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  • Male  (35)
  • American Association for the Advancement of Science (AAAS)  (35)
  • 2000-2004  (35)
  • 1995-1999
  • 2000  (35)
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  • American Association for the Advancement of Science (AAAS)  (35)
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  • 2000-2004  (35)
  • 1995-1999
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  • 1
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    Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: The hCHK2 gene encodes the human homolog of the yeast Cds1 and Rad53 G2 checkpoint kinases, whose activation in response to DNA damage prevents cellular entry into mitosis. Here, it is shown that heterozygous germ line mutations in hCHK2 occur in Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in the TP53 gene. These observations suggest that hCHK2 is a tumor suppressor gene conferring predisposition to sarcoma, breast cancer, and brain tumors, and they also provide a link between the central role of p53 inactivation in human cancer and the well-defined G2 checkpoint in yeast.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, D W -- Varley, J M -- Szydlo, T E -- Kang, D H -- Wahrer, D C -- Shannon, K E -- Lubratovich, M -- Verselis, S J -- Isselbacher, K J -- Fraumeni, J F -- Birch, J M -- Li, F P -- Garber, J E -- Haber, D A -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2528-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Center for Cancer Risk Analysis and Harvard Medical School, Building 149, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617473" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Apoptosis ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Checkpoint Kinase 2 ; Female ; G1 Phase ; *G2 Phase ; *Genes, Tumor Suppressor ; Genes, p53 ; Genetic Predisposition to Disease ; *Germ-Line Mutation ; Heterozygote ; Humans ; Li-Fraumeni Syndrome/enzymology/*genetics/pathology ; Male ; Pedigree ; Polymorphism, Genetic ; Protein Kinases/genetics ; Protein-Serine-Threonine Kinases/*genetics/metabolism ; Sarcoma/genetics ; Signal Transduction ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Role of brain insulin receptor in control of body weight and reproduction (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: Insulin receptors (IRs) and insulin signaling proteins are widely distributed throughout the central nervous system (CNS). To study the physiological role of insulin signaling in the brain, we created mice with a neuron-specific disruption of the IR gene (NIRKO mice). Inactivation of the IR had no impact on brain development or neuronal survival. However, female NIRKO mice showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia. NIRKO mice also exhibited impaired spermatogenesis and ovarian follicle maturation because of hypothalamic dysregulation of luteinizing hormone. Thus, IR signaling in the CNS plays an important role in regulation of energy disposal, fuel metabolism, and reproduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruning, J C -- Gautam, D -- Burks, D J -- Gillette, J -- Schubert, M -- Orban, P C -- Klein, R -- Krone, W -- Muller-Wieland, D -- Kahn, C R -- DK31036/DK/NIDDK NIH HHS/ -- DK55326-01A2/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 22;289(5487):2122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Klinik II und Poliklinik fur Innere Medizin and Center of Molecular Medicine (ZMMK) der Universitat zu Koln, Joseph Stelzmann Strasse 9, 50931 Cologne, Germany. jens.bruening@uni-koeln.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11000114" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Blood Glucose/analysis ; *Body Weight ; Brain/*metabolism ; Eating ; Female ; Hypertriglyceridemia/etiology ; Insulin/blood/*physiology ; Insulin Resistance ; Leptin/blood ; Leuprolide/pharmacology ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; Neurons/metabolism ; Obesity/etiology ; Ovarian Follicle/physiology ; Receptor, Insulin/genetics/*physiology ; *Reproduction ; Sex Characteristics ; Signal Transduction ; Spermatogenesis
