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  • Mice  (195)
  • Chemical Engineering
  • LUNAR AND PLANETARY EXPLORATION
  • Lunar and Planetary Science and Exploration
  • American Association for the Advancement of Science (AAAS)  (195)
  • 1995-1999  (195)
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  • 1
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    Inhibitors of HIV nucleocapsid protein zinc fingers as candidates for the treatment of AIDS (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-17
    Description: Strategies for the treatment of human immunodeficiency virus-type 1 (HIV-1) infection must contend with the obstacle of drug resistance. HIV-1 nucleocapsid protein zinc fingers are prime antiviral targets because they are mutationally intolerant and are required both for acute infection and virion assembly. Nontoxic disulfide-substituted benzamides were identified that attack the zinc fingers, inactivate cell-free virions, inhibit acute and chronic infections, and exhibit broad antiretroviral activity. The compounds were highly synergistic with other antiviral agents, and resistant mutants have not been detected. Zinc finger-reactive compounds may offer an anti-HIV strategy that restricts drug-resistance development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, W G -- Supko, J G -- Malspeis, L -- Buckheit, R W Jr -- Clanton, D -- Bu, M -- Graham, L -- Schaeffer, C A -- Turpin, J A -- Domagala, J -- Gogliotti, R -- Bader, J P -- Halliday, S M -- Coren, L -- Sowder, R C 2nd -- Arthur, L O -- Henderson, L E -- New York, N.Y. -- Science. 1995 Nov 17;270(5239):1194-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Antiviral Drug Mechanisms, PRI/DynCorp., National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502043" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antiviral Agents/chemistry/pharmacokinetics/*pharmacology ; Benzamides/chemistry/pharmacokinetics/*pharmacology ; Biological Availability ; Capsid/chemistry/*metabolism ; *Capsid Proteins ; Cell Line ; Disulfides/chemistry/pharmacokinetics/*pharmacology ; Drug Resistance, Microbial ; Drug Synergism ; Gene Products, gag/*antagonists & inhibitors/chemistry ; HIV-1/*drug effects/physiology ; Humans ; Male ; Mice ; Molecular Sequence Data ; *Viral Proteins ; Zinc Fingers/*drug effects ; gag Gene Products, Human Immunodeficiency Virus
    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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    Fas ligand: a sensor for DNA damage critical in skin cancer etiology (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed "cellular proofreading." Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, L L -- Ouhtit, A -- Loughlin, S M -- Kripke, M L -- Ananthaswamy, H N -- Owen-Schaub, L B -- CA45623/CA/NCI NIH HHS/ -- CA52457/CA/NCI NIH HHS/ -- F32 AI09351/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):898-900.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Texas, M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436160" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/genetics/physiology ; Apoptosis ; *DNA Damage ; Epidermis/*cytology/metabolism/radiation effects ; Fas Ligand Protein ; *Genes, p53 ; Keratinocytes/*cytology/metabolism/radiation effects ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C3H ; Mutation ; Skin Neoplasms/*etiology/pathology ; Ultraviolet Rays ; Up-Regulation
    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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    A mouse model with features of familial combined hyperlipidemia (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-17
    Description: Familial combined hyperlipidemia (FCHL) is a common inherited lipid disorder, affecting 1 to 2 percent of the population in Westernized societies. Individuals with FCHL have large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) and develop premature coronary heart disease. A mouse model displaying some of the features of FCHL was created by crossing mice carrying the human apolipoprotein C-III (APOC3) transgene with mice deficient in the LDL receptor. A synergistic interaction between the apolipoprotein C-III and the LDL receptor defects produced large quantities of VLDL and LDL and enhanced the development of atherosclerosis. This mouse model may provide clues to the origin of human FCHL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masucci-Magoulas, L -- Goldberg, I J -- Bisgaier, C L -- Serajuddin, H -- Francone, O L -- Breslow, J L -- Tall, A R -- HL 21006/HL/NHLBI NIH HHS/ -- HL 54591/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Columbia University, 630 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein C-III ; Apolipoproteins B/blood ; Apolipoproteins C/*genetics ; Apolipoproteins E/blood ; Arteriosclerosis/etiology ; Carrier Proteins/genetics ; Cholesterol/blood ; Cholesterol Ester Transfer Proteins ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Cholesterol, VLDL/blood ; Diet ; *Disease Models, Animal ; Disease Susceptibility ; Female ; *Glycoproteins ; Humans ; *Hyperlipidemia, Familial Combined/blood/genetics ; Hyperlipoproteinemia Type IV/genetics ; Lipoproteins/blood ; Lipoproteins, VLDL/blood ; Male ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Receptors, LDL/*genetics/metabolism ; Transgenes ; Triglycerides/blood
