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  • 1
    Publikationsdatum: 1999-04-09
    Beschreibung: The Ca2+-activated protein phosphatase calcineurin induces apoptosis, but the mechanism is unknown. Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. The Ca2+-induced dephosphorylation of BAD correlated with its dissociation from 14-3-3 in the cytosol and translocation to mitochondria where Bcl-xL resides. In hippocampal neurons, L-glutamate, an inducer of Ca2+ influx and calcineurin activation, triggered mitochondrial targeting of BAD and apoptosis, which were both suppressible by coexpression of a dominant-inhibitory mutant of calcineurin or pharmacological inhibitors of this phosphatase. Thus, a Ca2+-inducible mechanism for apoptosis induction operates by regulating BAD phosphorylation and localization in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H G -- Pathan, N -- Ethell, I M -- Krajewski, S -- Yamaguchi, Y -- Shibasaki, F -- McKeon, F -- Bobo, T -- Franke, T F -- Reed, J C -- AG-1593/AG/NIA NIH HHS/ -- CA-69381/CA/NCI NIH HHS/ -- HD25938/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):339-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195903" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 14-3-3 Proteins ; Animals ; *Apoptosis ; Calcineurin/genetics/*metabolism ; Calcineurin Inhibitors ; Calcium/*metabolism/pharmacology ; Carrier Proteins/chemistry/*metabolism ; Cell Line ; Cells, Cultured ; Dimerization ; Enzyme Inhibitors/pharmacology ; Glutamic Acid/pharmacology ; Hippocampus/cytology ; Humans ; Mitochondria/metabolism ; Neurons/cytology/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Transfection ; *Tyrosine 3-Monooxygenase ; bcl-Associated Death Protein ; bcl-X Protein
    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: 2015-06-05
    Beschreibung: Stem cells of the gastrointestinal tract, pancreas, liver and other columnar epithelia collectively resist cloning in their elemental states. Here we demonstrate the cloning and propagation of highly clonogenic, 'ground state' stem cells of the human intestine and colon. We show that derived stem-cell pedigrees sustain limited copy number and sequence variation despite extensive serial passaging and display exquisitely precise, cell-autonomous commitment to epithelial differentiation consistent with their origins along the intestinal tract. This developmentally patterned and epigenetically maintained commitment of stem cells is likely to enforce the functional specificity of the adult intestinal tract. Using clonally derived colonic epithelia, we show that toxins A or B of the enteric pathogen Clostridium difficile recapitulate the salient features of pseudomembranous colitis. The stability of the epigenetic commitment programs of these stem cells, coupled with their unlimited replicative expansion and maintained clonogenicity, suggests certain advantages for their use in disease modelling and regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xia -- Yamamoto, Yusuke -- Wilson, Lane H -- Zhang, Ting -- Howitt, Brooke E -- Farrow, Melissa A -- Kern, Florian -- Ning, Gang -- Hong, Yue -- Khor, Chiea Chuen -- Chevalier, Benoit -- Bertrand, Denis -- Wu, Lingyan -- Nagarajan, Niranjan -- Sylvester, Francisco A -- Hyams, Jeffrey S -- Devers, Thomas -- Bronson, Roderick -- Lacy, D Borden -- Ho, Khek Yu -- Crum, Christopher P -- McKeon, Frank -- Xian, Wa -- AI09575504/AI/NIAID NIH HHS/ -- R01 AI095755/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Jun 11;522(7555):173-8. doi: 10.1038/nature14484. Epub 2015 Jun 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Jackson Laboratory for Genomic Medicine, Farmington, Connecticut 06032, USA. ; 1] The Jackson Laboratory for Genomic Medicine, Farmington, Connecticut 06032, USA [2] Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut 06032, USA. ; Genome Institute of Singapore, Agency for Science, Technology and Research, 138672 Singapore. ; Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02118, USA. ; Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. ; 1] Genome Institute of Singapore, Agency for Science, Technology and Research, 138672 Singapore [2] Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, 119228 Singapore. ; Department of Pediatrics, Division of Gastroenterology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA. ; Division of Digestive Diseases, Hepatology, and Nutrition, Connecticut Children's Medical Center, Hartford, Connecticut 06106, USA. ; Department of Medicine, University of Connecticut Health Center, Farmington, Connecticut 06032, USA. ; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Medicine, National University of Singapore, 119228 Singapore. ; 1] The Jackson Laboratory for Genomic Medicine, Farmington, Connecticut 06032, USA [2] Genome Institute of Singapore, Agency for Science, Technology and Research, 138672 Singapore [3] Department of Medicine, National University of Singapore, 119228 Singapore [4] Multiclonal Therapeutics, Inc., Farmington, Connecticut 06032, USA. ; 1] The Jackson Laboratory for Genomic Medicine, Farmington, Connecticut 06032, USA [2] Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut 06032, USA [3] Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02118, USA [4] Department of Medicine, National University of Singapore, 119228 Singapore [5] Multiclonal Therapeutics, Inc., Farmington, Connecticut 06032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26040716" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Bacterial Toxins/pharmacology ; Cell Differentiation/drug effects ; Cell Lineage ; Cells, Cultured ; Clone Cells/cytology/metabolism ; Clostridium difficile/physiology ; Colon/cytology/drug effects ; Enterocolitis, Pseudomembranous/microbiology/pathology ; Epigenesis, Genetic/genetics ; Epithelium/drug effects/metabolism ; Fetus/cytology ; Genomic Instability/genetics ; Humans ; Intestine, Small/cytology ; Intestines/*cytology/drug effects ; Organoids/cytology/growth & development ; Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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