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  • Male  (77)
  • 2010-2014
  • 2000-2004  (51)
  • 1995-1999  (26)
  • 1955-1959
  • 1950-1954
  • 2002  (51)
  • 1999  (26)
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  • 2010-2014
  • 2000-2004  (51)
  • 1995-1999  (26)
  • 1955-1959
  • 1950-1954
Year
  • 1
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    A human genome diversity cell line panel (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cann, Howard M -- de Toma, Claudia -- Cazes, Lucien -- Legrand, Marie-Fernande -- Morel, Valerie -- Piouffre, Laurence -- Bodmer, Julia -- Bodmer, Walter F -- Bonne-Tamir, Batsheva -- Cambon-Thomsen, Anne -- Chen, Zhu -- Chu, J -- Carcassi, Carlo -- Contu, Licinio -- Du, Ruofu -- Excoffier, Laurent -- Ferrara, G B -- Friedlaender, Jonathan S -- Groot, Helena -- Gurwitz, David -- Jenkins, Trefor -- Herrera, Rene J -- Huang, Xiaoyi -- Kidd, Judith -- Kidd, Kenneth K -- Langaney, Andre -- Lin, Alice A -- Mehdi, S Qasim -- Parham, Peter -- Piazza, Alberto -- Pistillo, Maria Pia -- Qian, Yaping -- Shu, Qunfang -- Xu, Jiujin -- Zhu, S -- Weber, James L -- Greely, Henry T -- Feldman, Marcus W -- Thomas, Gilles -- Dausset, Jean -- Cavalli-Sforza, L Luca -- New York, N.Y. -- Science. 2002 Apr 12;296(5566):261-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11954565" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Specimen Banks ; *Cell Line ; Continental Population Groups/genetics ; DNA/genetics ; Databases, Factual ; Female ; *Genetic Variation ; *Genome, Human ; Haplotypes ; Humans ; Informed Consent ; *Lymphocytes ; Male ; Polymorphism, Single Nucleotide
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Regulation of intestinal alpha-defensin activation by the metalloproteinase matrilysin in innate host defense (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: Precursors of alpha-defensin peptides require activation for bactericidal activity. In mouse small intestine, matrilysin colocalized with alpha-defensins (cryptdins) in Paneth cell granules, and in vitro it cleaved the pro segment from cryptdin precursors. Matrilysin-deficient (MAT-/-) mice lacked mature cryptdins and accumulated precursor molecules. Intestinal peptide preparations from MAT-/- mice had decreased antimicrobial activity. Orally administered bacteria survived in greater numbers and were more virulent in MAT-/- mice than in MAT+/+ mice. Thus, matrilysin functions in intestinal mucosal defense by regulating the activity of defensins, which may be a common role for this metalloproteinase in its numerous epithelial sites of expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, C L -- Ouellette, A J -- Satchell, D P -- Ayabe, T -- Lopez-Boado, Y S -- Stratman, J L -- Hultgren, S J -- Matrisian, L M -- Parks, W C -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):113-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Division of Allergy and Pulmonary Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. wilson_c@kids.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Catalysis ; Cytoplasmic Granules/enzymology ; Escherichia coli/growth & development ; Escherichia coli Infections/immunology/microbiology ; Female ; Humans ; *Immunity, Innate ; *Immunity, Mucosal ; Intestinal Mucosa/enzymology/immunology/microbiology ; Intestine, Small/enzymology/*immunology/microbiology ; Male ; Matrix Metalloproteinase 7 ; Metalloendopeptidases/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Paneth Cells/enzymology ; Protein Precursors/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Salmonella typhimurium/growth & development/pathogenicity ; Tissue Extracts/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Reversal of bone loss in mice by nongenotropic signaling of sex steroids (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-26
    Description: We show that sex steroids protect the adult murine skeleton through a mechanism that is distinct from that used to preserve the mass and function of reproductive organs. The classical genotropic actions of sex steroid receptors are dispensable for their bone protective effects, but essential for their effects on reproductive tissues. A synthetic ligand (4-estren-3alpha,17beta-diol) that reproduces the nongenotropic effects of sex steroids, without affecting classical transcription, increases bone mass and strength in ovariectomized females above the level of the estrogen-replete state and is at least as effective as dihydrotestosterone in orchidectomized males, without affecting reproductive organs. Such ligands merit investigation as potential therapeutic alternatives to hormone replacement for osteoporosis in both women and men [corrected].〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kousteni, S -- Chen, J R -- Bellido, T -- Han, L -- Ali, A A -- O'Brien, C A -- Plotkin, L -- Fu, Q -- Mancino, A T -- Wen, Y -- Vertino, A M -- Powers, C C -- Stewart, S A -- Ebert, R -- Parfitt, A M -- Weinstein, R S -- Jilka, R L -- Manolagas, S C -- KO2-AR02127/AR/NIAMS NIH HHS/ -- P01-AG13918/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 25;298(5594):843-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology and Metabolism, Department of Internal Medicine, and Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12399595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Body Weight/drug effects ; Bone Density/*drug effects ; Bone and Bones/*drug effects/physiology ; Breast Neoplasms/pathology ; Cell Division/drug effects ; Cells, Cultured ; Compressive Strength/drug effects ; Dihydrotestosterone/pharmacology ; Estradiol/pharmacology ; Estrenes/metabolism/*pharmacology ; Female ; Humans ; Male ; Mice ; Orchiectomy ; Organ Size/drug effects ; Osteoblasts/*drug effects/physiology ; Osteocalcin/blood ; Osteoclasts/*drug effects/physiology ; Osteogenesis/drug effects ; Osteoporosis/drug therapy ; Ovariectomy ; Pyrazoles/pharmacology ; Receptors, Estrogen/metabolism ; Seminal Vesicles/drug effects ; Transcription, Genetic/drug effects ; Tumor Cells, Cultured ; Uterus/drug effects/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Activation of central melanocortin pathways by fenfluramine (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-27
    Description: D-fenfluramine (d-FEN) was once widely prescribed and was among the most effective weight loss drugs, but was withdrawn from clinical use because of reports of cardiac complications in a subset of patients. Discerning the neurobiology underlying the anorexic action of d-FEN may facilitate the development of new drugs to prevent and treat obesity. Through a combination of functional neuroanatomy, feeding, and electrophysiology studies in rodents, we show that d-FEN-induced anorexia requires activation of central nervous system melanocortin pathways. These results provide a mechanistic explanation of d-FEN's anorexic actions and indicate that drugs targeting these downstream melanocortin pathways may prove to be effective and more selective anti-obesity treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heisler, Lora K -- Cowley, Michael A -- Tecott, Laurence H -- Fan, Wei -- Low, Malcolm J -- Smart, James L -- Rubinstein, Marcelo -- Tatro, Jeffrey B -- Marcus, Jacob N -- Holstege, Henne -- Lee, Charlotte E -- Cone, Roger D -- Elmquist, Joel K -- F31HG00201/HG/NHGRI NIH HHS/ -- P01DK056116/DK/NIDDK NIH HHS/ -- P01DK55819/DK/NIDDK NIH HHS/ -- R01MH061583/MH/NIMH NIH HHS/ -- R01MH44694/MH/NIMH NIH HHS/ -- R01MH61624/MH/NIMH NIH HHS/ -- R03TW01233/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 26;297(5581):609-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12142539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite Depressants/*pharmacology ; Arcuate Nucleus of Hypothalamus/*drug effects/metabolism ; Feeding Behavior/*drug effects ; Fenfluramine/*pharmacology ; Male ; Melanocyte-Stimulating Hormones/pharmacology ; Mice ; Mice, Obese ; Mice, Transgenic ; Neurons/drug effects/metabolism ; Paraventricular Hypothalamic Nucleus/drug effects/metabolism ; Patch-Clamp Techniques ; Pro-Opiomelanocortin/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; Receptor, Serotonin, 5-HT2C ; Receptors, Corticotropin/metabolism ; Receptors, Serotonin/metabolism ; Serotonin/metabolism ; Serotonin Agents/pharmacology ; alpha-MSH/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Coordinated reactivation of distributed memory traces in primate neocortex (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-21
    Description: Conversion of new memories into a lasting form may involve the gradual refinement and linking together of neural representations stored widely throughout neocortex. This consolidation process may require coordinated reactivation of distributed components of memory traces while the cortex is "offline," i.e., not engaged in processing external stimuli. Simultaneous neural ensemble recordings from four sites in the macaque neocortex revealed such coordinated reactivation. In motor, somatosensory, and parietal cortex (but not prefrontal cortex), the behaviorally induced correlation structure and temporal patterning of neural ensembles within and between regions were preserved, confirming a major tenet of the trace-reactivation theory of memory consolidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, K L -- McNaughton, B L -- MH01565/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2002 Sep 20;297(5589):2070-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neural Systems, Memory, and Aging, University of Arizona, Tucson, AZ 85724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12242447" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain Mapping ; Cues ; Electrodes, Implanted ; Macaca mulatta ; Male ; Memory/*physiology ; Mental Recall/*physiology ; Motor Cortex/physiology ; Neocortex/*physiology ; Neurons/*physiology ; Parietal Lobe/physiology ; Prefrontal Cortex/physiology ; Somatosensory Cortex/physiology ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Defective angiogenesis in mice lacking endoglin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-29