    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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    Mediation of neuronal apoptosis by enhancement of outward potassium current (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (IK) current and loss of total intracellular K+. This IK augmentation was not seen in neurons undergoing excitotoxic necrosis or in older neurons resistant to staurosporine-induced apoptosis. Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented. Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis. Enhanced K+ efflux may mediate certain forms of neuronal apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C H -- Sensi, S L -- Gwag, B J -- Canzoniero, L M -- Farhangrazi, Z S -- Ying, H S -- Tian, M -- Dugan, L L -- Choi, D W -- 30337/PHS HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311914" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis/drug effects ; Benzopyrans/pharmacology ; Calcium/metabolism ; Cerebral Cortex/cytology ; Cromakalim ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; Gadolinium/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/metabolism ; Neuroprotective Agents/pharmacology ; Nifedipine/pharmacology ; Patch-Clamp Techniques ; Potassium/*metabolism ; Potassium Channels/drug effects/*metabolism ; Pyrroles/pharmacology ; Staurosporine/pharmacology ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Veratridine/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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  • 5
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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
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  • 6
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    An MTP inhibitor that normalizes atherogenic lipoprotein levels in WHHL rabbits (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: Patients with abetalipoproteinemia, a disease caused by defects in the microsomal triglyceride transfer protein (MTP), do not produce apolipoprotein B-containing lipoproteins. It was hypothesized that small molecule inhibitors of MTP would prevent the assembly and secretion of these atherogenic lipoproteins. To test this hypothesis, two compounds identified in a high-throughput screen for MTP inhibitors were used to direct the synthesis of a highly potent MTP inhibitor. This molecule (compound 9) inhibited the production of lipoprotein particles in rodent models and normalized plasma lipoprotein levels in Watanabe-heritable hyperlipidemic (WHHL) rabbits, which are a model for human homozygous familial hypercholesterolemia. These results suggest that compound 9, or derivatives thereof, has potential applications for the therapeutic lowering of atherogenic lipoprotein levels in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wetterau, J R -- Gregg, R E -- Harrity, T W -- Arbeeny, C -- Cap, M -- Connolly, F -- Chu, C H -- George, R J -- Gordon, D A -- Jamil, H -- Jolibois, K G -- Kunselman, L K -- Lan, S J -- Maccagnan, T J -- Ricci, B -- Yan, M -- Young, D -- Chen, Y -- Fryszman, O M -- Logan, J V -- Musial, C L -- Poss, M A -- Robl, J A -- Simpkins, L M -- Slusarchyk, W A -- Sulsky, R -- Taunk, P -- Magnin, D R -- Tino, J A -- Lawrence, R M -- Dickson, J K Jr -- Biller, S A -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):751-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Diseases, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543-4000, USA. Wetterau_John_R@msmail.bms.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784135" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine Transaminase/blood ; Animals ; Apolipoproteins B/*blood ; Aspartate Aminotransferases/blood ; Carrier Proteins/*antagonists & inhibitors ; Cholesterol/*blood ; Cricetinae ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Design ; Drug Evaluation, Preclinical ; Fluorenes/chemistry/pharmacokinetics/*pharmacology ; Humans ; Hyperlipidemias/blood/drug therapy ; Hyperlipoproteinemia Type II/*blood/drug therapy ; Lipids/blood ; Lipoproteins/blood ; Liver/metabolism ; Mice ; Piperidines/chemistry/pharmacokinetics/*pharmacology ; Rabbits ; Rats ; Triglycerides/*blood/metabolism ; 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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  • 7
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    Control of inflammation, cytokine expression, and germinal center formation by BCL-6 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: The gene encoding the BCL-6 transcriptional repressor is frequently translocated and mutated in diffuse large cell lymphoma. Mice with a disrupted BCL-6 gene developed myocarditis and pulmonary vasculitis, had no germinal centers, and had increased expression of T helper cell type 2 cytokines. The BCL-6 DNA recognition motif resembled sites bound by the STAT (signal transducers and activators of transcription) transcription factors, which mediate cytokine signaling. BCL-6 could repress interleukin-4 (IL-4)-induced transcription when bound to a site recognized by the IL-4-responsive transcription factor Stat6. Thus, dysregulation of STAT-responsive genes may underlie the inflammatory disease in BCL-6-deficient mice and participate in lymphoid malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dent, A L -- Shaffer, A L -- Yu, X -- Allman, D -- Staudt, L M -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):589-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, National Cancer 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/9110977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cells, Cultured ; Cytokines/*biosynthesis ; DNA-Binding Proteins/genetics/*physiology ; Ficoll/analogs & derivatives/immunology ; Germinal Center/*immunology ; Hemocyanin/immunology ; Immunoglobulins/biosynthesis ; Inflammation/*immunology/pathology ; Interferon-gamma/biosynthesis ; Interleukin-4/metabolism ; Interleukins/biosynthesis/metabolism ; Lymphocyte Activation ; Mice ; Myocarditis/immunology/pathology ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-6 ; Receptors, IgE/genetics ; STAT6 Transcription Factor ; Signal Transduction ; Spleen/immunology ; T-Lymphocytes/immunology ; Th2 Cells/immunology ; Trans-Activators/metabolism ; Transcription Factors/genetics/*physiology ; Transcription, Genetic ; Trinitrobenzenes/immunology ; Vasculitis/immunology/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Dopamine neuron agenesis in Nurr1-deficient mice (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-11
