aspartate residues at the cytoplasmic entrance and a carbonyl funnel at the periplasmic side of the pore.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eshaghi, Said -- Niegowski, Damian -- Kohl, Andreas -- Martinez Molina, Daniel -- Lesley, Scott A -- Nordlund, Par -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):354-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biophysics, Department of Medical Biochemistry and Biophysics, Karolinska Institute, SE-171 77 Stockholm, Sweden. Said.Eshaghi@ki.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857941" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/*chemistry/metabolism ; Binding Sites ; Cation Transport Proteins/*chemistry/metabolism ; Chlorides/analysis/metabolism ; Cobalt/chemistry/*metabolism ; Crystallography, X-Ray ; Hydrophobic and Hydrophilic Interactions ; Magnesium/chemistry/*metabolism ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Sequence Alignment ; Thermotoga maritima/*chemistry ; Water/chemistry
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  • 67
    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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  • 68
    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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  • 69
    Publication Date: 2006-07-29
    Description: Comparative genomics of 45 epidemiologically varied variola virus isolates from the past 30 years of the smallpox era indicate low sequence diversity, suggesting that there is probably little difference in the isolates' functional gene content. Phylogenetic clustering inferred three clades coincident with their geographical origin and case-fatality rate; the latter implicated putative proteins that mediate viral virulence differences. Analysis of the viral linear DNA genome suggests that its evolution involved direct descent and DNA end-region recombination events. Knowing the sequences will help understand the viral proteome and improve diagnostic test precision, therapeutics, and systems for their assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esposito, Joseph J -- Sammons, Scott A -- Frace, A Michael -- Osborne, John D -- Olsen-Rasmussen, Melissa -- Zhang, Ming -- Govil, Dhwani -- Damon, Inger K -- Kline, Richard -- Laker, Miriam -- Li, Yu -- Smith, Geoffrey L -- Meyer, Hermann -- Leduc, James W -- Wohlhueter, Robert M -- G0501257/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):807-12. Epub 2006 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Core Facility Branch, Division of Scientific Resources, National Center for Preparedness, Detection, and Control of Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30329, USA. jesposito@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873609" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Viral/*genetics ; Disease Outbreaks ; *Evolution, Molecular ; Gene Deletion ; *Genetic Variation ; *Genome, Viral ; Genomics ; Humans ; Molecular Sequence Data ; Open Reading Frames ; Phylogeny ; Proteome/analysis/genetics ; Recombination, Genetic ; Sequence Analysis, DNA ; Smallpox/epidemiology/mortality/*virology ; Variola virus/classification/*genetics/isolation & purification/pathogenicity ; Viral Proteins/chemistry/genetics ; Virulence/genetics
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  • 70
    Publication Date: 2006-07-22
    Description: Resistance to the limited number of available antifungal drugs is a serious problem in the treatment of Candida albicans. We found that aneuploidy in general and a specific segmental aneuploidy, consisting of an isochromosome composed of the two left arms of chromosome 5, were associated with azole resistance. The isochromosome forms around a single centromere flanked by an inverted repeat and was found as an independent chromosome or fused at the telomere to a full-length homolog of chromosome 5. Increases and decreases in drug resistance were strongly associated with gain and loss of this isochromosome, which bears genes expressing the enzyme in the ergosterol pathway targeted by azole drugs, efflux pumps, and a transcription factor that positively regulates a subset of efflux pump genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1717021/" 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/PMC1717021/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selmecki, Anna -- Forche, Anja -- Berman, Judith -- DE10641-S/DE/NIDCR NIH HHS/ -- R01 AI062427/AI/NIAID NIH HHS/ -- R01 AIO62427/PHS HHS/ -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):367-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Cell Biology, and Development, University of Minnesota, 6-160 Jackson Hall, 321 Church Street SE, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857942" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Antifungal Agents/*pharmacology ; Azoles/pharmacology ; Candida albicans/*drug effects/*genetics/growth & development ; Centromere/ultrastructure ; Chromosomes, Fungal ; Cytochrome P-450 Enzyme System/genetics/metabolism ; Drug Resistance, Fungal/*genetics ; Ergosterol/biosynthesis ; Fluconazole/*pharmacology ; Fungal Proteins/genetics/metabolism ; Gene Dosage ; Gene Expression Profiling ; Genes, Fungal ; *Isochromosomes ; Karyotyping ; Molecular Sequence Data ; Repetitive Sequences, Nucleic Acid ; Sequence Analysis, DNA ; Transcription Factors/genetics/metabolism ; Trisomy
