Predominant requirement of Bax for apoptosis in HCT116 cells is determined by Mcl-1's inhibitory effect on Bak.
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Mitochondria, cholesterol and cancer cell metabolismImproving anticancer drug development begins with cell culture: misinformation perpetrated by the misuse of cytotoxicity assaysBOK Is a Non-canonical BCL-2 Family Effector of Apoptosis Regulated by ER-Associated DegradationInhibition of MARCH5 ubiquitin ligase abrogates MCL1-dependent resistance to BH3 mimetics via NOXACaspase-8 activation by TRAIL monotherapy predicts responses to IAPi and TRAIL combination treatment in breast cancer cell linesUSP22 Induces Cisplatin Resistance in Lung Adenocarcinoma by Regulating γH2AX-Mediated DNA Damage Repair and Ku70/Bax-Mediated ApoptosisThe virus-induced protein APOBEC3G inhibits anoikis by activation of Akt kinase in pancreatic cancer cells.ERBB3 knockdown induces cell cycle arrest and activation of Bak and Bax-dependent apoptosis in colon cancer cells.Disruption of the VDAC2-Bak interaction by Bcl-x(S) mediates efficient induction of apoptosis in melanoma cells.Bcl-2 stabilization by paxillin confers 5-fluorouracil resistance in colorectal cancer.Reversal of Mutant KRAS-Mediated Apoptosis Resistance by Concurrent Noxa/Bik Induction and Bcl-2/Bcl-xL Antagonism in Colon Cancer Cells.The combination of thioxodihydroquinazolinones and platinum drugs reverses platinum resistance in tumor cells by inducing mitochondrial apoptosis independent of Bax and BakProapoptotic activities of protein disulfide isomerase (PDI) and PDIA3 protein, a role of the Bcl-2 protein Bak.Bax/Bak-independent mitochondrial depolarization and reactive oxygen species induction by sorafenib overcome resistance to apoptosis in renal cell carcinoma.Conversion of cell-survival activity of Akt into apoptotic death of cancer cells by two mutations on the BIM BH3 domain.miR-150 inhibits terminal erythroid proliferation and differentiation.N-(3-oxo-acyl) homoserine lactone inhibits tumor growth independent of Bcl-2 proteins.Cardiolipin or MTCH2 can serve as tBID receptors during apoptosisBAX-BAK1-independent LC3B lipidation by BH3 mimetics is unrelated to BH3 mimetic activity and has only minimal effects on autophagic flux.Bax/Bak activation in the absence of Bid, Bim, Puma, and p53.Loss of the proteins Bak and Bax prevents apoptosis mediated by histone deacetylase inhibitors.Blocking downstream signaling pathways in the context of HDAC inhibition promotes apoptosis preferentially in cells harboring mutant Ras.Activation of the proapoptotic Bcl-2 protein Bax by a small molecule induces tumor cell apoptosis.That which does not kill me makes me stronger; combining ERK1/2 pathway inhibitors and BH3 mimetics to kill tumour cells and prevent acquired resistance.Mitochondrial apoptosis: killing cancer using the enemy within.Chemoresistance is associated with overexpression of HAX-1, inhibition of which resensitizes drug-resistant breast cancer cells to chemotherapy.Transcriptional regulation of Mcl-1 plays an important role of cellular protective effector of vincristine-triggered autophagy in oral cancer cells.The small-molecule compound BM-1197 inhibits the antiapoptotic regulators Bcl-2/Bcl-xL and triggers apoptotic cell death in human colorectal cancer cells.Novel combination of mitochondrial division inhibitor 1 (mdivi-1) and platinum agents produces synergistic pro-apoptotic effect in drug resistant tumor cells.TAT-RasGAP317-326-mediated tumor cell death sensitization can occur independently of Bax and Bak.Targeting Bax interaction sites reveals that only homo-oligomerization sites are essential for its activation.The BH3 mimetic ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to promote BIM-dependent tumour cell death and inhibit acquired resistance.Chemotherapy-triggered cathepsin B release in myeloid-derived suppressor cells activates the Nlrp3 inflammasome and promotes tumor growth.Bak and Mcl-1 are essential for Temozolomide induced cell death in human glioma.Immune effects of 5-fluorouracil: Ambivalence matters.Live-cell imaging to measure BAX recruitment kinetics to mitochondria during apoptosis.Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity.The C-terminal helix of Bcl-x(L) mediates Bax retrotranslocation from the mitochondria.Parkin promotes proteasomal degradation of misregulated BAX.Mcl-1 and Bcl-xL sequestration of Bak confers differential resistance to BH3-only proteins.
P2860
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P2860
Predominant requirement of Bax for apoptosis in HCT116 cells is determined by Mcl-1's inhibitory effect on Bak.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Predominant requirement of Bax ...... -1's inhibitory effect on Bak.
@ast
Predominant requirement of Bax ...... -1's inhibitory effect on Bak.
@en
type
label
Predominant requirement of Bax ...... -1's inhibitory effect on Bak.
@ast
Predominant requirement of Bax ...... -1's inhibitory effect on Bak.
@en
prefLabel
Predominant requirement of Bax ...... -1's inhibitory effect on Bak.
@ast
Predominant requirement of Bax ...... -1's inhibitory effect on Bak.
@en
P2860
P356
P1433
P1476
Predominant requirement of Bax ...... l-1's inhibitory effect on Bak
@en
P2093
P2860
P2888
P304
P356
10.1038/ONC.2011.497
P407
P50
P577
2011-11-07T00:00:00Z