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抗Mouse (Murine) NCOR1 抗体:
抗Rat (Rattus) NCOR1 抗体:
抗Human NCOR1 抗体:
Human Polyclonal NCOR1 Primary Antibody for IHC (p), ELISA - ABIN543314
Ishizuka, Lazar: The N-CoR/histone deacetylase 3 complex is required for repression by thyroid hormone receptor. in Molecular and cellular biology 2003
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Human Polyclonal NCOR1 Primary Antibody for ChIP, IP - ABIN188815
Dai, Hussain: NR2F1 disrupts synergistic activation of the MTTP gene transcription by HNF-4α and HNF-1α. in Journal of lipid research 2012
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Human Monoclonal NCOR1 Primary Antibody for IHC, ELISA - ABIN969310
Zhang, Yoon, Wong: JMJD2A is a novel N-CoR-interacting protein and is involved in repression of the human transcription factor achaete scute-like homologue 2 (ASCL2/Hash2). in Molecular and cellular biology 2005
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Human Monoclonal NCOR1 Primary Antibody for IHC, ELISA - ABIN966640
Atsumi, Tomita, Kiyoi, Naoe: Histone deacetylase 3 (HDAC3) is recruited to target promoters by PML-RARalpha as a component of the N-CoR co-repressor complex to repress transcription in vivo. in Biochemical and biophysical research communications 2006
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Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive myelopoiesis
NCoR1 functions as a negative modulator for hepatic de novo fatty acid synthesis and mitochondria energy adaptation, playing distinct roles in regeneration or carcinogenesis
Liver-Specific Ablation of NCoR1 Induces Hepatic Steatosis and Does Not Prevent Hypothyroidism-Induced Hypercholesterolemia.
the nuclear receptor NCoR1 suppresses Bim1 to inhibit negative selection and promote thymocyte survival.
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 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 repressing complex, which is indispensable for NF-kappaB/AP1-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 action
NCOR1 interacts with Rev-Erbalpha to regulate circadian expression of Tshb mRNA independent of thyroid hormone.
these data indicate that interactions between NCoR1 and TR control a specific pathway involved in regulation of cholesterol metabolism and clearance.
Demonstrate that interaction with NCOR is essential for deacetylase-independent function of HDAC3 in liver.
Study shows that NCoR1 is a key target of proteolysis and physically interacts with the transcription factor CREB, the genome-wide map described here ties proteolysis in mammalian cells to active enhancers and to promoters of specific gene families.
A major effect of NCoR KOknockout in macrophages is to derepress LXR, which leads to the induction of lipogenic pathway genes. This causes increased biosynthesis of palmitoleic acid and omega3 fatty acids within macrophages, which exert robust local anti-inflammatory effects and are associated with the in vivo insulin sensitive phenotype.
NCOR1 has a role in regulating in vivo actions of a mutated thyroid hormone receptor alpha in mice
HDAC3 enzyme activity is undetectable in mice bearing point mutations in the deacetylase-activating domain of both NCOR1 and SMRT.
the repressive effect of NCoR1 on oxidative phosphorylation gene expression specifically antagonizes PGC-1alpha-mediated coactivation of ERRalpha
The specificity of TLR tolerance is dictated by evolutionally conserved nucleic acid motifs that bound by NF-kappaB and the NcoR repressosome.
19 patients with neurodevelopmental disorders harboring a rare deletion inherited from a healthy parent were investigated by whole-exome sequencing to search for SNV on the contralateral segment. This strategy allowed us to identify a candidate variant in two patients in the NUP214 and NCOR1 genes.
Microarray analysis revealed differential expression of three vitamin D associated genes in the aortic adventitia in rheumatoid arthritis (RA) and non-RA patients with coronary artery disease: while the expression of GADD45A and NCOR1 was higher, the expression of PON2 was lower in RA patients.
verexpression of COPS5, through its isopeptidase activity, leads to ubiquitination and proteasome-mediated degradation of NCoR, a key corepressor for ERalpha and tamoxifen-mediated suppression of ERalpha target genes.
the NCOR/HDAC3 complex is a major suppressor of differentiation in rhabdomyosarcoma
Authors previously shown that Nuclear Receptor Corepressor 1 (NCoR) and the thyroid hormone receptor beta1 (TRbeta) inhibit tumor invasion. Here they show that these molecules repress VEGF-C and VEGF-D gene transcription in breast cancer cells, reducing lymphatic vessel density and sentinel lymph node invasion in tumor xenografts.
Nuclear Receptor Corepressor 1 is an important transcriptional regulator that interacts with nuclear receptors and other transcription factors. Recent results have shown the presence of inactivating mutations or deletions of the nuclear receptor corepressor 1 gene in human tumors.
NCOR1 function declines with prostate cancer progression. Reduction in NCOR1 levels causes bicalutamide resistance in LNCaP cells and compromises response to bicalutamide in mouse prostate in vivo
USP44 contributes to N-CoR functions in regulating gene expression and is required for efficient invasiveness of triple-negative breast cancer cells.
PDCD2 and NCoR1 may act as tumor suppressors in Gastrointestinal stromal tumors cells through the Smad 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-ETO 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 (holocarboxylase synthetase) with NCOR1 (nuclear receptor corepressor 1) and HDAC1 (histone deacetylase 1) 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 was essential for the misfolding and loss of N-CoR protein.
The aberrant cytoplasmic expression of NCoR1 in retinoblastoma appears to be associated with the proliferative and/or dedifferentiated properties of retinoblastoma.
Corepressor molecules NCoR and SMRT are present at 1,25(OH)2D3 activated gene enhancers
NCOR1 and HDAC3 are instrumental in the repression of glucocorticoid receptor gene transcription.
Data provide in vivo evidence for targeted recruitment of N-CoR/SMRT-TBLR1 complexes by unliganded thyroid hormone 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