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  • Humans  (4)
  • Female  (3)
  • Life and Medical Sciences
  • Polymer and Materials Science
  • American Association for the Advancement of Science (AAAS)  (6)
  • 1995-1999  (6)
  • 1970-1974
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (6)
  • Wiley-Blackwell  (30)
Years
Year
  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, M -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):617, 619.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9988653" target="_blank"〉PubMed〈/a〉
    Keywords: Bioethics ; Cell Division ; *Cloning, Organism/legislation & jurisprudence ; Embryo Research ; *Embryo, Mammalian/cytology ; Ethical Review ; Government Regulation ; Humans ; Korea ; Nuclear Transfer Techniques ; Public Policy
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, M -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):16-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917255" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Bioethics ; *Cloning, Organism ; Embryo Research ; Female ; Government Regulation ; Humans ; Korea ; Nuclear Transfer Techniques ; Research
    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
    Publication Date: 1997-08-08
    Description: TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheridan, J P -- Marsters, S A -- Pitti, R M -- Gurney, A -- Skubatch, M -- Baldwin, D -- Ramakrishnan, L -- Gray, C L -- Baker, K -- Wood, W I -- Goddard, A D -- Godowski, P -- Ashkenazi, A -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, South San Francisco, CA 94080-4918, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242611" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Membrane/metabolism ; Cells, Cultured ; GPI-Linked Proteins ; Glycosylphosphatidylinositols/metabolism ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-25
    Description: REVIEW There is substantial cytogenetic data indicating that the process of sex determination can evolve relatively rapidly. However, recent molecular studies on the evolution of the regulatory genes that control sex determination in the insect Drosophila melanogaster, the nematode Caenorhabditis elegans, and mammals suggest that, although certain sex determination regulatory genes have evolved relatively rapidly, other sex determination regulatory genes are quite conserved. Thus, studies of the evolution of sex determination, a process that appears to have elements that undergo substantial evolutionary change and others that may be conserved, could provide substantial insights into the kinds of forces that both drive and constrain the evolution of developmental hierarchies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marin, I -- Baker, B S -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):1990-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9748152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Female ; Gene Expression Regulation ; Male ; Mutation ; Selection, Genetic ; Sex Chromosomes/genetics ; *Sex Determination Processes
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1995-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohman, J C -- Slanina, M -- Baker, G -- Mensforth, R P -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):587-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7725113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomechanical Phenomena ; Hominidae/*anatomy & histology ; Humans ; Metacarpophalangeal Joint/anatomy & histology ; Metacarpus ; Motor Skills ; Thumb/*anatomy & histology
    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
    Publication Date: 1995-07-28
    Description: C57BL/6J mice with a mutation in the obese (ob) gene are obese, diabetic, and exhibit reduced activity, metabolism, and body temperature. Daily intraperitoneal injection of these mice with recombinant OB protein lowered their body weight, percent body fat, food intake, and serum concentrations of glucose and insulin. In addition, metabolic rate, body temperature, and activity levels were increased by this treatment. None of these parameters was altered beyond the level observed in lean controls, suggesting that the OB protein normalized the metabolic status of the ob/ob mice. Lean animals injected with OB protein maintained a smaller weight loss throughout the 28-day study and showed no changes in any of the metabolic parameters. These data suggest that the OB protein regulates body weight and fat deposition through effects on metabolism and appetite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pelleymounter, M A -- Cullen, M J -- Baker, M B -- Hecht, R -- Winters, D -- Boone, T -- Collins, F -- New York, N.Y. -- Science. 1995 Jul 28;269(5223):540-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Amgen, Inc., Thousand Oaks, CA 91320, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624776" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/drug effects ; Analysis of Variance ; Animals ; Blood Glucose/analysis ; Body Composition/drug effects ; Body Temperature/drug effects ; Dose-Response Relationship, Drug ; Drinking/drug effects ; Eating/*drug effects ; Energy Metabolism/drug effects ; Female ; Insulin/blood ; Leptin ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Motor Activity/drug effects ; Obesity/genetics/*physiopathology ; Oxygen Consumption/drug effects ; Proteins/genetics/*pharmacology ; Recombinant Proteins/pharmacology ; 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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