    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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    Insect population control using a dominant, repressible, lethal genetic system (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: A major modification to the sterile insect technique is described, in which transgenic insects homozygous for a dominant, repressible, female-specific lethal gene system are used. We demonstrate two methods that give the required genetic characteristics in an otherwise wild-type genetic background. The first system uses a sex-specific promoter or enhancer to drive the expression of a repressible transcription factor, which in turn controls the expression of a toxic gene product. The second system uses non-sex-specific expression of the repressible transcription factor to regulate a selectively lethal gene product. Both methods work efficiently in Drosophila melanogaster, and we expect these principles to be widely applicable to more economically important organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, D D -- Donnelly, C A -- Wood, R J -- Alphey, L S -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2474-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741964" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Crosses, Genetic ; DNA-Binding Proteins ; *Drosophila Proteins ; Drosophila melanogaster/*genetics ; Egg Proteins/genetics ; Enhancer Elements, Genetic ; Fat Body/metabolism ; Female ; Gene Expression Regulation ; *Genes, Dominant ; *Genes, Insect ; *Genes, Lethal ; Genes, ras ; Homozygote ; Male ; Models, Biological ; Nuclear Proteins/genetics ; *Pest Control, Biological ; Promoter Regions, Genetic ; Tetracycline/pharmacology ; Trans-Activators/genetics ; Transcription Factors/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Hematopoietic stem cell quiescence maintained by p21cip1/waf1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: Relative quiescence is a defining characteristic of hematopoietic stem cells, while their progeny have dramatic proliferative ability and inexorably move toward terminal differentiation. The quiescence of stem cells has been conjectured to be of critical biologic importance in protecting the stem cell compartment, which we directly assessed using mice engineered to be deficient in the G1 checkpoint regulator, cyclin-dependent kinase inhibitor, p21cip1/waf1 (p21). In the absence of p21, hematopoietic stem cell proliferation and absolute number were increased under normal homeostatic conditions. Exposing the animals to cell cycle-specific myelotoxic injury resulted in premature death due to hematopoietic cell depletion. Further, self-renewal of primitive cells was impaired in serially transplanted bone marrow from p21-/- mice, leading to hematopoietic failure. Therefore, p21 is the molecular switch governing the entry of stem cells into the cell cycle, and in its absence, increased cell cycling leads to stem cell exhaustion. Under conditions of stress, restricted cell cycling is crucial to prevent premature stem cell depletion and hematopoietic death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, T -- Rodrigues, N -- Shen, H -- Yang, Y -- Dombkowski, D -- Sykes, M -- Scadden, D T -- AI07387/AI/NIAID NIH HHS/ -- DK50234/DK/NIDDK NIH HHS/ -- HL44851/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1804-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Hematology, AIDS Research Center, Massachusetts General Hospital Cancer Center, Transplantation Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimetabolites/pharmacology ; Blood Cell Count ; Bone Marrow Transplantation ; Cell Count ; *Cell Cycle ; Cell Death ; Cell Differentiation ; Cell Division ; Coculture Techniques ; Colony-Forming Units Assay ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics/*physiology ; Female ; Fluorouracil/pharmacology ; *Hematopoiesis ; Hematopoietic Stem Cells/*cytology/drug effects/physiology ; Homeostasis ; Male ; Mice ; Mice, Inbred Strains
    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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    Requirement for RORgamma in thymocyte survival and lymphoid organ development (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-06
    Description: Most developing thymocytes undergo apoptosis because they cannot interact productively with molecules encoded by the major histocompatibility complex. Here, we show that mice lacking the orphan nuclear hormone receptor RORgamma lose thymic expression of the anti-apoptotic factor Bcl-xL. RORgamma thus regulates the survival of CD4+8+ thymocytes and may control the temporal window during which thymocytes can undergo positive selection. RORgamma was also required for development of lymph nodes and Peyer's patches, but not splenic follicles. In its absence, there was loss of a population of CD3-CD4+CD45+ cells that normally express RORgamma and that are likely early progenitors of lymphoid organs. Hence, RORgamma has critical functions in T cell repertoire selection and lymphoid organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Z -- Unutmaz, D -- Zou, Y R -- Sunshine, M J -- Pierani, A -- Brenner-Morton, S -- Mebius, R E -- Littman, D R -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; Cell Count ; Cell Cycle ; Cell Survival ; Crosses, Genetic ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Targeting ; Inhibitor of Differentiation Protein 2 ; Lymphoid Tissue/cytology/embryology/*growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; *Receptors, Retinoic Acid ; *Receptors, Thyroid Hormone ; *Repressor Proteins ; T-Lymphocyte Subsets/*cytology ; Thymus Gland/*cytology ; *Transcription Factors ; bcl-X Protein