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  • 71
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    American Association for the Advancement of Science (AAAS)
    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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  • 72
    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
    Print ISSN: 0036-8075
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  • 73
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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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  • 74
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    Unknown
    American Association for the Advancement of Science (AAAS)
    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
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  • 75
    Publication Date: 2006-07-11
    Description: The spindle checkpoint delays cell cycle progression until microtubules attach each pair of sister chromosomes to opposite poles of the mitotic spindle. Following sister chromatid separation, however, the checkpoint ignores chromosomes whose kinetochores are attached to only one spindle pole, a state that activates the checkpoint prior to metaphase. We demonstrate that, in budding yeast, mutual inhibition between the anaphase-promoting complex (APC) and Mps1, an essential component of the checkpoint, leads to sustained inactivation of the spindle checkpoint. Mps1 protein abundance decreases in anaphase, and Mps1 is a target of the APC. Furthermore, expression of Mps1 in anaphase, or repression of the APC in anaphase, reactivates the spindle checkpoint. This APC-Mps1 feedback circuit allows cells to irreversibly inactivate the checkpoint during anaphase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palframan, William J -- Meehl, Janet B -- Jaspersen, Sue L -- Winey, Mark -- Murray, Andrew W -- GM43987/GM/NIGMS NIH HHS/ -- GM51312/GM/NIGMS NIH HHS/ -- R37 GM043987/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):680-4. Epub 2006 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Biological Laboratories, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825537" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anaphase/*physiology ; Anaphase-Promoting Complex-Cyclosome ; Cdc20 Proteins ; Cell Cycle Proteins/metabolism ; Chromosomes, Fungal/physiology ; Feedback, Physiological ; GTP-Binding Proteins/metabolism ; Kinetochores/physiology ; Mad2 Proteins ; Mitosis ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/*cytology/metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Securin ; Spindle Apparatus/*physiology ; Ubiquitin-Protein Ligase Complexes/*metabolism
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  • 76
    Publication Date: 2006-12-16
    Description: A methanogenic archaeon isolated from deep-sea hydrothermal vent fluid was found to reduce N(2) to NH(3) at up to 92 degrees C, which is 28 degrees C higher than the current upper temperature limit of biological nitrogen fixation. The 16S ribosomal RNA gene of the hyperthermophilic nitrogen fixer, designated FS406-22, was 99% similar to that of non-nitrogen fixing Methanocaldococcus jannaschii DSM 2661. At its optimal growth temperature of 90 degrees C, FS406-22 incorporated (15)N(2) and expressed nifH messenger RNA. This increase in the temperature limit of nitrogen fixation could reveal a broader range of conditions for life in the subseafloor biosphere and other nitrogen-limited ecosystems than previously estimated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mehta, Mausmi P -- Baross, John A -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1783-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Oceanography, University of Washington, Seattle, WA 98195, USA. mausmi@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170307" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Archaea/classification/genetics/*isolation & purification/*metabolism ; Archaeal Proteins/chemistry/genetics/metabolism ; Base Sequence ; *Ecosystem ; Genes, Archaeal ; Genes, rRNA ; Geologic Sediments/microbiology ; *Hot Temperature ; Molecular Sequence Data ; Nitrogen/metabolism ; *Nitrogen Fixation/genetics ; Nitrogenase/chemistry/*genetics/metabolism ; Operon ; Oxidation-Reduction ; Oxidoreductases/chemistry/genetics/metabolism ; Pacific Ocean ; Phylogeny ; RNA, Ribosomal, 16S/genetics ; Seawater/*microbiology ; Volcanic Eruptions
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  • 77
