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anti-Human NCOR2 Antibodies:
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Human Monoclonal NCOR2 Primary Antibody for IP, WB - ABIN152352
Wu, Li, Park, Chen: SMRTE inhibits MEF2C transcriptional activation by targeting HDAC4 and 5 to nuclear domains. in The Journal of biological chemistry 2001
Show all 3 Pubmed References
Human Polyclonal NCOR2 Primary Antibody for IP, PLA - ABIN188817
Zhou, Li, Hu, Gong, Drescher, Chen: miR-16 targets transcriptional corepressor SMRT and modulates NF-kappaB-regulated transactivation of interleukin-8 gene. in PLoS ONE 2012
Human Monoclonal NCOR2 Primary Antibody for ChIP, IHC (fro) - ABIN266935
Catalano, Mauro, Bonofiglio, Pellegrino, Qi, Rizza, Vizza, Bossi, Andò: In vivo and in vitro evidence that PPARγ ligands are antagonists of leptin signaling in breast cancer. in The American journal of pathology 2011
Human Polyclonal NCOR2 Primary Antibody for ELISA, WB - ABIN564153
Zhang, Gong, Lau, Yang, Wong, Cheung, Tsang, Chan, Khoo: SpliceArray profiling of breast cancer reveals a novel variant of NCOR2/SMRT that is associated with tamoxifen resistance and control of ER? transcriptional activity. in Cancer research 2013
Human Monoclonal NCOR2 Primary Antibody for WB - ABIN2668570
Huang, Zhang, Miska, Guenther, Kouzarides, Lazar: Nuclear receptor corepressors partner with class II histone deacetylases in a Sin3-independent repression pathway. in Genes & development 2000
MIR22HG inhibited HCC progression in part through the miR-10a-5p/NCOR2 signaling.
this report tried to address the molecular basis for the direct interaction between CSL and SMRT.
The pregnane X receptor (PXR) and the nuclear receptor corepressor 2 (NCoR2) modulate cell growth in head and neck squamous cell carcinoma
Cellular Differentiation of Human Monocytes Is Regulated by Time-Dependent Interleukin-4 Signaling and the Transcriptional Regulator NCOR2.
The mechanism of IL-6-induced AR activation is mediated through enhancing AR-SRC-1 interaction and inhibiting AR-SMRT interaction.
IL-6-mediated AR antagonism induced by cypermethrin is related to repress the recruitment of co-regulators SRC-1 and SMRT to the AR in a ligand-independent manner
this study identifies NCOR2 as a new gene for FVC, indicating the importance of further research into the role of vitamin A intake/supplementation and its interactions with related genes in the regulation of FVC.
Molecular basis for the specific interactions between HDAC4 and the SMRT corepressor.
SNPs in Notch pathway genes may be predictors of cutaneous melanoma disease-specific survival.
Significant methylation changes in the SLC23A2 and NCOR2 regulatory regions.
A repeated peptide motif present in both SMRT and NCoR is sufficient to mediate specific interaction, with micromolar affinity, with all the Class IIa Histone Deacetylases (HDACs 4, 5, 7, and 9).
SMRT enhances cell growth of estrogen receptor-alpha-positive breast cancer cells by promotion of cell cycle progression and inhibition of apoptosis.
Phosphorylation of the CK2 site on SMRT significantly increased affinity for SHARP.
model where p53 binding to the SMRT deacetylase activation domain (DAD) limits HDAC3 interaction with this coregulator, thereby facilitating SMRT coactivation of p53-dependent gene expression
SMRT is responsible for basal repression of Wip1,a phosphatase that de-phosphorylates and inactivates Chk2, thus affecting a feedback loop responsible for licensing the correct timing of Chk2 activation and the proper execution of the DNA repair process.
a model in which TNFalpha-induced beta-TrCP1 accumulation promotes SMRT degradation and the subsequent induction of proinflammatory gene expression.