    Description: Dopamine neurons of the substantia nigra and ventral tegmental area regulate movement and affective behavior and degenerate in Parkinson's disease. The orphan nuclear receptor Nurr1 was shown to be expressed in developing dopamine neurons before the appearance of known phenotypic markers for these cells. Mice lacking Nurr1 failed to generate midbrain dopaminergic neurons, were hypoactive, and died soon after birth. Nurr1 expression continued into adulthood, and brains of heterozygous animals, otherwise apparently healthy, contained reduced dopamine levels. These results suggest that putative Nurr1 ligands may be useful for treatment of Parkinson's disease and other disorders of midbrain dopamine circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zetterstrom, R H -- Solomin, L -- Jansson, L -- Hoffer, B J -- Olson, L -- Perlmann, T -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):248-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Karolinska Institute, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092472" target="_blank"〉PubMed〈/a〉
    Keywords: 3,4-Dihydroxyphenylacetic Acid/metabolism ; Animals ; Cell Differentiation ; Chromatography, High Pressure Liquid ; Corpus Striatum/metabolism ; *DNA-Binding Proteins ; Dopamine/biosynthesis/*metabolism ; Gene Targeting ; Heterozygote ; Ligands ; Mesencephalon/abnormalities/*cytology/growth & development/metabolism ; Mice ; Nerve Tissue Proteins/genetics/*metabolism ; Neurons/*cytology/*metabolism ; Nuclear Receptor Subfamily 4, Group A, Member 2 ; RNA, Messenger/genetics/metabolism ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    A small, nonpeptidyl mimic of granulocyte-colony-stimulating factor [see commetns] (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-10
    Description: A nonpeptidyl small molecule SB 247464, capable of activating granulocyte-colony-stimulating factor (G-CSF) signal transduction pathways, was identified in a high-throughput assay in cultured cells. Like G-CSF, SB 247464 induced tyrosine phosphorylation of multiple signaling proteins and stimulated primary murine bone marrow cells to form granulocytic colonies in vitro. It also elevated peripheral blood neutrophil counts in mice. The extracellular domain of the murine G-CSF receptor was required for the activity of SB 247464, suggesting that the compound acts by oligomerizing receptor chains. The results indicate that a small molecule can activate a receptor that normally binds a relatively large protein ligand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, S S -- Lamb, P -- King, A G -- Miller, S G -- Kessler, L -- Luengo, J I -- Averill, L -- Johnson, R K -- Gleason, J G -- Pelus, L M -- Dillon, S B -- Rosen, J -- New York, N.Y. -- Science. 1998 Jul 10;281(5374):257-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Transcription Research, Ligand Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9657720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/metabolism/*pharmacology ; Cell Line ; Colony-Forming Units Assay ; DNA-Binding Proteins/metabolism ; Dimerization ; Female ; Granulocyte Colony-Stimulating Factor/metabolism/pharmacology ; Granulocytes/cytology ; Guanidines/chemistry/metabolism/*pharmacology ; Humans ; Janus Kinase 1 ; Janus Kinase 2 ; Leukocyte Count ; Leukopoiesis ; Mice ; Mice, Inbred C57BL ; *Milk Proteins ; Neutrophils/cytology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; *Proto-Oncogene Proteins ; Receptors, Granulocyte Colony-Stimulating Factor/chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; STAT3 Transcription Factor ; STAT5 Transcription Factor ; Signal Transduction/drug effects ; Species Specificity ; Trans-Activators/metabolism ; Transfection ; Tumor Cells, Cultured
    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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    Weight-reducing effects of the plasma protein encoded by the obese gene (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-28
    Description: The gene product of the ob locus is important in the regulation of body weight. The ob product was shown to be present as a 16-kilodalton protein in mouse and human plasma but was undetectable in plasma from C57BL/6J ob/ob mice. Plasma levels of this protein were increased in diabetic (db) mice, a mutant thought to be resistant to the effects of ob. Daily intraperitoneal injections of either mouse or human recombinant OB protein reduced the body weight of ob/ob mice by 30 percent after 2 weeks of treatment with no apparent toxicity but had no effect on db/db mice. The protein reduced food intake and increased energy expenditure in ob/ob mice. Injections of wild-type mice twice daily with the mouse protein resulted in a sustained 12 percent weight loss, decreased food intake, and a reduction of body fat from 12.2 to 0.7 percent. These data suggest that the OB protein serves an endocrine function to regulate body fat stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halaas, J L -- Gajiwala, K S -- Maffei, M -- Cohen, S L -- Chait, B T -- Rabinowitz, D -- Lallone, R L -- Burley, S K -- Friedman, J M -- DK41096/DK/NIDDK NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1995 Jul 28;269(5223):543-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Howard Hughes Medical Institute, Rockfeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624777" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/drug effects ; Animals ; Blood Glucose/analysis ; Body Composition/drug effects ; Diabetes Mellitus/blood/physiopathology ; Eating/drug effects ; Energy Metabolism/drug effects ; Female ; Humans ; Leptin ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Obesity/blood/genetics/*physiopathology ; Proteins/analysis/genetics/*pharmacology/physiology ; Recombinant Proteins/administration & dosage/pharmacology ; Weight Loss/*drug effects
    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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