    Description: Endoglin is a transforming growth factor-beta (TGF-beta) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENG cause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-beta, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, D Y -- Sorensen, L K -- Brooke, B S -- Urness, L D -- Davis, E C -- Taylor, D G -- Boak, B B -- Wendel, D P -- K08 HL03490-03/HL/NHLBI NIH HHS/ -- T35 HL07744-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 May 28;284(5419):1534-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-5330, USA. dean.li@hci.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10348742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, CD31/analysis ; Blood Vessels/cytology/*embryology/metabolism ; Cell Differentiation ; Crosses, Genetic ; Endothelium, Vascular/cytology/*embryology/metabolism ; Female ; Gene Targeting ; In Situ Hybridization ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Muscle, Smooth, Vascular/cytology/*embryology ; *Neovascularization, Physiologic ; Receptors, Cell Surface ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Vascular Cell Adhesion Molecule-1/genetics/*physiology ; Yolk Sac/ultrastructure
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-05
    Description: Protein tyrosine phosphatase-1B (PTP-1B) has been implicated in the negative regulation of insulin signaling. Disruption of the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP-1B+/+ littermates. The enhanced insulin sensitivity of the PTP-1B-/- mice was also evident in glucose and insulin tolerance tests. The PTP-1B-/- mice showed increased phosphorylation of the insulin receptor in liver and muscle tissue after insulin injection in comparison to PTP-1B+/+ mice. On a high-fat diet, the PTP-1B-/- and PTP-1B+/- mice were resistant to weight gain and remained insulin sensitive, whereas the PTP-1B+/+ mice rapidly gained weight and became insulin resistant. These results demonstrate that PTP-1B has a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing it as a potential therapeutic target in the treatment of type 2 diabetes and obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elchebly, M -- Payette, P -- Michaliszyn, E -- Cromlish, W -- Collins, S -- Loy, A L -- Normandin, D -- Cheng, A -- Himms-Hagen, J -- Chan, C C -- Ramachandran, C -- Gresser, M J -- Tremblay, M L -- Kennedy, B P -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1544-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada, H3G 1Y6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066179" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/therapy ; Dietary Fats/administration & dosage ; Gene Targeting ; Glucose Tolerance Test ; Insulin/blood/*metabolism/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Muscle, Skeletal/metabolism ; Obesity/*metabolism/therapy ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatases/*genetics/*metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Structural maturation of neural pathways in children and adolescents: in vivo study (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-19
    Description: Structural maturation of fiber tracts in the human brain, including an increase in the diameter and myelination of axons, may play a role in cognitive development during childhood and adolescence. A computational analysis of structural magnetic resonance images obtained in 111 children and adolescents revealed age-related increases in white matter density in fiber tracts constituting putative corticospinal and frontotemporal pathways. The maturation of the corticospinal tract was bilateral, whereas that of the frontotemporal pathway was found predominantly in the left (speech-dominant) hemisphere. These findings provide evidence for a gradual maturation, during late childhood and adolescence, of fiber pathways presumably supporting motor and speech functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paus, T -- Zijdenbos, A -- Worsley, K -- Collins, D L -- Blumenthal, J -- Giedd, J N -- Rapoport, J L -- Evans, A C -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1908-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, Quebec H3A 2B4, Canada. tomas@bic.mni.mcgill.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082463" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; *Aging ; Axons/physiology/ultrastructure ; Brain/anatomy & histology/*growth & development ; Brain Mapping ; Child ; Child, Preschool ; Female ; Frontal Lobe/anatomy & histology/growth & development ; Humans ; Magnetic Resonance Imaging ; Male ; Motor Skills ; Myelin Sheath/ultrastructure ; Nerve Fibers/ultrastructure ; Neural Conduction ; Neural Pathways/anatomy & histology/*growth & development ; Regression Analysis ; Speech ; Spinal Cord/anatomy & histology ; Synaptic Transmission ; Temporal Lobe/anatomy & histology/growth & development
