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Human Polyclonal NCOA2 Primary Antibody für ICC, IF - ABIN151282
Tognoni, Chadwick, Ackeifi, Tetel: Nuclear receptor coactivators are coexpressed with steroid receptors and regulated by estradiol in mouse brain. in Neuroendocrinology 2011
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Human Polyclonal NCOA2 Primary Antibody für IP, WB - ABIN151852
Long, Udy, Dumont: Hec1 Tail Phosphorylation Differentially Regulates Mammalian Kinetochore Coupling to Polymerizing and Depolymerizing Microtubules. in Current biology : CB 2018
Cow (Bovine) Polyclonal NCOA2 Primary Antibody für WB - ABIN2780788
Strehl, Nebral, König, Harbott, Strobl, Ratei, Struski, Bielorai, Lessard, Zimmermann, Haas, Izraeli: ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations. in Clinical cancer research : an official journal of the American Association for Cancer Research 2008
Case Reports/Review: indeterminate dendritic cell tumor lacking the ETV3-NCOA2 translocation.
Using quantitative biochemical, biophysical, and solution structural methods study shows that ligand and DNA cooperatively recruit the intrinsically disordered steroid receptor coactivator-2 (SRC-2/TIF2/GRIP1/NCoA-2) receptor interaction domain to peroxisome proliferator-activated receptor gamma-retinoid X receptor alpha (PPARgamma-RXRalpha) heterodimer and reveal the binding determinants of the complex.
T3 promotes differentiation towards chondrocytes-like cells in our in vitro model, that this differentiation is mediated by steroid receptor co-activator 2 (SRC2) and does not induce hypertrophy
Pancreatic involvement occurs in mesenchymal chondrosarcoma harboring the HEY1-NCOA2 gene fusion.
Data suggest that steroid receptor coactivators (NCOA1, NCOA2, NCOA3) are over-expressed in a number of hormone-dependent cancers where they promote tumor growth, invasion, metastasis, and chemo-resistance; with their multiple roles in cancer, steroid receptor coactivators are promising targets for development of antineoplastic agents that can interfere with their function. [REVIEW]
SRC-2 may exhibit oncogenic or tumor suppressor activity depending on the target genes and nuclear receptors that are expressed in distinct tissues
NCOA2ETV4 protein would contain the helixloophelix, PAS_9 and PAS_11, CITED domains, the SRC1 domain of NCOA2 and the ETS DNAbinding domain of ETV4.
Altered expression of TIF2 may play a role in adenomyosis development and treatment outcome with levonorgestrel-releasing intrauterine system.
evaluating if NCOA2 relative copy-number gain presents prognostic value for prostate cancer
Report NcoA2-regulation of the AhR-ARNT-HIF-1a interaction.
Data suggest that LRH1/NR5A2 (liver receptor homologue-1) exhibits phospholipid-mediated allosteric control of protein-protein binding interface in interactions with TIF2 and SHP (co-repressor; small heterodimer partner protein).
NCOA2 is a novel negative growth regulatory gene repressing the Wnt/beta-catenin pathway in colorectal cancer, where recurrent fusion with LACTB2 contributes to its disruption.
Suggest a possible association between NCOA2 rs10504473 polymorphism and obesity in Chinese Han population.
miR-137 has a role in targeting p160 steroid receptor coactivators SRC1, SRC2, and SRC3 and inhibits cell proliferation
results suggest that CCNC temporarily protects SRC-2 against degradation and this event is involved in the transcriptional regulation of SRC-2 cell cycle target genes.
Data suggest that over-stimulating the steroid seceptor coactivators SRC-1, SRC-2, and SRC-3 oncogenic program can be an effective strategy to kill cancer cells.
SRC-2 is a prominent metabolic coordinator of cancer metastasis.
Because deregulation of endometrial SRC-2 expression has been associated with common gynecological disorders of reproductive-age women, this signaling pathway, involving SRC-2 and PFKFB3.
the PAX3-NCOA2 fusion gene has a dual role in the tumorigenesis of rhabdomyosarcoma
increased levels of SRC-2 impairs murine endometrial function
Results suggest that SRC-2 coordinates cardiomyocyte secretion of VEGF downstream of the two major angiogenic stimuli occurring during pressure overload bridging both hypertrophic and hypoxia-stimulated paracrine signaling.
studies demonstrate that SRC-2 provides an essential link between the behavioral activities influenced by light cues and the metabolic homeostasis maintained by the liver
the expression of MOZ-TIF2 fusion protein represses the transcription of p16INK4a and p19ARF and blocks senescence.
findings position SRC-2 as a major regulator of polygenic inputs to metabolic gene regulation and perhaps identify a previously unappreciated model that helps to explain the clinical spectrum of glucose dysregulation
fetal lungs produce signals to initiate labor when mature, and SRC-1/-2-dependent production of SP-A and PAF is crucial for this process
In a murine model, overexpression of NCoA2 in the prostate epithelium resulted in neoplasia.