    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
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  • 78
    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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  • 79
    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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  • 80
    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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  • 81
    Publication Date: 2006-04-08
    Description: Biological responses to histone methylation critically depend on the faithful readout and transduction of the methyl-lysine signal by "effector" proteins, yet our understanding of methyl-lysine recognition has so far been limited to the study of histone binding by chromodomain and WD40-repeat proteins. The double tudor domain of JMJD2A, a Jmjc domain-containing histone demethylase, binds methylated histone H3-K4 and H4-K20. We found that the double tudor domain has an interdigitated structure, and the unusual fold is required for its ability to bind methylated histone tails. The cocrystal structure of the JMJD2A double tudor domain with a trimethylated H3-K4 peptide reveals that the trimethyl-K4 is bound in a cage of three aromatic residues, two of which are from the tudor-2 motif, whereas the binding specificity is determined by side-chain interactions involving amino acids from the tudor-1 motif. Our study provides mechanistic insights into recognition of methylated histone tails by tudor domains and reveals the structural intricacy of methyl-lysine recognition by two closely spaced effector domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Ying -- Fang, Jia -- Bedford, Mark T -- Zhang, Yi -- Xu, Rui-Ming -- DK62248/DK/NIDDK NIH HHS/ -- GM 63718/GM/NIGMS NIH HHS/ -- GM68804/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 5;312(5774):748-51. Epub 2006 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉W. M. Keck Structural Biology Laboratory, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601153" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Binding Sites ; Crystallography, X-Ray ; DNA-Binding Proteins/*chemistry/genetics/*metabolism ; Histones/*chemistry/*metabolism ; Humans ; Hydrogen Bonding ; Jumonji Domain-Containing Histone Demethylases ; Lysine/metabolism ; Methylation ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Oxidoreductases, N-Demethylating ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Structure, Tertiary ; Static Electricity ; Transcription Factors/*chemistry/genetics/*metabolism
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  • 82
    Publication Date: 2006-10-28
    Description: Large-conductance calcium- and voltage-activated potassium channels (BKCa) are dually activated by membrane depolarization and elevation of cytosolic calcium ions (Ca2+). Under normal cellular conditions, BKCa channel activation requires Ca2+ concentrations that typically occur in close proximity to Ca2+ sources. We show that BKCa channels affinity-purified from rat brain are assembled into macromolecular complexes with the voltage-gated calcium channels Cav1.2 (L-type), Cav2.1 (P/Q-type), and Cav2.2 (N-type). Heterologously expressed BKCa-Cav complexes reconstitute a functional "Ca2+ nanodomain" where Ca2+ influx through the Cav channel activates BKCa in the physiological voltage range with submillisecond kinetics. Complex formation with distinct Cav channels enables BKCa-mediated membrane hyperpolarization that controls neuronal firing pattern and release of hormones and transmitters in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berkefeld, Henrike -- Sailer, Claudia A -- Bildl, Wolfgang -- Rohde, Volker -- Thumfart, Jorg-Oliver -- Eble, Silke -- Klugbauer, Norbert -- Reisinger, Ellen -- Bischofberger, Josef -- Oliver, Dominik -- Knaus, Hans-Gunther -- Schulte, Uwe -- Fakler, Bernd -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):615-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology, University of Freiburg, Hermann-Herder-Strasse 7, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068255" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain Chemistry ; CHO Cells ; Calcium/*metabolism ; Calcium Channels, L-Type/drug effects/isolation & purification/*metabolism ; Calcium Channels, N-Type/drug effects/isolation & purification/*metabolism ; Calcium Signaling ; Chromaffin Cells/drug effects/metabolism ; Cricetinae ; Cricetulus ; Egtazic Acid/analogs & derivatives/pharmacology ; Large-Conductance Calcium-Activated Potassium Channels/drug effects/isolation & ; purification/*metabolism ; Membrane Potentials/drug effects ; Molecular Sequence Data ; Patch-Clamp Techniques ; Potassium/*metabolism ; Rats ; *Signal Transduction ; Transfection ; Xenopus
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  • 83
    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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  • 84