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    An allele of COL9A2 associated with intervertebral disc disease (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-20
    Description: Intervertebral disc disease is one of the most common musculoskeletal disorders. A number of environmental and anthropometric risk factors may contribute to it, and recent reports have suggested the importance of genetic factors as well. The COL9A2 gene, which codes for one of the polypeptide chains of collagen IX that is expressed in the intervertebral disc, was screened for sequence variations in individuals with intervertebral disc disease. The analysis identified a putative disease-causing sequence variation that converted a codon for glutamine to one for tryptophan in six out of the 157 individuals but in none of 174 controls. The tryptophan allele cosegregated with the disease phenotype in the four families studied, giving a lod score (logarithm of odds ratio) for linkage of 4.5, and subsequent linkage disequilibrium analysis conditional on linkage gave an additional lod score of 7.1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Annunen, S -- Paassilta, P -- Lohiniva, J -- Perala, M -- Pihlajamaa, T -- Karppinen, J -- Tervonen, O -- Kroger, H -- Lahde, S -- Vanharanta, H -- Ryhanen, L -- Goring, H H -- Ott, J -- Prockop, D J -- Ala-Kokko, L -- AR39740/AR/NIAMS NIH HHS/ -- HG00008/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 16;285(5426):409-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Collagen Research Unit, Biocenter and Department of Medical Biochemistry, University of Oulu, 90220 Oulu, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10411504" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Alleles ; Amino Acid Substitution ; Case-Control Studies ; Codon ; Collagen/chemistry/*genetics ; *Collagen Type IX ; Female ; Genetic Linkage ; *Genetic Predisposition to Disease ; Humans ; Intervertebral Disc Displacement/*genetics ; Linkage Disequilibrium ; Male ; Middle Aged ; Mutation ; Penetrance ; Polymorphism, Genetic ; Sciatica/*genetics ; Tryptophan/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Impaired B cell development and proliferation in absence of phosphoinositide 3-kinase p85alpha (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: Phosphoinositide 3-kinase (PI3K) activation has been implicated in many cellular responses, including fibroblast growth, transformation, survival, and chemotaxis. Although PI3K is activated by several agents that stimulate T and B cells, the role of PI3K in lymphocyte function is not clear. The mouse gene encoding the PI3K adapter subunit p85alpha and its splice variants p55alpha and p50alpha was disrupted. Most p85alpha-p55alpha-p50alpha-/- mice die within days after birth. Lymphocyte development and function was studied with the use of the RAG2-deficient blastocyst complementation system. Chimeric mice had reduced numbers of peripheral mature B cells and decreased serum immunoglobulin. The B cells that developed had diminished proliferative responses to antibody to immunoglobulin M, antibody to CD40, and lipopolysaccharide stimulation and decreased survival after incubation with interleukin-4. In contrast, T cell development and proliferation was normal. This phenotype is similar to defects observed in mice lacking the tyrosine kinase Btk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fruman, D A -- Snapper, S B -- Yballe, C M -- Davidson, L -- Yu, J Y -- Alt, F W -- Cantley, L C -- R01 GM041890/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):393-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. dfruman@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD45/analysis ; Apoptosis ; B-Lymphocytes/cytology/enzymology/*immunology ; Catalytic Domain ; Cell Cycle ; Chimera ; Chromones/pharmacology ; Enzyme Inhibitors/pharmacology ; Female ; Gene Targeting ; Immunoglobulins/*blood ; *Lymphocyte Activation ; Lymphocyte Count ; Male ; Mice ; Mice, Inbred C57BL ; Morpholines/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/metabolism ; Spleen/immunology ; T-Lymphocytes/cytology/enzymology/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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