Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT-mTORC1 activation. [electronic resource]
Producer: 20171002Description: 1055-1062 p. digitalISSN:- 1546-170X
- Azepines -- pharmacology
- Blotting, Western
- Cell Cycle Proteins
- Cell Line, Tumor
- Cell Proliferation -- drug effects
- Cell Survival
- Drug Resistance, Neoplasm
- Gene Expression Profiling
- Humans
- Immunoprecipitation
- Male
- Mechanistic Target of Rapamycin Complex 1
- Molecular Targeted Therapy
- Multiprotein Complexes -- drug effects
- Mutation
- Nuclear Proteins -- antagonists & inhibitors
- Prostatic Neoplasms -- drug therapy
- Proteasome Endopeptidase Complex -- drug effects
- Protein Serine-Threonine Kinases -- antagonists & inhibitors
- Proto-Oncogene Proteins c-akt -- drug effects
- RNA-Binding Proteins -- antagonists & inhibitors
- Repressor Proteins -- genetics
- Reverse Transcriptase Polymerase Chain Reaction
- TOR Serine-Threonine Kinases -- drug effects
- Transcription Factors -- antagonists & inhibitors
- Triazoles -- pharmacology
- rac1 GTP-Binding Protein -- genetics
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Publication Type: Journal Article
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