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Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive myelopoiesis
Loss of NCOR1 is associated with Thyroid Cancer.
These studies support a model in which NCOR1/2 mediates direct Retinoic acid-dependent repression of Fgf8 in caudal progenitors in order to control somitogenesis.
demonstrate that the binding of HDAC3 (show HDAC3 Proteins) to IR nGREs in vivo is mediated through interaction with SMRT/NCoR1
GR SUMOylation site is mandatory for the formation of a GR-small ubiquitin-related modifiers (SUMOs)-SMRT/NCoR1-HDAC3 (show HDAC3 Proteins) repressing complex, which is indispensable for NF-kappaB (show NFKB1 Proteins)/AP1 (show JUN Proteins)-mediated GC-induced tethered indirect transrepression in vitro
dexamethasone, a powerful regulator of metabolism and of adipocyte differentiation, confers this change in NCoR mRNA splicing in cultured adipocytes.
Phosphorylation-mediated recruitment switch of NCoR1 between nuclear receptor subsets provides a mechanism by which corepressors can selectively modulate liver energy metabolism during the fasting-feeding transition
NCOR1 protein levels were significantly reduced.
corepressor specificity exists in vivo and that nuclear receptor corepressor1 is the principal regulator of thyroid hormone (show PTH Proteins) action
NCOR1 interacts with Rev-Erbalpha (show NR1D1 Proteins) to regulate circadian expression of Tshb (show TSHB Proteins) mRNA independent of thyroid hormone (show PTH Proteins).
these data indicate that interactions between NCoR1 and TR control a specific pathway involved in regulation of cholesterol metabolism and clearance.
USP44 (show USP44 Proteins) contributes to N-CoR functions in regulating gene expression and is required for efficient invasiveness of triple-negative breast cancer cells.
PDCD2 (show PDCD2 Proteins) and NCoR1 may act as tumor suppressors in Gastrointestinal stromal tumors cells through the Smad (show SMAD1 Proteins) signaling pathway.
Data suggest that complexes of HDAC3-H1.3 with NCOR1 and NCOR2/SMRT accumulate on chromatin in synchronized HeLa cells in late G2 phase and mitosis; deacetylation activity of HDAC3 is activated via phosphorylation of Ser-424 by CK2 only in mitosis.
NCoR depletion enhances cancer cell invasion and increases tumor growth and metastatic potential.
loss of nuclear NCoR results in upregulation of a specific cancer-related genetic signature, and is significantly associated with malignant melanoma progression.
The co-localization of AML1 (show RUNX1 Proteins)-ETO (show RUNX1T1 Proteins) with the N-CoR co-repressor to be primarily on genomic regions distal to transcriptional start sites. (NcoR1)
Data suggest that direct interactions of HLCS (show HLCS Proteins) (holocarboxylase synthetase) with NCOR1 (nuclear receptor corepressor 1) and HDAC1 (histone deacetylase 1 (show HDAC1 Proteins)) contribute toward transcriptional repression of repeats, presumably increasing genome stability.
Low NCoR expression is associated with glioblastoma.
Site directed mutagenic analysis of N-CoR identified serine 1450 as the crucial residue whose phosphorylation by Akt (show AKT1 Proteins) was essential for the misfolding and loss of N-CoR protein.
Study shows that NCoR1 is a key target of proteolysis and physically interacts with the transcription factor CREB (show CREB1 Proteins), the genome-wide map described here ties proteolysis in mammalian cells to active enhancers and to promoters of specific gene families.
Data provide in vivo evidence for targeted recruitment of N-CoR/SMRT-TBLR1 (show TBL1XR1 Proteins) complexes by unliganded thyroid hormone (show PTH Proteins) receptors in transcriptional repression during vertebrate development
This gene encodes a protein that mediates ligand-independent transcription repression of thyroid-hormone and retinoic-acid receptors by promoting chromatin condensation and preventing access of the transcription machinery. It is part of a complex which also includes histone deacetylases and transcriptional regulators similar to the yeast protein Sin3p. This gene is located between the Charcot-Marie-Tooth and Smith-Magenis syndrome critical regions on chromosome 17. Alternate splicing results in multiple transcript variants. Pseudogenes of this gene are found on chromosomes 17 and 20.
nuclear receptor corepressor 1
, nuclear receptor co-repressor 1
, retinoid X receptor interacting protein 13
, retinoid X receptor-interacting protein 13
, N-Cor/SMRT corepressor Rip13
, N-Cor/SMRT corepressor, Rip13
, thyroid hormone- and retinoic acid receptor-associated corepressor 1