Bcl-x(L) can inhibit apoptosis in cells that have undergone Fas-induced protease activation.
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Proteins associated with the exon junction complex also control the alternative splicing of apoptotic regulatorsThe c-IAP-1 and c-IAP-2 proteins are direct inhibitors of specific caspasesNF-kappaB induces expression of the Bcl-2 homologue A1/Bfl-1 to preferentially suppress chemotherapy-induced apoptosisUpstream regulatory role for XIAP in receptor-mediated apoptosisCaspases are activated in a branched protease cascade and control distinct downstream processes in Fas-induced apoptosisMitochondrial release of caspase-2 and -9 during the apoptotic processThe Role of Alternative Splicing in the Control of Immune Homeostasis and Cellular DifferentiationCaspase-mediated cleavage of DNA topoisomerase I at unconventional sites during apoptosisTwo CD95 (APO-1/Fas) signaling pathwaysResistance to induced apoptosis in the human neuroblastoma cell line SK-N-SH in relation to neuronal differentiation. Role of Bcl-2 protein family.Glucose uptake and glycolysis reduce hypoxia-induced apoptosis in cultured neonatal rat cardiac myocytes.Relevance of Bcl-x expression in different types of endometrial tissues.Distinct biology of Kaposi's sarcoma-associated herpesvirus from primary lesions and body cavity lymphomas.Commitment and effector phases of the physiological cell death pathway elucidated with respect to Bcl-2 caspase, and cyclin-dependent kinase activities.Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization.Mitochondria play no roles in Mn(II)-induced apoptosis in HeLa cells.The Rel/NF-kappaB family directly activates expression of the apoptosis inhibitor Bcl-x(L).Enhanced signaling through the IL-2 receptor in CD8+ T cells regulated by antigen recognition results in preferential proliferation and expansion of responding CD8+ T cells rather than promotion of cell deathAnalysis of human immunodeficiency virus type 1 Gag dimerization-induced assemblyAutoimmune lymphoproliferative syndrome type III: an indefinite disorder.Autoimmune lymphoproliferative syndrome type III, an indefinite disorder.The effect of drugs and toxins on the process of apoptosis.Role of Acinus in regulating retinoic acid-responsive gene pre-mRNA splicing.Role of factors downstream of caspases in nuclear disassembly during apoptotic execution.CD34 cells from patients with trisomy 8 myelodysplastic syndrome (MDS) express early apoptotic markers but avoid programmed cell death by up-regulation of antiapoptotic proteins.The Proto-oncogene PKCι regulates the alternative splicing of Bcl-x pre-mRNA.Increased expression but not sensitivity to Fas/CD95 in glioblastoma cells depleted of mitochondrial DNA.Transition from caspase-dependent to caspase-independent mechanisms at the onset of apoptotic execution.E1B 19K inhibits Fas-mediated apoptosis through FADD-dependent sequestration of FLICE.E4orf4, a novel adenovirus death factor that induces p53-independent apoptosis by a pathway that is not inhibited by zVAD-fmkRequirement for transforming growth factor beta1 in controlling T cell apoptosisActivation of CPP32-like proteases is not sufficient to trigger apoptosis: inhibition of apoptosis by agents that suppress activation of AP24, but not CPP32-like activity.The permeability transition pore complex: a target for apoptosis regulation by caspases and bcl-2-related proteins.Receptor-mediated uptake of an extracellular Bcl-x(L) fusion protein inhibits apoptosis.Anti-apoptotic Activity of Ginsenoside Rb1 in Hydrogen Peroxide-treated Chondrocytes: Stabilization of Mitochondria and the Inhibition of Caspase-3.Direct T cell activation via CD40 ligand generates high avidity CD8+ T cells capable of breaking immunological tolerance for the control of tumors.Role of Bcl-2 family members in caspase-independent apoptosis during Chlamydia infection.Inhibition of apoptosis in chlamydia-infected cells: blockade of mitochondrial cytochrome c release and caspase activation.Antiapoptotic activity of the herpesvirus saimiri-encoded Bcl-2 homolog: stabilization of mitochondria and inhibition of caspase-3-like activity.Antiapoptotic proteins Bcl-2 and Bcl-XL inhibit Clostridium difficile toxin A-induced cell death in human epithelial cells.
P2860
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P2860
Bcl-x(L) can inhibit apoptosis in cells that have undergone Fas-induced protease activation.
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年論文
@yue
1997年論文
@zh-hant
1997年論文
@zh-hk
1997年論文
@zh-mo
1997年論文
@zh-tw
1997年论文
@wuu
1997年论文
@zh
1997年论文
@zh-cn
name
Bcl-x(L) can inhibit apoptosis ...... s-induced protease activation.
@ast
Bcl-x(L) can inhibit apoptosis ...... s-induced protease activation.
@en
type
label
Bcl-x(L) can inhibit apoptosis ...... s-induced protease activation.
@ast
Bcl-x(L) can inhibit apoptosis ...... s-induced protease activation.
@en
prefLabel
Bcl-x(L) can inhibit apoptosis ...... s-induced protease activation.
@ast
Bcl-x(L) can inhibit apoptosis ...... s-induced protease activation.
@en
P2860
P356
P1476
Bcl-x(L) can inhibit apoptosis ...... s-induced protease activation.
@en
P2093
P2860
P304
P356
10.1073/PNAS.94.8.3759
P407
P577
1997-04-01T00:00:00Z