2024年12月25日 · NCOR2 (Nuclear Receptor Corepressor 2) is a Protein Coding gene. Diseases associated with NCOR2 include Hematologic Cancer and Plasma Cell Neoplasm. Among its related pathways are Constitutive Signaling by NOTCH1 HD+PEST Domain Mutants and Transcriptional Regulation by MECP2.

The nuclear receptor co-repressor 2 (NCOR2) is a transcriptional coregulatory protein that contains several nuclear receptor -interacting domains. In addition, NCOR2 appears to recruit histone deacetylases to DNA promoter regions.

2025年2月19日 · Title: Nuclear corepressors NCOR1/NCOR2 regulate B cell development, maintain genomic integrity and prevent transformation. Screening of organoids derived from patients with breast cancer implicates the repressor NCOR2 in cytotoxic stress response and antitumor immunity.

2022年10月31日 · Herein, we demonstrate that Ncor1/2 deletion limits B cell differentiation via impaired recombination, attenuates pre-BCR signaling and enhances STAT5-dependent transcription. Furthermore,...

2015年6月29日 · NCOR2 is a transcriptional corepressor that maintains the 'off state' of nonliganded nuclear receptors. Its interaction with nuclear receptors is mediated by 2 C-terminal receptor-interacting domains (RIDs).

2019年1月21日 · Nuclear receptor corepressor 1 (NCOR1) and NCOR2 (also known as SMRT) regulate gene expression by activating histone deacetylase 3 through their deacetylase activation domain (DAD). We show...

In this review, we summarize the literature on the mechanism, regulation, and function of the core components of NCoR/SMRT complexes in the context of their involvement in cancers and leukemias.

NCOR2 is a prognostic marker in Cervical squamous cell carcinoma and endocervical adenocarcinoma, Ovary serous cystadenocarcinoma

NCOR2 is a nuclear co-repressor that was firstly known for its transcriptional silencing role of retinoid and thyroid hormone receptors and is referred to as SMRT (silencing mediator for retinoid and thyroid hormone receptors) (Hussein-Fikret and Fuller 2005; Sasaki et al. 2008).

Herein, we demonstrate that Ncor1/2 deletion limits B cell differentiation via impaired recombination, attenuates pre-BCR signaling and enhances STAT5-dependent transcription. Furthermore, NCOR1/2-deficient B cells exhibited derepression of EZH2-repressed gene modules, including the p53 pathway.