Bcl-xL overexpression attenuates glutathione depletion in FL5.12 cells following interleukin-3 withdrawal
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Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channelA novel, high conductance channel of mitochondria linked to apoptosis in mammalian cells and Bax expression in yeastFanconi anemia group C protein prevents apoptosis in hematopoietic cells through redox regulation of GSTP1Tubulin-perturbing naphthoquinone spiroketals.Oxidative stress by targeted agents promotes cytotoxicity in hematologic malignancies.Signalling apoptosis: a radical approach.Changes of sFas and sFasL, oxidative stress markers in serum and follicular fluid of patients undergoing IVF.Inhibition of mitochondrial respiration and rapid depletion of mitochondrial glutathione by β-phenethyl isothiocyanate: mechanisms for anti-leukemia activity.Apoptosis as a novel target for cancer chemoprevention.Redox mechanisms of cytoprotection by Bcl-2.Key Roles of Glutamine Pathways in Reprogramming the Cancer Metabolism.Glutathione efflux and cell death.T cells expanded in presence of IL-15 exhibit increased antioxidant capacity and innate effector molecules.Interaction between glutathione and apoptosis in systemic lupus erythematosus.Functional significance of the GAG trinucleotide-repeat polymorphism in the gene for the catalytic subunit of gamma-glutamylcysteine ligase.Plasma membrane glutathione transporters and their roles in cell physiology and pathophysiologyGlutathione dysregulation and the etiology and progression of human diseases.Bcl-x L blocks mitochondrial multiple conductance channel activation and inhibits 6-OHDA-induced death in SH-SY5Y cells.GSH depletion enhances adenoviral bax-induced apoptosis in lung cancer cells.Bax gene expression alters Ca(2+) signal transduction without affecting apoptosis in an epithelial cell line.Protection against hydrogen peroxide cytotoxicity in rat-1 fibroblasts provided by the oncoprotein Bcl-2: maintenance of calcium homoeostasis is secondary to the effect of Bcl-2 on cellular glutathione.A relationship between 5-lipoxygenase-activating protein and bcl-xL expression in murine pro-B lymphocytic FL5.12 cells.Elevated skeletal muscle apoptotic signaling following glutathione depletion.BCL-2 is involved in preventing oxidant-induced cell death and in decreasing oxygen radical production.Decreased glutathione levels potentiate the apoptotic efficacy of selenium: possible involvement of p38 and JNK MAPKs--in vitro studies.Inducible nitric oxide synthase up-regulation and mitochondrial glutathione depletion mediate cyanide-induced necrosis in mesencephalic cells.Glutathione is a factor of resistance of Jurkat leukemia cells to nitric oxide-mediated apoptosis.
P2860
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P2860
Bcl-xL overexpression attenuates glutathione depletion in FL5.12 cells following interleukin-3 withdrawal
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-xL overexpression attenuat ...... owing interleukin-3 withdrawal
@en
type
label
Bcl-xL overexpression attenuat ...... owing interleukin-3 withdrawal
@en
prefLabel
Bcl-xL overexpression attenuat ...... owing interleukin-3 withdrawal
@en
P2093
P2860
P356
P1433
P1476
Bcl-xL overexpression attenuat ...... owing interleukin-3 withdrawal
@en
P2093
J P Kehrer
P Simonian
P2860
P304
P356
10.1042/BJ3250315
P407
P478
325 ( Pt 2)
P577
1997-07-01T00:00:00Z