    Publication Date: 2006-10-28
    Description: Neuropeptides, critical brain peptides that modulate animal behavior by affecting the activity of almost every neuronal circuit, are inherently difficult to predict directly from a nascent genome sequence because of extensive posttranslational processing. The combination of bioinformatics and proteomics allows unprecedented neuropeptide discovery from an unannotated genome. Within the Apis mellifera genome, we have inferred more than 200 neuropeptides and have confirmed the sequences of 100 peptides. This study lays the groundwork for future molecular studies of Apis neuropeptides with the identification of 36 genes, 33 of which were previously unreported.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hummon, Amanda B -- Richmond, Timothy A -- Verleyen, Peter -- Baggerman, Geert -- Huybrechts, Jurgen -- Ewing, Michael A -- Vierstraete, Evy -- Rodriguez-Zas, Sandra L -- Schoofs, Liliane -- Robinson, Gene E -- Sweedler, Jonathan V -- DC006395/DC/NIDCD NIH HHS/ -- GM068946/GM/NIGMS NIH HHS/ -- NS31609/NS/NINDS NIH HHS/ -- P30 DA01830/DA/NIDA NIH HHS/ -- P30 DA018310/DA/NIDA NIH HHS/ -- R01 GM068946/GM/NIGMS NIH HHS/ -- R01 NS031609/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):647-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Illinois, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068263" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Bees/*chemistry/*genetics ; Brain Chemistry ; Codon ; Computational Biology ; *Genes, Insect ; Genome, Insect ; Insect Proteins/*chemistry/*genetics ; Mass Spectrometry ; Molecular Sequence Data ; Neuropeptides/*chemistry/*genetics ; Protein Precursors/chemistry/genetics ; Proteome
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  • 85
    Publication Date: 2006-04-29
    Description: Rice blast is caused by the fungus Magnaporthe grisea, which elaborates specialized infection cells called appressoria to penetrate the tough outer cuticle of the rice plant Oryza sativa. We found that the formation of an appressorium required, sequentially, the completion of mitosis, nuclear migration, and death of the conidium (fungal spore) from which the infection originated. Genetic intervention during mitosis prevented both appressorium development and conidium death. Impairment of autophagy, by the targeted mutation of the MgATG8 gene, arrested conidial cell death but rendered the fungus nonpathogenic. Thus, the initiation of rice blast requires autophagic cell death of the conidium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Veneault-Fourrey, Claire -- Barooah, Madhumita -- Egan, Martin -- Wakley, Gavin -- Talbot, Nicholas J -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):580-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biosciences, University of Exeter, Washington Singer Laboratories, Perry Road, Exeter EX4 4QG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645096" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Autophagy ; Benomyl/pharmacology ; Cell Nucleus/physiology ; Cell Nucleus Division ; Genes, Fungal ; Hydroxyurea/pharmacology ; Magnaporthe/*cytology/genetics/pathogenicity/*physiology ; Microtubule-Associated Proteins/genetics/physiology ; Mitosis/drug effects ; Molecular Sequence Data ; Morphogenesis ; Mutation ; Oryza/*microbiology ; Plant Diseases/*microbiology ; Spores, Fungal/cytology/*physiology
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  • 86
    Publication Date: 2006-12-23
    Description: Cartilaginous fishes represent the living group of jawed vertebrates that diverged from the common ancestor of human and teleost fish lineages about 530 million years ago. We generated approximately 1.4x genome sequence coverage for a cartilaginous fish, the elephant shark (Callorhinchus milii), and compared this genome with the human genome to identify conserved noncoding elements (CNEs). The elephant shark sequence revealed twice as many CNEs as were identified by whole-genome comparisons between teleost fishes and human. The ancient vertebrate-specific CNEs in the elephant shark and human genomes are likely to play key regulatory roles in vertebrate gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venkatesh, Byrappa -- Kirkness, Ewen F -- Loh, Yong-Hwee -- Halpern, Aaron L -- Lee, Alison P -- Johnson, Justin -- Dandona, Nidhi -- Viswanathan, Lakshmi D -- Tay, Alice -- Venter, J Craig -- Strausberg, Robert L -- Brenner, Sydney -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1892.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cell Biology, 61 Biopolis Drive, Singapore 138673. mcbbv@imcb.a-star.edu.sg〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Conserved Sequence ; DNA, Intergenic ; Enhancer Elements, Genetic ; Evolution, Molecular ; Genome ; *Genome, Human ; Humans ; Molecular Sequence Data ; *Regulatory Sequences, Nucleic Acid ; Sharks/*genetics ; Takifugu/genetics ; Zebrafish/genetics
