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  • Mice  (9)
  • ASTROPHYSICS
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  • American Association for the Advancement of Science (AAAS)  (9)
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  • 1
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    Extended longevity in mice lacking the insulin receptor in adipose tissue (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-25
    Description: Caloric restriction has been shown to increase longevity in organisms ranging from yeast to mammals. In some organisms, this has been associated with a decreased fat mass and alterations in insulin/insulin-like growth factor 1 (IGF-1) pathways. To further explore these associations with enhanced longevity, we studied mice with a fat-specific insulin receptor knockout (FIRKO). These animals have reduced fat mass and are protected against age-related obesity and its subsequent metabolic abnormalities, although their food intake is normal. Both male and female FIRKO mice were found to have an increase in mean life-span of approximately 134 days (18%), with parallel increases in median and maximum life-spans. Thus, a reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bluher, Matthias -- Kahn, Barbara B -- Kahn, C Ronald -- DK 30136/DK/NIDDK NIH HHS/ -- DK 43051/DK/NIDDK NIH HHS/ -- DK 56116/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):572-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center and Department of Medicine, Harvard Medical School, One Joslin Place, Boston, MA, 02215 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543978" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*anatomy & histology/*metabolism ; Aging ; Animals ; Body Constitution ; Body Weight ; Caloric Restriction ; Eating ; Female ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; *Longevity ; Male ; Mice ; Mice, Knockout ; Receptor, Insulin/*genetics/metabolism ; Signal Transduction ; *Thinness
    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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    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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    Tumstatin, an endothelial cell-specific inhibitor of protein synthesis (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-05
    Description: Tumstatin is a 28-kilodalton fragment of type IV collagen that displays both anti-angiogenic and proapoptotic activity. Here we show that tumstatin functions as an endothelial cell-specific inhibitor of protein synthesis. Through a requisite interaction with alphaVbeta3 integrin, tumstatin inhibits activation of focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3-kinase), protein kinase B (PKB/Akt), and mammalian target of rapamycin (mTOR), and it prevents the dissociation of eukaryotic initiation factor 4E protein (eIF4E) from 4E-binding protein 1. These results establish a role for integrins in mediating cell-specific inhibition of cap-dependent protein synthesis and suggest a potential mechanism for tumstatin's selective effects on endothelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeshima, Yohei -- Sudhakar, Akulapalli -- Lively, Julie C -- Ueki, Kohjiro -- Kharbanda, Surender -- Kahn, C Ronald -- Sonenberg, Nahum -- Hynes, Richard O -- Kalluri, Raghu -- DK-51711/DK/NIDDK NIH HHS/ -- DK-55001/DK/NIDDK NIH HHS/ -- P01-HL66105/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jan 4;295(5552):140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Matrix Biology, Department of Medicine and the Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11778052" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Autoantigens/chemistry/metabolism/*pharmacology ; Carrier Proteins/metabolism ; Cattle ; Cells, Cultured ; Collagen Type IV/chemistry/metabolism/*pharmacology ; Endothelium, Vascular/*cytology/drug effects/*metabolism ; Enzyme Activation/drug effects ; Eukaryotic Initiation Factor-4E ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Humans ; Mice ; Molecular Sequence Data ; Peptide Fragments/pharmacology ; Peptide Initiation Factors/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; *Protein Biosynthesis/drug effects ; Protein Kinase Inhibitors ; Protein Kinases/metabolism ; Protein Synthesis Inhibitors/*pharmacology ; *Protein-Serine-Threonine Kinases ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; RNA Caps/metabolism ; RNA, Messenger/genetics/metabolism ; Receptors, Vitronectin/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases ; 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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  • 4
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    Medicine. Can we nip obesity in its vascular bud? (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-10-25
