Pro-caspase-8 is predominantly localized in mitochondria and released into cytoplasm upon apoptotic stimulation.
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FLASH links the CD95 signaling pathway to the cell nucleus and nuclear bodiesInactivation of caspase-8 on mitochondria of Bcl-xL-expressing MCF7-Fas cells: role for the bifunctional apoptosis regulator proteinp38 activation is required upstream of potassium current enhancement and caspase cleavage in thiol oxidant-induced neuronal apoptosisActive caspase-8 translocates into the nucleus of apoptotic cells to inactivate poly(ADP-ribose) polymerase-2PICK1, an anchoring protein that specifically targets protein kinase Calpha to mitochondria selectively upon serum stimulation in NIH 3T3 cellsIan4 is required for mitochondrial integrity and T cell survivalAssociation of active caspase 8 with the mitochondrial membrane during apoptosis: potential roles in cleaving BAP31 and caspase 3 and mediating mitochondrion-endoplasmic reticulum cross talk in etoposide-induced cell deathAutophagy is involved in cytotoxic effects of crotoxin in human breast cancer cell line MCF-7 cells.Alcohol dehydrogenase accentuates ethanol-induced myocardial dysfunction and mitochondrial damage in mice: role of mitochondrial death pathway.Voltage dependent anion channel-1 regulates death receptor mediated apoptosis by enabling cleavage of caspase-8.Mitochondrial accumulation of polyubiquitinated proteins and differential regulation of apoptosis by polyubiquitination sites Lys-48 and -63Deoxycholic acid (DCA) causes ligand-independent activation of epidermal growth factor receptor (EGFR) and FAS receptor in primary hepatocytes: inhibition of EGFR/mitogen-activated protein kinase-signaling module enhances DCA-induced apoptosis.Hsp72 and stress kinase c-jun N-terminal kinase regulate the bid-dependent pathway in tumor necrosis factor-induced apoptosis.Reovirus-induced apoptosis requires mitochondrial release of Smac/DIABLO and involves reduction of cellular inhibitor of apoptosis protein levels.Acute focal brain damage alters mitochondrial dynamics and autophagy in axotomized neurons.The role of mitochondrial factors in apoptosis: a Russian roulette with more than one bullet.The HIV-1-specific protein Casp8p41 induces death of infected cells through Bax/Bak.Toxic proteins released from mitochondria in cell death.DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosisAutophagosomal membrane serves as platform for intracellular death-inducing signaling complex (iDISC)-mediated caspase-8 activation and apoptosis.FOXO3a regulates oxygen-responsive expression of tumor necrosis factor receptor 2 in human dermal microvascular endothelial cells.Caspases indirectly regulate cleavage of the mitochondrial fusion GTPase OPA1 in neurons undergoing apoptosis.Apoptosis induction by interleukin-2-activated cytotoxic lymphocytes in a squamous cell carcinoma cell line and Daudi cells - involvement of reactive oxygen species-dependent cytochrome c and reactive oxygen species-independent apoptosis-inducing faMitochondrially localized active caspase-9 and caspase-3 result mostly from translocation from the cytosol and partly from caspase-mediated activation in the organelle. Lack of evidence for Apaf-1-mediated procaspase-9 activation in the mitochondriaBasic fibroblast growth factor (bFGF)-induced cell death is mediated through a caspase-dependent and p53-independent cell death receptor pathway.Dandelion root extract affects colorectal cancer proliferation and survival through the activation of multiple death signalling pathways.Subcellular localization of CrmA: identification of a novel leucine-rich nuclear export signal conserved in anti-apoptotic serpins.BID is cleaved by caspase-8 within a native complex on the mitochondrial membrane.Pre-processed caspase-9 contained in mitochondria participates in apoptosis.Caspases are not localized in mitochondria during life or death.In vivo calpain/caspase cross-talk during 3-nitropropionic acid-induced striatal degeneration: implication of a calpain-mediated cleavage of active caspase-3.Activation of caspases-9, -3 and -8 in human platelets triggered by BH3-only mimetic ABT-737 and calcium ionophore A23187: caspase-8 is activated via bypass of the death receptors.Bistability analyses of a caspase activation model for receptor-induced apoptosis.Therapeutic effect of SN50, an inhibitor of nuclear factor-κB, in treatment of TBI in mice.Temporal and spatial profile of caspase 8 expression and proteolysis after experimental traumatic brain injury
P2860
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P2860
Pro-caspase-8 is predominantly localized in mitochondria and released into cytoplasm upon apoptotic stimulation.
description
2000 nî lūn-bûn
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2000年の論文
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2000年学术文章
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2000年学术文章
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2000年学术文章
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name
Pro-caspase-8 is predominantly ...... sm upon apoptotic stimulation.
@en
Pro-caspase-8 is predominantly ...... sm upon apoptotic stimulation.
@nl
type
label
Pro-caspase-8 is predominantly ...... sm upon apoptotic stimulation.
@en
Pro-caspase-8 is predominantly ...... sm upon apoptotic stimulation.
@nl
prefLabel
Pro-caspase-8 is predominantly ...... sm upon apoptotic stimulation.
@en
Pro-caspase-8 is predominantly ...... sm upon apoptotic stimulation.
@nl
P2093
P2860
P356
P1476
Pro-caspase-8 is predominantly ...... sm upon apoptotic stimulation.
@en
P2093
DiFiglia M
P2860
P304
P356
10.1074/JBC.M007028200
P407
P577
2000-12-01T00:00:00Z