نتایج جستجو برای: caspase programmed cell death

تعداد نتایج: 1883179  

Journal: :Archives of Surgery 1998

2009
Gamze Tanriover Angeliki Louvi

Background and Purpose—Mutations in the Programmed Cell Death 10 (PDCD10) gene cause autosomal dominant familial cerebral cavernous malformations (CCM3). To date, little is known about the function of this gene and its role in disease pathogenesis. Methods—We examined the effects of overexpression of wild-type and 2 human disease-causing variants of PDCD10 on cell death using 3 different method...

Journal: :Journal of immunology 2014
Edward S Mocarski William J Kaiser Devon Livingston-Rosanoff Jason W Upton Lisa P Daley-Bauer

Programmed necrosis mediated by receptor interacting protein kinase (RIP)3 (also called RIPK3) has emerged as an alternate death pathway triggered by TNF family death receptors, pathogen sensors, IFNRs, Ag-specific TCR activation, and genotoxic stress. Necrosis leads to cell leakage and acts as a "trap door," eliminating cells that cannot die by apoptosis because of the elaboration of pathogen-...

Journal: :مجله علوم اعصاب شفای خاتم 0
ali jahanbazi jahan-abad shefa neuroscience research center, khatam alanbia hospital, tehran, iran leila alizadeh shefa neuroscience research center, khatam alanbia hospital, tehran, iran sajad sahab negah a. shefa neuroscience research center, khatam alanbia hospital, tehran, iran b. department of neuroscience, mashhad university of medical sciences, mashhad, iran parastoo barati shefa neuroscience research center, khatam alanbia hospital, tehran, iran maryam khaleghi ghadiri department of neurosurgery, wilhelms-universität münster, münster, germany sven g meuth department of neurology, westfälische wilhelms-universität münster, münster, germany

introduction: repetitive cortical spreading depression (csd) can lead to cell death in immature brain tissue. caspases are involved in neuronal cell death in several csd-related neurological disorders. yet, whether repetitive csd itself can induce caspase activation in adult or juvenile tissue remains unknown. inducing repetitive csd in somatosensory cortices of juvenile and adult rats in vivo,...

Journal: :Stroke 2009
Leiling Chen Gamze Tanriover Hiroko Yano Robert Friedlander Angeliki Louvi Murat Gunel

BACKGROUND AND PURPOSE Mutations in the Programmed Cell Death 10 (PDCD10) gene cause autosomal dominant familial cerebral cavernous malformations (CCM3). To date, little is known about the function of this gene and its role in disease pathogenesis. METHODS We examined the effects of overexpression of wild-type and 2 human disease-causing variants of PDCD10 on cell death using 3 different meth...

Journal: :Genetics 2007
Peter W Reddien Erik C Andersen Michael C Huang H Robert Horvitz

The genes egl-1, ced-9, ced-4, and ced-3 play major roles in programmed cell death in Caenorhabditis elegans. To identify genes that have more subtle activities, we sought mutations that confer strong cell-death defects in a genetically sensitized mutant background. Specifically, we screened for mutations that enhance the cell-death defects caused by a partial loss-of-function allele of the ced...

Journal: :Plant physiology 2002
Ernst J Woltering Arie van der Bent Frank A Hoeberichts

Programmed cell death (PCD) is a functional concept that refers to cell death that is part of the normal life of a multicellular organism; it involves controlled disassembly of the cell. In animal systems PCD is synonymous with apoptosis, a cell death process characterized by a distinct set of morphological and biochemical features, mediated by a class of specific Cys proteases called cysteinyl...

Journal: :The EMBO journal 2010
Cédric Artus Hanan Boujrad Aïda Bouharrour Marie-Noëlle Brunelle Sylviane Hoos Victor J Yuste Pascal Lenormand Jean-Claude Rousselle Abdelkader Namane Patrick England Hans K Lorenzo Santos A Susin

Programmed necrosis induced by DNA alkylating agents, such as MNNG, is a caspase-independent mode of cell death mediated by apoptosis-inducing factor (AIF). After poly(ADP-ribose) polymerase 1, calpain, and Bax activation, AIF moves from the mitochondria to the nucleus where it induces chromatinolysis and cell death. The mechanisms underlying the nuclear action of AIF are, however, largely unkn...

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