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  • 87
    Publication Date: 2006-12-02
    Description: We describe a transgenesis platform for Drosophila melanogaster that integrates three recently developed technologies: a conditionally amplifiable bacterial artificial chromosome (BAC), recombineering, and bacteriophage PhiC31-mediated transgenesis. The BAC is maintained at low copy number, facilitating plasmid maintenance and recombineering, but is induced to high copy number for plasmid isolation. Recombineering allows gap repair and mutagenesis in bacteria. Gap repair efficiently retrieves DNA fragments up to 133 kilobases long from P1 or BAC clones. PhiC31-mediated transgenesis integrates these large DNA fragments at specific sites in the genome, allowing the rescue of lethal mutations in the corresponding genes. This transgenesis platform should greatly facilitate structure/function analyses of most Drosophila genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venken, Koen J T -- He, Yuchun -- Hoskins, Roger A -- Bellen, Hugo J -- GM067858-05/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1747-51. Epub 2006 Nov 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Developmental Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17138868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; *Chromosomes, Artificial, Bacterial ; Cloning, Molecular/*methods ; DNA Repair ; *DNA Transposable Elements ; Drosophila melanogaster/*genetics ; *Gene Transfer Techniques ; Genes, Insect ; Genetic Vectors ; Molecular Sequence Data ; Mutagenesis ; Plasmids ; Recombination, Genetic ; Siphoviridae/*genetics ; Transgenes ; Transposases/metabolism
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  • 88
    Publication Date: 2006-06-24
    Description: Organisms ranging from bacteria to humans synchronize their internal clocks to daily cycles of light and dark. Photic entrainment of the Drosophila clock is mediated by proteasomal degradation of the clock protein TIMELESS (TIM). We have identified mutations in jetlag-a gene coding for an F-box protein with leucine-rich repeats-that result in reduced light sensitivity of the circadian clock. Mutant flies show rhythmic behavior in constant light, reduced phase shifts in response to light pulses, and reduced light-dependent degradation of TIM. Expression of JET along with the circadian photoreceptor cryptochrome (CRY) in cultured S2R cells confers light-dependent degradation onto TIM, thereby reconstituting the acute response + of the circadian clock to light in a cell culture system. Our results suggest that JET is essential for resetting the clock by transmitting light signals from CRY to TIM.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2767177/" 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/PMC2767177/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, Kyunghee -- Zheng, Xiangzhong -- Sehgal, Amita -- NS048471/NS/NINDS NIH HHS/ -- R01 NS048471/NS/NINDS NIH HHS/ -- R01 NS048471-02/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1809-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794082" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cells, Cultured ; *Circadian Rhythm ; Cryptochromes ; Drosophila/chemistry/genetics/physiology ; Drosophila Proteins/chemistry/*genetics/*metabolism/*physiology ; Drosophila melanogaster/chemistry/*genetics/*physiology ; Eye Proteins/metabolism ; F-Box Proteins/chemistry/*genetics/*physiology ; Female ; *Light ; Male ; Models, Biological ; Molecular Sequence Data ; Mutation ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled/metabolism ; Transgenes ; Ubiquitin/metabolism
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  • 89
    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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  • 90
    Publication Date: 2006-12-23
    Description: The germinal center (GC) is an important site for the generation and selection of B cells bearing high-affinity antibodies, yet GC cell migration and interaction dynamics have not been directly observed. Using two-photon microscopy of mouse lymph nodes, we revealed that GC B cells are highly motile and extend long cell processes. They transited between GC dark and light zones and divided in both regions, although these B cells resided for only several hours in the light zone where antigen is displayed. GC B cells formed few stable contacts with GC T cells despite frequent encounters, and T cells were seen to carry dead B cell blebs. On the basis of these observations, we propose a model in which competition for T cell help plays a more dominant role in the selection of GC B cells than previously appreciated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, Christopher D C -- Okada, Takaharu -- Tang, H Lucy -- Cyster, Jason G -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):528-31. Epub 2006 Dec 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Affinity ; B-Lymphocytes/*cytology/*immunology/physiology ; Cell Cycle ; Cell Death ; Cell Movement ; Dendritic Cells, Follicular/cytology/physiology ; Germinal Center/cytology/*immunology ; Macrophages/physiology ; Mice ; Mice, Inbred C57BL ; Microscopy/methods ; Models, Immunological ; Mutation ; T-Lymphocytes/cytology/immunology/physiology
