Withdrawal of IL-7 induces Bax translocation from cytosol to mitochondria through a rise in intracellular pH.
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BH3 domains other than Bim and Bid can directly activate Bax/BakTrophic factor withdrawal: p38 mitogen-activated protein kinase activates NHE1, which induces intracellular alkalinizationGrowth factors can influence cell growth and survival through effects on glucose metabolismCaspase-resistant BAP31 inhibits fas-mediated apoptotic membrane fragmentation and release of cytochrome c from mitochondriaRetinoid-related orphan receptor gamma (RORgamma) is essential for lymphoid organogenesis and controls apoptosis during thymopoiesisChlamydia inhibit host cell apoptosis by degradation of proapoptotic BH3-only proteinsBAX unleashed: the biochemical transformation of an inactive cytosolic monomer into a toxic mitochondrial poreCristae remodeling causes acidification detected by integrated graphene sensor during mitochondrial outer membrane permeabilization14-3-3 Interacts directly with and negatively regulates pro-apoptotic BaxCytochrome c release upon Fas receptor activation depends on translocation of full-length bid and the induction of the mitochondrial permeability transitionBuilding blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosisActivation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injuryApoptosis induction is associated with decreased NHE1 expression in neonatal unilateral ureteric obstructionConsidering protonation as a posttranslational modification regulating protein structure and function.Roles of Na⁺/H⁺ exchanger type 1 and intracellular pH in angiotensin II-induced reactive oxygen species generation and podocyte apoptosis.Interleukin-3 withdrawal induces an early increase in mitochondrial membrane potential unrelated to the Bcl-2 family. Roles of intracellular pH, ADP transport, and F(0)F(1)-ATPase.Bax kappa, a novel Bax splice variant from ischemic rat brain lacking an ART domain, promotes neuronal cell death.The N-terminus and alpha-5, alpha-6 helices of the pro-apoptotic protein Bax, modulate functional interactions with the anti-apoptotic protein Bcl-xL.Bax contains two functional mitochondrial targeting sequences and translocates to mitochondria in a conformational change- and homo-oligomerization-driven process.Interleukin-7 regulates Bim proapoptotic activity in peripheral T-cell survival.Overcoming chemotherapy drug resistance by targeting inhibitors of apoptosis proteins (IAPs)Interleukin-7 mediates glucose utilization in lymphocytes through transcriptional regulation of the hexokinase II geneDoes closure of acid-sensing ion channels reduce ischemia/reperfusion injury in the rat brain?Myc potentiates apoptosis by stimulating Bax activity at the mitochondria.Lipopolysaccharide protects primary B lymphocytes from apoptosis by preventing mitochondrial dysfunction and bax translocation to mitochondriaJunD/AP-1-mediated gene expression promotes lymphocyte growth dependent on interleukin-7 signal transduction.The multidomain proapoptotic molecules Bax and Bak are directly activated by heat.Study of PTPC composition during apoptosis for identification of viral protein target.Life and death in the thymus--cell death signaling during T cell development.Potential therapeutic role of Tridham in human hepatocellular carcinoma cell line through induction of p53 independent apoptosisROS production is essential for the apoptotic function of E2F1 in pheochromocytoma and neuroblastoma cell lines.Homeostatic control of lymphocyte survival: potential origins and implications.Structure and function of the NHE1 isoform of the Na+/H+ exchanger.BAX supports the mitochondrial network, promoting bioenergetics in nonapoptotic cellsDistinct regions of the interleukin-7 receptor regulate different Bcl2 family members.Death and Baxes: mechanisms of lymphotrophic cytokines.Mitochondria in apoptosis: Bcl-2 family members and mitochondrial dynamics.Peg3/Pw1 promotes p53-mediated apoptosis by inducing Bax translocation from cytosol to mitochondria.The c-MYC oncoprotein as a treatment target in cancer and other disorders of cell growth.B-cell homeostasis: digital survival or analog growth?
P2860
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P2860
Withdrawal of IL-7 induces Bax translocation from cytosol to mitochondria through a rise in intracellular pH.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
Withdrawal of IL-7 induces Bax ...... gh a rise in intracellular pH.
@en
type
label
Withdrawal of IL-7 induces Bax ...... gh a rise in intracellular pH.
@en
prefLabel
Withdrawal of IL-7 induces Bax ...... gh a rise in intracellular pH.
@en
P2093
P2860
P356
P1476
Withdrawal of IL-7 induces Bax ...... gh a rise in intracellular pH.
@en
P2093
P2860
P304
14476-14481
P356
10.1073/PNAS.96.25.14476
P407
P577
1999-12-01T00:00:00Z