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  • 1
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    ABIN-1 is a ubiquitin sensor that restricts cell death and sustains embryonic development (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-12-09
    Description: Proteins that directly regulate tumour necrosis factor receptor (TNFR) signalling have critical roles in regulating cellular activation and survival. ABIN-1 (A20 binding and inhibitor of NF-kappaB) is a novel protein that is thought to inhibit NF-kappaB signalling. Here we show that mice deficient for ABIN-1 die during embryogenesis with fetal liver apoptosis, anaemia and hypoplasia. ABIN-1 deficient cells are hypersensitive to tumour necrosis factor (TNF)-induced programmed cell death, and TNF deficiency rescues ABIN-1 deficient embryos. ABIN-1 inhibits caspase 8 recruitment to FADD (Fas-associated death domain-containing protein) in TNF-induced signalling complexes, preventing caspase 8 cleavage and programmed cell death. Moreover, ABIN-1 directly binds polyubiquitin chains and this ubiquitin sensing activity is required for ABIN-1's anti-apoptotic activity. These studies provide insights into how ubiquitination and ubiquitin sensing proteins regulate cellular and organismal survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2642523/" 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/PMC2642523/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oshima, Shigeru -- Turer, Emre E -- Callahan, Joseph A -- Chai, Sophia -- Advincula, Rommel -- Barrera, Julio -- Shifrin, Nataliya -- Lee, Bettina -- Benedict Yen, T S -- Woo, Tammy -- Malynn, Barbara A -- Ma, Averil -- R01 DK071939/DK/NIDDK NIH HHS/ -- R01 DK071939-01/DK/NIDDK NIH HHS/ -- R01 DK071939-02/DK/NIDDK NIH HHS/ -- R01 DK071939-03/DK/NIDDK NIH HHS/ -- R01 DK071939-04/DK/NIDDK NIH HHS/ -- England -- Nature. 2009 Feb 12;457(7231):906-9. doi: 10.1038/nature07575. Epub 2008 Dec 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California at San Francisco, 513 Parnassus Avenue, S-1057, San Francisco, California 94143-0451, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19060883" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Apoptosis/*physiology ; Cell Line ; DNA-Binding Proteins/chemistry/*metabolism ; Embryonic Development/genetics/*physiology ; Gene Expression Regulation, Developmental ; Humans ; Intracellular Signaling Peptides and Proteins/chemistry/metabolism ; Jurkat Cells ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Sequence Alignment ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitin/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Menin controls growth of pancreatic beta-cells in pregnant mice and promotes gestational diabetes mellitus (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-03
    Description: During pregnancy, maternal pancreatic islets grow to match dynamic physiological demands, but the mechanisms regulating adaptive islet growth in this setting are poorly understood. Here we show that menin, a protein previously characterized as an endocrine tumor suppressor and transcriptional regulator, controls islet growth in pregnant mice. Pregnancy stimulated proliferation of maternal pancreatic islet beta-cells that was accompanied by reduced islet levels of menin and its targets. Transgenic expression of menin in maternal beta-cells prevented islet expansion and led to hyperglycemia and impaired glucose tolerance, hallmark features of gestational diabetes. Prolactin, a hormonal regulator of pregnancy, repressed islet menin levels and stimulated beta-cell proliferation. These results expand our understanding of mechanisms underlying diabetes pathogenesis and reveal potential targets for therapy in diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karnik, Satyajit K -- Chen, Hainan -- McLean, Graeme W -- Heit, Jeremy J -- Gu, Xueying -- Zhang, Andrew Y -- Fontaine, Magali -- Yen, Michael H -- Kim, Seung K -- T32DK007217-32/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975067" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Diabetes, Gestational/*etiology/metabolism ; Female ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Obesity/metabolism ; Pregnancy ; Prolactin/metabolism ; Proto-Oncogene Proteins/*physiology ; Tumor Cells, Cultured
    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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