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  • 91
    Publication Date: 2006-12-16
    Description: Genetically matched pluripotent embryonic stem (ES) cells generated via nuclear transfer or parthenogenesis (pES cells) are a potential source of histocompatible cells and tissues for transplantation. After parthenogenetic activation of murine oocytes and interruption of meiosis I or II, we isolated and genotyped pES cells and characterized those that carried the full complement of major histocompatibility complex (MHC) antigens of the oocyte donor. Differentiated tissues from these pES cells engrafted in immunocompetent MHC-matched mouse recipients, demonstrating that selected pES cells can serve as a source of histocompatible tissues for transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kitai -- Lerou, Paul -- Yabuuchi, Akiko -- Lengerke, Claudia -- Ng, Kitwa -- West, Jason -- Kirby, Andrew -- Daly, Mark J -- Daley, George Q -- T32: HD07466/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):482-6. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and Dana Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chromosome Segregation ; Embryonic Stem Cells/cytology/*immunology/physiology ; Female ; Genotype ; H-2 Antigens/*genetics/*immunology ; Heterozygote ; *Histocompatibility ; Histocompatibility Antigens Class II/genetics/immunology ; *Major Histocompatibility Complex ; Meiosis ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Oocytes/cytology/immunology ; *Parthenogenesis ; Pluripotent Stem Cells/cytology/*immunology/physiology ; Polymerase Chain Reaction ; Recombination, Genetic ; Stem Cell Transplantation
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  • 92
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2006-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhuri, Jayanta -- Jasin, Maria -- R01 GM054668/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):335-6. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA. chaudhuj@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; B-Lymphocytes/*immunology ; Cytidine Deaminase/genetics/*metabolism ; DNA Breaks, Double-Stranded ; DNA Repair ; Deoxyribonucleases, Type II Site-Specific/*metabolism ; Genes, Immunoglobulin Heavy Chain ; *Immunoglobulin Class Switching ; *Immunoglobulin Switch Region ; Mice ; Mutation ; Recombination, Genetic ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae Proteins ; Transcription, Genetic
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  • 93
    Publication Date: 2006-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):515.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastomyces/cytology/enzymology/*genetics/*pathogenicity ; Blastomycosis/microbiology ; Fungal Proteins/genetics/physiology ; Genes, Fungal ; Lung Diseases, Fungal/microbiology ; Mice ; Mutation ; Protein Kinases/*genetics/*physiology ; RNA Interference ; Soil Microbiology ; Spores, Fungal/physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
    Publication Date: 2006-02-18
    Description: Progerias are rare genetic diseases characterized by premature aging. Several progeroid disorders are caused by mutations that lead to the accumulation of a lipid-modified (farnesylated) form of prelamin A, a protein that contributes to the structural scaffolding for the cell nucleus. In progeria, the accumulation of farnesyl-prelamin A disrupts this scaffolding, leading to misshapen nuclei. Previous studies have shown that farnesyltransferase inhibitors (FTIs) reverse this cellular abnormality. We tested the efficacy of an FTI (ABT-100) in Zmpste24-deficient mice, a mouse model of progeria. The FTI-treated mice exhibited improved body weight, grip strength, bone integrity, and percent survival at 20 weeks of age. These results suggest that FTIs may have beneficial effects in humans with progeria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fong, Loren G -- Frost, David -- Meta, Margarita -- Qiao, Xin -- Yang, Shao H -- Coffinier, Catherine -- Young, Stephen G -- AR050200/AR/NIAMS NIH HHS/ -- HL76839/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1621-3. Epub 2006 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA. lfong@mednet.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484451" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Weight/drug effects ; Disease Models, Animal ; Enzyme Inhibitors/pharmacology/*therapeutic use ; Farnesyltranstransferase/*antagonists & inhibitors ; Female ; Hand Strength ; Imidazoles/pharmacology/*therapeutic use ; Lamin Type A ; Male ; Membrane Proteins/deficiency/genetics ; Metalloendopeptidases/deficiency/genetics ; Mice ; Nuclear Proteins/metabolism ; Progeria/*drug therapy/physiopathology ; Protein Precursors/metabolism ; Protein Prenylation/drug effects ; Rib Fractures/prevention & control ; Survival Rate