    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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    Mitotic misregulation and human aging (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: Messenger RNA levels were measured in actively dividing fibroblasts isolated from young, middle-age, and old-age humans and humans with progeria, a rare genetic disorder characterized by accelerated aging. Genes whose expression is associated with age-related phenotypes and diseases were identified. The data also suggest that an underlying mechanism of the aging process involves increasing errors in the mitotic machinery of dividing cells in the postreproductive stage of life. We propose that this dysfunction leads to chromosomal pathologies that result in misregulation of genes involved in the aging process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ly, D H -- Lockhart, D J -- Lerner, R A -- Schultz, P G -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2486-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741968" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Aging/*genetics/pathology ; Biochemical Phenomena ; Cell Division ; Cell Line ; Cell Nucleus/ultrastructure ; Child ; Chromosome Segregation/genetics ; Disease/etiology ; Extracellular Matrix/metabolism ; Female ; Fibroblasts/cytology/*metabolism ; *Gene Expression Profiling ; *Gene Expression Regulation ; Humans ; Male ; Middle Aged ; *Mitosis/genetics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Progeria/*genetics/pathology ; RNA, Messenger/genetics/metabolism ; Spindle Apparatus/metabolism ; Transcription Factors/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Natural selection and parallel speciation in sympatric sticklebacks (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: Natural selection plays a fundamental role in most theories of speciation, but empirical evidence from the wild has been lacking. Here the post-Pleistocene radiation of threespine sticklebacks was used to infer natural selection in the origin of species. Populations of sticklebacks that evolved under different ecological conditions show strong reproductive isolation, whereas populations that evolved independently under similar ecological conditions lack isolation. Speciation has proceeded in this adaptive radiation in a repeatable fashion, ultimately as a consequence of adaptation to alternative environments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rundle, H D -- Nagel, L -- Wenrick Boughman, J -- Schluter, D -- New York, N.Y. -- Science. 2000 Jan 14;287(5451):306-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of British Columbia, 6270 University Boulevard, Vancouver, British Columbia V6T 1Z4 Canada. rundle@zoology.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10634785" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; *Biological Evolution ; British Columbia ; DNA, Mitochondrial/genetics ; Female ; Fishes/classification/*genetics/physiology ; Male ; Phylogeny ; Probability ; Reproduction ; *Selection, Genetic ; Sexual Behavior, Animal
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-01
    Description: Several nuclear hormone receptors involved in lipid metabolism form obligate heterodimers with retinoid X receptors (RXRs) and are activated by RXR agonists such as rexinoids. Animals treated with rexinoids exhibited marked changes in cholesterol balance, including inhibition of cholesterol absorption and repressed bile acid synthesis. Studies with receptor-selective agonists revealed that oxysterol receptors (LXRs) and the bile acid receptor (FXR) are the RXR heterodimeric partners that mediate these effects by regulating expression of the reverse cholesterol transporter, ABC1, and the rate-limiting enzyme of bile acid synthesis, CYP7A1, respectively. Thus, these RXR heterodimers serve as key regulators of cholesterol homeostasis by governing reverse cholesterol transport from peripheral tissues, bile acid synthesis in liver, and cholesterol absorption in intestine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Repa, J J -- Turley, S D -- Lobaccaro, J A -- Medina, J -- Li, L -- Lustig, K -- Shan, B -- Heyman, R A -- Dietschy, J M -- Mangelsdorf, D J -- R37 HL 09610/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1524-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968783" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/*metabolism ; Animals ; Bile Acids and Salts/biosynthesis ; Biological Transport/drug effects ; Cholesterol/*metabolism ; Cholesterol 7-alpha-Hydroxylase/metabolism ; Cholesterol, Dietary/administration & dosage ; Cricetinae ; DNA-Binding Proteins/metabolism ; Dimerization ; Gene Expression Regulation/drug effects ; Glycoproteins/genetics/*metabolism ; Homeostasis/drug effects ; Intestinal Absorption/*drug effects ; Intestine, Small/*metabolism ; Ligands ; Liver/*metabolism ; Macrophages, Peritoneal/metabolism ; Male ; Mesocricetus ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Orphan Nuclear Receptors ; *Receptors, Cytoplasmic and Nuclear ; Receptors, Retinoic Acid/agonists/genetics/*metabolism ; Receptors, Thyroid Hormone/agonists/genetics/metabolism ; Retinoid X Receptors ; Transcription Factors/agonists/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Reduced food intake and body weight in mice treated with fatty acid synthase inhibitors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-06