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351775/" 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/PMC4351775/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kahn, C Ronald -- P30 DK036836/DK/NIDDK NIH HHS/ -- R01 DK082659/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 24;322(5901):542-3. doi: 10.1126/science.1165667.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA. c.ronald.kahn@joslin.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948531" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*cytology/metabolism ; Adipocytes, Brown/cytology/metabolism ; Adipocytes, White/*cytology/metabolism ; Adipogenesis ; Adipose Tissue/*blood supply/cytology/metabolism ; Adiposity ; Animals ; Cell Lineage ; Gene Expression ; Humans ; Mesenchymal Stromal Cells/cytology ; Mice ; Multipotent Stem Cells/*cytology/metabolism ; Pericytes/*cytology/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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    A bacterial guanine nucleotide exchange factor activates ARF on Legionella phagosomes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-26
    Description: The intracellular pathogen Legionella pneumophila subverts vesicle traffic in eukaryotic host cells to create a vacuole that supports replication. The dot/icm genes encode a protein secretion apparatus that L. pneumophila require for biogenesis of this vacuole. Here we show that L. pneumophila produce a protein called RalF that functions as an exchange factor for the ADP ribosylation factor (ARF) family of guanosine triphosphatases (GTPases). The RalF protein is required for the localization of ARF on phagosomes containing L. pneumophila. Translocation of RalF protein through the phagosomal membrane is a dot/icm-dependent process. Thus, RalF is a substrate of the Dot/Icm secretion apparatus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nagai, Hiroki -- Kagan, Jonathan C -- Zhu, Xinjun -- Kahn, Richard A -- Roy, Craig R -- R01 AI44371/AI/NIAID NIH HHS/ -- R29 AI41699/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2002 Jan 25;295(5555):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11809974" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factor 1/genetics/*metabolism ; ADP-Ribosylation Factors/metabolism ; Acanthamoeba/microbiology ; Amino Acid Sequence ; Animals ; Bacterial Proteins/genetics/metabolism ; Carrier Proteins/genetics/metabolism ; Cell Line ; Genes, Bacterial ; Guanine Nucleotide Exchange Factors/chemistry/genetics/*metabolism ; Humans ; Legionella/genetics ; Legionella pneumophila/genetics/growth & development/*metabolism ; Macrophages/microbiology ; Mice ; Mice, Inbred A ; Molecular Sequence Data ; Phagosomes/*metabolism/*microbiology ; Protein Structure, Tertiary ; Protein Transport ; RNA, Bacterial/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Homology, Amino Acid
    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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    Suppression of aging in mice by the hormone Klotho (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-27
    Description: A defect in Klotho gene expression in mice accelerates the degeneration of multiple age-sensitive traits. Here, we show that overexpression of Klotho in mice extends life span. Klotho protein functions as a circulating hormone that binds to a cell-surface receptor and represses intracellular signals of insulin and insulin-like growth factor 1 (IGF1), an evolutionarily conserved mechanism for extending life span. Alleviation of aging-like phenotypes in Klotho-deficient mice was observed by perturbing insulin and IGF1 signaling, suggesting that Klotho-mediated inhibition of insulin and IGF1 signaling contributes to its anti-aging properties. Klotho protein may function as an anti-aging hormone in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536606/" 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/PMC2536606/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurosu, Hiroshi -- Yamamoto, Masaya -- Clark, Jeremy D -- Pastor, Johanne V -- Nandi, Animesh -- Gurnani, Prem -- McGuinness, Owen P -- Chikuda, Hirotaka -- Yamaguchi, Masayuki -- Kawaguchi, Hiroshi -- Shimomura, Iichiro -- Takayama, Yoshiharu -- Herz, Joachim -- Kahn, C Ronald -- Rosenblatt, Kevin P -- Kuro-o, Makoto -- R01 AG019712/AG/NIA NIH HHS/ -- R01 AG019712-05/AG/NIA NIH HHS/ -- R01 AG025326/AG/NIA NIH HHS/ -- R01 AG025326-03/AG/NIA NIH HHS/ -- R01AG19712/AG/NIA NIH HHS/ -- R01AG25326/AG/NIA NIH HHS/ -- R37 HL063762/HL/NHLBI NIH HHS/ -- U24 DK059637/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1829-33. Epub 2005 Aug 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Texas (UT) Southwestern Medical Center at Dallas, 5323 Harry Hines Bouleuvard, Dallas, TX 75390-9072, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123266" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/*physiology ; Animals ; Blood Glucose/analysis ; Cell Line ; Cell Line, Tumor ; Eating ; Female ; Glucuronidase ; Insulin/blood/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Ligands ; Longevity/genetics/*physiology ; Male ; Membrane Proteins/chemistry/*genetics/pharmacology/*physiology ; Mice ; Mice, Transgenic ; Myoblasts/metabolism ; Oxygen Consumption ; Peptide Fragments/chemistry/pharmacology ; Phosphorylation ; Receptor, IGF Type 1/metabolism ; Receptor, Insulin/metabolism ; Receptors, Cell Surface/metabolism ; Recombinant Proteins/chemistry/isolation & purification/metabolism ; Signal Transduction
