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Article

Destruction of full-length androgen receptor by wild-type SPOP, but not prostate-cancer-associated mutants.

Cell reports - 27 Feb 2014

An Jian, Wang Chenji, Deng Yibin, Yu Long, Huang Haojie

Abstract excerpt

The SPOP E3 ubiquitin ligase gene is frequently mutated in human prostate cancers. Here, we demonstrate that SPOP recognizes a Ser/Thr-rich degron in the hinge domain of androgen receptor (AR) and induces degradation of full-length AR and inhibition of AR-mediated gene transcription and prostate cancer cell growth. AR splicing variants, most of which lack the hinge domain, escape SPOP-mediated degradation....

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 24508459
DOI: 10.1016/j.celrep.2014.01.013
PMCID: PMC4361392

Genes

SPOP

Provenance

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Related research

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Destruction of full-length androgen receptor by wild-type SPOP, but not prostate-cancer-associated mutants.PMID 24508459Read ↗

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SPOP Gene Mutations in Prostate Cancer: Deciphering Their Role in Disease Characterization and Targeted Interventions on AR SignalingSemantic proximity Read ↗

Mutated SPOP E3 Ligase Promotes 17βHSD4 Protein Degradation to Drive Androgenesis and Prostate Cancer Progression.Semantic proximity Read ↗

Prostate cancer. Ubiquitylome analysis identifies dysregulation of effector substrates in SPOP-mutant prostate cancer.Semantic proximity Read ↗

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