    Description: With the escalation of obesity-related disease, there is great interest in defining the mechanisms that control appetite and body weight. We have identified a link between anabolic energy metabolism and appetite control. Both systemic and intracerebroventricular treatment of mice with fatty acid synthase (FAS) inhibitors (cerulenin and a synthetic compound C75) led to inhibition of feeding and dramatic weight loss. C75 inhibited expression of the prophagic signal neuropeptide Y in the hypothalamus and acted in a leptin-independent manner that appears to be mediated by malonyl-coenzyme A. Thus, FAS may represent an important link in feeding regulation and may be a potential therapeutic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loftus, T M -- Jaworsky, D E -- Frehywot, G L -- Townsend, C A -- Ronnett, G V -- Lane, M D -- Kuhajda, F P -- DC02979/DC/NIDCD NIH HHS/ -- DK09623/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2379-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, The 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/10875926" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyl-CoA Carboxylase/antagonists & inhibitors/metabolism ; Animals ; Appetite/*drug effects ; Appetite Depressants/administration & dosage/chemical synthesis/*pharmacology ; Cerulenin/pharmacology ; Dose-Response Relationship, Drug ; Eating/drug effects ; Enzyme Inhibitors/administration & dosage/chemical synthesis/*pharmacology ; Fasting ; Fatty Acid Synthases/*antagonists & inhibitors/metabolism ; Female ; Hypothalamus/drug effects/metabolism ; Injections, Intraventricular ; Leptin/metabolism ; Liver/drug effects/metabolism ; Male ; Malonyl Coenzyme A/metabolism ; Mice ; Mice, Inbred BALB C ; Neurons/drug effects/metabolism ; Neuropeptide Y/administration & dosage/genetics/metabolism/pharmacology ; RNA, Messenger/genetics/metabolism ; Weight Loss/*drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Regulation of cell fate decision of undifferentiated spermatogonia by GDNF (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: The molecular control of self-renewal and differentiation of stem cells has remained enigmatic. Transgenic loss-of-function and overexpression models now show that the dosage of glial cell line-derived neurotrophic factor (GDNF), produced by Sertoli cells, regulates cell fate decisions of undifferentiated spermatogonial cells that include the stem cells for spermatogenesis. Gene-targeted mice with one GDNF-null allele show depletion of stem cell reserves, whereas mice overexpressing GDNF show accumulation of undifferentiated spermatogonia. They are unable to respond properly to differentiation signals and undergo apoptosis upon retinoic acid treatment. Nonmetastatic testicular tumors are regularly formed in older GDNF-overexpressing mice. Thus, GDNF contributes to paracrine regulation of spermatogonial self-renewal and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meng, X -- Lindahl, M -- Hyvonen, M E -- Parvinen, M -- de Rooij, D G -- Hess, M W -- Raatikainen-Ahokas, A -- Sainio, K -- Rauvala, H -- Lakso, M -- Pichel, J G -- Westphal, H -- Saarma, M -- Sariola, H -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1489-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Programs of Developmental Biology, Molecular Neurobiology, Electron Microscopy Unit, Institute of Biotechnology, Viikki Biocenter, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Cell Cycle ; Cell Differentiation/drug effects ; Cobalt/metabolism ; *Drosophila Proteins ; Female ; Gene Expression ; Gene Targeting ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Male ; Mice ; Mice, Transgenic ; Mitosis ; *Nerve Growth Factors ; Nerve Tissue Proteins/genetics/*physiology ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Receptor Protein-Tyrosine Kinases/genetics/metabolism ; Sertoli Cells/cytology/physiology ; *Spermatogenesis ; Spermatogonia/*cytology/drug effects ; Stem Cells/*cytology ; Testicular Neoplasms/pathology ; Testis/anatomy & histology ; Vitamin A/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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