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  • 1
    Publikationsdatum: 2010-03-13
    Beschreibung: Chromosome fragmentation is a hallmark of apoptosis, conserved in diverse organisms. In mammals, caspases activate apoptotic chromosome fragmentation by cleaving and inactivating an apoptotic nuclease inhibitor. We report that inactivation of the Caenorhabditis elegans dcr-1 gene, which encodes the Dicer ribonuclease important for processing of small RNAs, compromises apoptosis and blocks apoptotic chromosome fragmentation. DCR-1 was cleaved by the CED-3 caspase to generate a C-terminal fragment with deoxyribonuclease activity, which produced 3' hydroxyl DNA breaks on chromosomes and promoted apoptosis. Thus, caspase-mediated activation of apoptotic DNA degradation is conserved. DCR-1 functions in fragmenting chromosomal DNA during apoptosis, in addition to processing of small RNAs, and undergoes a protease-mediated conversion from a ribonuclease to a deoxyribonuclease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4313557/" 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/PMC4313557/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakagawa, Akihisa -- Shi, Yong -- Kage-Nakadai, Eriko -- Mitani, Shohei -- Xue, Ding -- R01 GM059083/GM/NIGMS NIH HHS/ -- R01 GM079097/GM/NIGMS NIH HHS/ -- R01 GM59083/GM/NIGMS NIH HHS/ -- R01 GM79097/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 16;328(5976):327-34. doi: 10.1126/science.1182374. Epub 2010 Mar 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20223951" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Genetically Modified ; *Apoptosis ; Caenorhabditis elegans/cytology/*enzymology/genetics/physiology ; Caenorhabditis elegans Proteins/chemistry/genetics/*metabolism ; Caspases/genetics/*metabolism ; Catalytic Domain ; *DNA Fragmentation ; DNA, Helminth/*metabolism ; Deoxyribonucleases/*metabolism ; In Situ Nick-End Labeling ; RNA Interference ; RNA, Double-Stranded/metabolism ; RNA, Helminth/metabolism ; Recombinant Fusion Proteins/metabolism ; Ribonuclease III/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2008-04-26
    Beschreibung: The asymmetrical distribution of phospholipids on the plasma membrane is critical for maintaining cell integrity and physiology and for regulating intracellular signaling and important cellular events such as clearance of apoptotic cells. How phospholipid asymmetry is established and maintained is not fully understood. We report that the Caenorhabditis elegans P-type adenosine triphosphatase homolog, TAT-1, is critical for maintaining cell surface asymmetry of phosphatidylserine (PS). In animals deficient in tat-1, PS is abnormally exposed on the cell surface, and normally living cells are randomly lost through a mechanism dependent on PSR-1, a PS-recognizing phagocyte receptor, and CED-1, which contributes to recognition and engulfment of apoptotic cells. Thus, tat-1 appears to function in preventing appearance of PS in the outer leaflet of plasma membrane, and ectopic exposure of PS on the cell surface may result in removal of living cells by neighboring phagocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darland-Ransom, Monica -- Wang, Xiaochen -- Sun, Chun-Ling -- Mapes, James -- Gengyo-Ando, Keiko -- Mitani, Shohei -- Xue, Ding -- R01 GM59083/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):528-31. doi: 10.1126/science.1155847.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436785" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Genetically Modified ; Apoptosis ; Caenorhabditis elegans/cytology/genetics/*metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Membrane/*metabolism ; Germ Cells/cytology/metabolism ; Muscle Cells/cytology/metabolism ; Neurons/cytology/metabolism ; Phagocytosis ; Phosphatidylserines/*metabolism ; Phospholipid Transfer Proteins/genetics/*metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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