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
    Publication Date: 2006-12-23
    Description: Double-stranded RNA, processed to small interfering RNAs (siRNAs) by Dicer and incorporated into the RNA-induced silencing complex (RISC), triggers gene silencing by a variety of pathways in eukaryotes. RNA interference involving the degradation of homologous transcripts is the best-characterized mechanism. However, the fate of the RNA fragments resulting from siRNA-directed cleavage is poorly understood. We have identified a gene (MUT68) in the unicellular green alga Chlamydomonas reinhardtii that is required for the efficient decay of siRNA-targeted transcripts. MUT68 encodes a noncanonical polyadenylate polymerase that adds untemplated adenines to the 5' RNA fragments after siRNA-mediated cleavage and appears to stimulate their exosome-dependent degradation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibrahim, Fadia -- Rohr, Jennifer -- Jeong, Won-Joong -- Hesson, Jennifer -- Cerutti, Heriberto -- GM62915/GM/NIGMS NIH HHS/ -- R01 GM062915-06/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1893.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Sciences and Plant Science Initiative, University of Nebraska, Lincoln, NE 68588, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185594" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine Nucleotides/*metabolism ; Animals ; Chlamydomonas reinhardtii/enzymology/*genetics/*metabolism ; Exoribonucleases/metabolism ; Molecular Sequence Data ; Oligoribonucleotides/*metabolism ; Polynucleotide Adenylyltransferase/genetics/*metabolism ; RNA, Messenger/genetics/*metabolism ; RNA, Small Interfering/metabolism ; RNA-Induced Silencing Complex/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Templates, Genetic ; Transgenes ; Tryptophan Synthase/genetics ; Uracil Nucleotides/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
    Publication Date: 2006-02-14
    Description: Mice experiencing repeated aggression develop a long-lasting aversion to social contact, which can be normalized by chronic, but not acute, administration of antidepressant. Using viral-mediated, mesolimbic dopamine pathway-specific knockdown of brain-derived neurotrophic factor (BDNF), we showed that BDNF is required for the development of this experience-dependent social aversion. Gene profiling in the nucleus accumbens indicates that local knockdown of BDNF obliterates most of the effects of repeated aggression on gene expression within this circuit, with similar effects being produced by chronic treatment with antidepressant. These results establish an essential role for BDNF in mediating long-term neural and behavioral plasticity in response to aversive social experiences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berton, Olivier -- McClung, Colleen A -- Dileone, Ralph J -- Krishnan, Vaishnav -- Renthal, William -- Russo, Scott J -- Graham, Danielle -- Tsankova, Nadia M -- Bolanos, Carlos A -- Rios, Maribel -- Monteggia, Lisa M -- Self, David W -- Nestler, Eric J -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):864-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Center for Basic Neuroscience, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9070, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469931" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Animals ; Antidepressive Agents/pharmacology ; Brain-Derived Neurotrophic Factor/genetics/*physiology ; Depression/physiopathology ; Dominance-Subordination ; Dopamine/*physiology ; Fluoxetine/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Imipramine/pharmacology ; Limbic System/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/physiology ; Nucleus Accumbens/*physiology ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/biosynthesis ; *Social Behavior ; Social Isolation ; *Stress, Psychological ; Ventral Tegmental Area/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
    Publication Date: 2006-11-04
