GNL3 orchestrates AR transcriptional programs to drive castration-resistant prostate cancer and immune evasion
Ontology highlight
ABSTRACT: Androgen receptor (AR) signaling is a primary oncogenic driver of castration-resistant prostate cancer (CRPC), yet the mechanism remains incompletely understood. Dysregulation of the AR co-regulatory network has emerged as a key driver of castration resistance. To identify AR-interacting proteins linked to CRPC progression, we performed proteomics-based rapid immunoprecipitation of endogenous proteins (RIME) analysis targeting AR in the CRPC cell line C4-2B.
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Malignant Cell, Cell Culture
DISEASE(S): Prostate Cancer
SUBMITTER:
Cuiting Zhang
LAB HEAD: Edwin Cheung
PROVIDER: PXD067138 | Pride | 2026-06-08
REPOSITORIES: Pride
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