Transcription factor 23 (Tcf23), a basic-helix-loop-helix transcription factor, is a new progesterone-induced target gene that requires SRC-2 for full induction.
SRC-2 is a transcriptional coactivator for BMAL1:CLOCK. Ablation of SRC-2 disrupts the central clock.
SRC-2 is critical to transcriptional control modulated by MEF2, GATA-4, and Tbx5, thereby enhancing gene expression associated with cardiac growth.
SRC2 regulates anxiety response with SRC2(-/-) females showing decreased anxiety in novel environments.
Our results indicate that SRC-2 is involved in maintenance of the steady-state adult heart transcriptional profile, with its ablation inducing transcriptional changes that mimic a stressed heart.
Deletion of Ncoa2/Src-2 in mice predisposes to diethylnitrosamine-induced liver tumorigenesis.
SRC-1 and TIF2 can modulate the expression of the uncoupling protein 3 in an antagonistic manner and that enhanced SRC-1 levels in TIF2-deficient myofibers are critically involved in the metabolic changes of TIF2(i)skm-/- mice.
Pre-treatment with T0901317 before LPS stimulation can suppress the expressions of IRF3 and GRIP1 to inhibit inflammation and Kupffer cell activation.
differentially regulates PKA-stimulated transcriptional activity of steroidogenic factor 1
synergistic activation of constitutively active androstane receptor (CAR) by glucocorticoid receptor-interacting protein 1 (GRIP1) results from both nuclear translocation and activation of CAR.
cyclin D-cdk4 activity modulates the subnuclear localization and interaction of MEF2 with SRC-family coactivators, GRIP-1 during skeletal muscle differentiation
Data show that TIF2 plays a critical role in mouse reproductive functions. Though TIF2, SRC-1, and p/CIP exhibit sequence homology and similar activity in vitro, their genetic eliminations result in distinct pathologies in vivo.
results indicate a potential role of PIAS3 as transcriptional modulator of TIF2-mediated signalling
The tif2 is involved in embryogenesis and in primitive hematopoiesis. tif2-knockdown zebrafish embryos are smaller than controls.
SNP 1718 in the NCOA2 gene was significant for early pregnancy probability (P=0.02) and age at first calving (P=0.03), and SNP 2038 in the same gene was significant for days to calving (P=0.03).
The NCOA2 gene encodes nuclear receptor coactivator 2, which aids in the function of nuclear hormone receptors. Nuclear hormone receptors are conditional transcription factors that play important roles in various aspects of cell growth, development, and homeostasis by controlling expression of specific genes. Members of the nuclear hormone receptor superfamily, which includes the 5 steroid receptors and class II nuclear receptors (see below), are structurally characterized by 3 distinct domains: an N-terminal transcriptional activation domain, a central DNA-binding domain, and a C-terminal hormone-binding domain. Before the binding of hormone, steroid receptors, which are sometimes called class I of the nuclear hormone receptor family, remain inactive in a complex with heat-shock protein-90 (MIM 140571) and other stress family proteins. Binding of hormone induces critical conformational changes in steroid receptors that cause them to dissociate from the inhibitory complex, bind as homodimers to specific DNA enhancer elements associated with target genes, and modulate that gene's transcription. After binding to enhancer elements, transcription factors require transcriptional coactivator proteins to mediate their stimulation of transcription initiation (Hong et al., 1997
class E basic helix-loop-helix protein 75
, glucocorticoid receptor-interacting protein-1
, transcriptional intermediary factor 2
, glucocorticoid receptor interacting protein 1
, glucocorticoid receptor-interacting protein 1
, steroid receptor coactivator 2
, nuclear receptor coactivator 2
, transcriptional intermediary factor-2
, Transcriptional intermediary factor 2
, nuclear receptor coactivator 2-like