    Description: Mathematical reaction-diffusion models have been suggested to describe formation of animal pigmentation patterns and distribution of epidermal appendages. However, the crucial signals and in vivo mechanisms are still elusive. Here we identify WNT and its inhibitor DKK as primary determinants of murine hair follicle spacing, using a combined experimental and computational modeling approach. Transgenic DKK overexpression reduces overall appendage density. Moderate suppression of endogenous WNT signaling forces follicles to form clusters during an otherwise normal morphogenetic program. These results confirm predictions of a WNT/DKK-specific mathematical model and provide in vivo corroboration of the reaction-diffusion mechanism for epidermal appendage formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sick, Stefanie -- Reinker, Stefan -- Timmer, Jens -- Schlake, Thomas -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1447-50. Epub 2006 Nov 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck Institute of Immunobiology, Stuebeweg 51, 79108 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082421" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Diffusion ; Forkhead Transcription Factors/genetics ; Hair/growth & development ; Hair Follicle/embryology/*growth & development/metabolism ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism ; Mathematics ; Mesoderm/metabolism ; Mice ; Mice, Transgenic ; *Models, Biological ; Morphogenesis ; *Signal Transduction ; Wnt Proteins/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 2006-08-12
    Description: The Arabidopsis CLAVATA3 (CLV3) gene encodes a stem cell-specific protein presumed to be a precursor of a secreted peptide hormone. Matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS) applied to in situ Arabidopsis tissues determined the structure of a modified 12-amino acid peptide (MCLV3), which was derived from a conserved motif in the CLV3 sequence. Synthetic MCLV3 induced shoot and root meristem consumption as cells differentiated into other organs, displaying the typical phenotype of transgenic plants overexpressing CLV3. These results suggest that the functional peptide of CLV3 is MCLV3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, Tatsuhiko -- Sawa, Shinichiro -- Kinoshita, Atsuko -- Mizuno, Satoko -- Kakimoto, Tatsuo -- Fukuda, Hiroo -- Sakagami, Youji -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):845-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya, 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902141" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/*cytology/genetics/metabolism ; Arabidopsis Proteins/*chemistry/genetics/*metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Hydroxyproline/chemistry ; Meristem/*cytology/drug effects/metabolism ; Molecular Sequence Data ; Oligopeptides/chemistry/*metabolism/pharmacology ; Plant Roots/growth & development ; Plants, Genetically Modified ; Signal Transduction ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Stem Cells/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
    Publication Date: 2006-04-15
    Description: Loss of seed shattering was a key event in the domestication of major cereals. We revealed that the qSH1 gene, a major quantitative trait locus of seed shattering in rice, encodes a BEL1-type homeobox gene and demonstrated that a single-nucleotide polymorphism (SNP) in the 5' regulatory region of the qSH1 gene caused loss of seed shattering owing to the absence of abscission layer formation. Haplotype analysis and association analysis in various rice collections revealed that the SNP was highly associated with shattering among japonica subspecies of rice, implying that it was a target of artificial selection during rice domestication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Konishi, Saeko -- Izawa, Takeshi -- Lin, Shao Yang -- Ebana, Kaworu -- Fukuta, Yoshimichi -- Sasaki, Takuji -- Yano, Masahiro -- New York, N.Y. -- Science. 2006 Jun 2;312(5778):1392-6. Epub 2006 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of the Society for Techno-Innovation of Agriculture, Forestry, and Fisheries, 446-1 Ippaizuka, Kamiyokoba Tsukuba, Ibaraki 305-0854, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16614172" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/*history ; Alleles ; Chromosome Mapping ; Chromosomes, Plant ; Crops, Agricultural/*genetics/history ; Genes, Plant ; History, Ancient ; Humans ; Molecular Sequence Data ; Oryza/*genetics/history ; Plant Proteins/genetics ; *Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; *Seeds ; Transcription Factors/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2006-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitetta, Ellen S -- Ghetie, Victor F -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):308-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Immunobiology Center, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75235-8576, USA. ellen.vitetta@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857927" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/administration & dosage/adverse ; effects/immunology/*therapeutic use ; Antibodies, Monoclonal, Humanized ; Antibody Affinity ; Binding Sites, Antibody ; *Clinical Trials as Topic ; Combined Modality Therapy ; Cytokines/metabolism ; Drug Evaluation, Preclinical ; Half-Life ; Humans ; Immunoglobulin Fc Fragments/immunology ; Immunoglobulin G/chemistry/immunology/metabolism ; *Immunotherapy ; Lymphocyte Activation ; Mice ; Neoplasms/*therapy ; Protein Engineering ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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