    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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    Molecular biology. HNFs--linking the liver and pancreatic islets in diabetes (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kulkarni, Rohit N -- Kahn, C Ronald -- New York, N.Y. -- Science. 2004 Feb 27;303(5662):1311-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Physiology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA. rohit.kulkarni@joslin.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14988544" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; DNA-Binding Proteins/metabolism ; Diabetes Mellitus, Type 2/*genetics/metabolism ; *Gene Expression Regulation ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Hepatocyte Nuclear Factor 3-beta ; Hepatocyte Nuclear Factor 4 ; Hepatocyte Nuclear Factor 6 ; Hepatocytes/*metabolism ; Homeodomain Proteins/genetics/metabolism ; Humans ; Insulin/metabolism ; Insulin Resistance ; Islets of Langerhans/*metabolism ; Mice ; Mutation ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Phosphoproteins/genetics/metabolism ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Signal Transduction ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
    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 blood and lymphatic vascular separation by signaling proteins SLP-76 and Syk (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-11
    Description: Lymphatic vessels develop from specialized endothelial cells in preexisting blood vessels, but the molecular signals that regulate this separation are unknown. Here we identify a failure to separate emerging lymphatic vessels from blood vessels in mice lacking the hematopoietic signaling protein SLP-76 or Syk. Blood-lymphatic connections lead to embryonic hemorrhage and arteriovenous shunting. Expression of slp-76 could not be detected in endothelial cells, and blood-filled lymphatics also arose in wild-type mice reconstituted with SLP-76-deficient bone marrow. These studies reveal a hematopoietic signaling pathway required for separation of the two major vascular networks in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982679/" 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/PMC2982679/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abtahian, Farhad -- Guerriero, Anastasia -- Sebzda, Eric -- Lu, Min-Min -- Zhou, Rong -- Mocsai, Attila -- Myers, Erin E -- Huang, Bin -- Jackson, David G -- Ferrari, Victor A -- Tybulewicz, Victor -- Lowell, Clifford A -- Lepore, John J -- Koretzky, Gary A -- Kahn, Mark L -- R21 EB002473/EB/NIBIB NIH HHS/ -- R21 EB002473-02/EB/NIBIB NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):247-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signal Transduction Program, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522250" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Animals, Newborn ; Antigens, CD34/metabolism ; Blood Vessels/abnormalities/cytology/*embryology/metabolism ; Bone Marrow Cells/cytology/physiology ; Bone Marrow Transplantation ; Dextrans ; Endothelium, Lymphatic/cytology/metabolism ; Endothelium, Vascular/cytology/metabolism ; Enzyme Precursors/genetics/*metabolism ; Fluorescein-5-isothiocyanate/*analogs & derivatives ; Glycoproteins/metabolism ; Hemorrhage ; Homeodomain Proteins/genetics/metabolism ; Intestines/blood supply ; Intracellular Signaling Peptides and Proteins ; Lymphatic System/abnormalities/cytology/*embryology/metabolism ; Mesenteric Arteries/abnormalities ; Mesenteric Veins/abnormalities ; Mice ; Phosphoproteins/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/*metabolism ; *Signal Transduction ; Stem Cells/physiology ; Tumor Suppressor Proteins ; Vascular Endothelial Growth Factor Receptor-3/metabolism ; Veins/cytology/embryology/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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    Radioimmunoassay of the insulin receptor: a new probe of receptor structure and function (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-02-09
    Description: A sensitive and specific radioimmunoassay for the insulin receptor has been developed employing receptor autoantibodies from the serum of a patient with insulin-resistant diabetes. The assay detects insulin binding sites at concentrations as low as 0.1 nanomolar; distinguishes between receptors originating from human placental membranes, human lymphoblastoid cells, and mouse liver membranes; and measures the receptor independently of its binding function. Down-regulation, or loss of binding after exposure to insulin, is associated with loss of immunoreactive receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrison, L C -- Flier, J -- Itin, A -- Kahn, C R -- Roth, J -- New York, N.Y. -- Science. 1979 Feb 9;203(4380):544-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/83675" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Reactions ; Binding Sites ; Binding Sites, Antibody ; Epitopes ; Female ; Humans ; Liver/analysis ; Lymphocytes/analysis ; Mice ; Placenta/analysis ; Pregnancy ; Radioimmunoassay/methods ; Receptor, Insulin/analysis/*immunology ; Solubility
    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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