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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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| Hoofdauteurs: | , , , , , , , , , , |
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| Formaat: | Artigo |
| Taal: | Inglês |
| Gepubliceerd in: |
2010
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| Onderwerpen: | |
| Online toegang: | 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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