Corepressor molecules NCoR and SMRT are present at 1,25(OH)2D3 activated gene enhancers
SMRT may be recruited in the SXR-cofactor complex even in the presence of ligand; SMRTmay be involved not only in SXR-mediated suppression without ligand, but also in ligand-activated transcription to suppress the overactivation of transcription
There was no association between SMRT expression and overall survival for patients, regardless of whether they received tamoxifen
expression of the transcriptional corepressor complex subunits GPS2 and SMRT was significantly reduced in obese adipose tissue, inversely correlated to inflammatory status
Both the acetylation and SUMOylation status of the PXR protein is affected by its ability to associate with the lysine de-acetylating enzyme HDAC3 in a complex with SMRT.
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
changes in dietary components can consistently, if moderately, modulate the total transcript levels and the mRNA splicing of NCoR and SMRT in both cultured cells and intact mice.
SMRT regulates glucocorticoid action in adipocytes.
While silencing mediator of retinoid and thyroid hormone receptor played little role in TH-regulated pathways, when disrupted in combination with nuclear receptor corepressor, it greatly accentuated the synthesis and storage of hepatic lipid
HDAC3 enzyme activity is undetectable in mice bearing point mutations in the deacetylase-activating domain of both NCOR1 and SMRT.
These results reveal that Bcl6-SMRT/NCoR complexes constrain immune responses and contribute to the prevention of atherosclerosis.
SMRT is an adipogenic gatekeeper as it directly fine-tunes transcription of pro- and antiadipogenic genes.
miR-184 downregulated nuclear receptor corepressor 2 (Ncor2) by targeting its 3' untranslated region through inhibiting NCOR2 protein translation
Data show that knock-in mutations of the nuclear co-repressor SMRT in C57BL/6 mice produces a previously unidentified respiratory distress syndrome caused by prematurity of the type I pneumocyte.
essential role of nuclear receptor corepressors in maintaining metabolic homeostasis and describe an essential role for SMRT in regulating the progression, severity, and therapeutic outcome of metabolic diseases
Nuclear receptor corepressor SMRT regulates mitochondrial oxidative metabolism and mediates aging-related metabolic deterioration.
SMRT regulates leptin expression and limits the ability of fat mass to expand with increased caloric intake, but SMRT also negatively regulates adipocyte insulin sensitivity
TR surfaces and conformations required to bind nuclear receptor corepressor
Nuclear receptor corepressor-dependent repression of peroxisome-proliferator-activated receptor delta-mediated transactivation
The transcription factor B-Myb is maintained in an inhibited state in target cells through its interaction with the nuclear corepressors N-CoR and SMRT.
the loss of the molecular events of AML1-ETO C-terminal NCoR/SMRT-interacting domain transforms AML1-ETO into a potent leukemogenic protein.
differential mRNA splicing of SMRT serves to customize corepressor function in different cells, allowing the transcriptional properties of nuclear receptors to be adapted to different contexts
Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive myelopoiesis
A novel regulatory mechanism for Ncor2 through Fos-Vegfd-Notch signaling cascade during hematopoietic stem cell development in zebrafish embryos.
rar-ncor2 corepressor complex may be part of an embryonic, epigenetic switch that keeps retinoic acid responsive genes off before retinoic becomes available to the embryo
This gene encodes a nuclear receptor co-repressor that mediates transcriptional silencing of certain target genes. The encoded protein is a member of a family of thyroid hormone- and retinoic acid receptor-associated co-repressors. This protein acts as part of a multisubunit complex which includes histone deacetylases to modify chromatin structure that prevents basal transcriptional activity of target genes. Aberrant expression of this gene is associated with certain cancers. Alternate splicing results in multiple transcript variants encoding different isoforms.
CTG repeat protein 26
, T3 receptor-associating factor
, silencing mediator for retinoid and thyroid hormone receptors
, thyroid-, retinoic-acid-receptor-associated corepressor
, nuclear receptor corepressor 2
, nuclear receptor co-repressor 2
, silencing mediator of retinoic acid and thyroid hormone receptor
, silencing mediator of retinoid acid and thyroid hormone receptor
, silencing mediator
, thyroid hormone receptor