17AAG and MEK1/2 inhibitors kill GI tumor cells via Ca(2+)-dependent suppression of GRP78/BiP and induction of ceramide and ROS

The present studies determined in greater detail the molecular mechanisms upstream of the CD95 death receptor by which geldanamycin HSP90 inhibitors and MEK1/2 inhibitors interact to kill carcinoma cells. MEK1/2 inhibition enhanced 17AAG toxicity that was suppressed in cells deleted for mutant activ...

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מידע ביבליוגרפי
Main Authors: Walker, Teneille, Mitchell, Clint, Park, Margaret A., Yacoub, Adly, Rahmani, Mohamed, Häussinger, Dieter, Reinehr, Roland, Voelkel-Johnson, Christina, Fisher, Paul B., Grant, Steven, Dent, Paul
פורמט: Artigo
שפה:Inglês
יצא לאור: 2010
נושאים:
Article
גישה מקוונת:https://ncbi.nlm.nih.gov/pmc/articles/PMC2868106/
https://ncbi.nlm.nih.gov/pubmed/20442308
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1158/1535-7163.MCT-09-1131
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