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AKT is involved in regulating AIB1 recruitment to the PS2 promoter region in the presence of IGF-1. AIB1 overexpression in breast cancer cells increases AKT activity, as well as enhances PI3K/AKT-mediated cell cycle S phase entry.
Study shows that oxidative stress plays a crucial role in controlling steroid receptor coactivator 3 expression, which influences the migration and tube formation abilities of endothelial cells through the PI3K/Akt/mTOR signaling pathways.
stable knockdown of FOXO3, NCOA3, and TCF7L2 restored growth in low glucose but reduced MEK/MAPK phosphorylation, reduced anchorage-independent growth, and modulated expressions of GLUT1 and Ras pathway related proteins.
The Authors reveal a gender difference in the prognostic value of concomitant AIB1 and HER2 copy number gain (CNG) in glioma patients which were barely noticed before. These observations indicated that genetic alterations synergistic with essential respects of sex determination influence glioma biology and patients outcomes.
NCOA3 maintained the molecular signature of chondrocytes dedifferentiating in vitro or exposed to IL-1 beta and NCOA3 lose promotes posttraumatic OA at least partially by enhancing NF-kappaB activation.
Data suggest that NEAT1, SRC3, and IGF1R are highly expressed in prostate cancer cells; NEAT1 appears to interact with SRC3 and promote cell proliferation via up-regulation of SRC3/IGF1R/AKT signaling pathway. (NEAT1 = nuclear paraspeckle assembly transcript-1; SRC3 = steroid receptor coactivator protein-3; IGF1R = insulin-like growth factor 1 receptor)
findings suggest that the Warburg pathway enzyme PFKFB4 acts as a molecular fulcrum that couples sugar metabolism to transcriptional activation by stimulating SRC-3 to promote aggressive metastatic tumours
Findings demonstrate how SRC3 and Cx43 regulation between BMSCs and myeloma cells mediate cell growth and disease progression.
RAC3 bound tightly to the ARE enhancer region of the HO-1 promoter via Nrf2 binding.
Hypoxia inhibits the RAC3 gene expression leading to the autophagy process, allowing tumor cells to survive until angiogenesis occurs
RAC3 is an inhibitor of senescence whose downregulation in aged individuals could be probably a tumor suppressor mechanism.
The model had 92% sensitivity and 92% specificity. We obtained similar results in the independent validation cohort. AIB1 and EIF5A2 show promise for the noninvasive detection of bladder cancer. The model based on AIB1, EIF5A2, and NMP22 outperformed each of the three individual biomarkers for detecting Bladder cancer.
our study implicates that AIB1 is a molecular target of sorafenib and downregulation of AIB1 contributes to the anti-tumor effects of sorafenib
our studies illustrate that SRC-3 overexpression is clinically and functionally relevant to the progression of human ESCC.
Data indicate that phosphorylated cortactin recruits Vav2 to activate Rac3 and promote invadopodial maturation in invasive breast cancer cells.
Estrogen receptor recruits steroid receptor coactivator-3 primary coactivator and secondary coactivators, p300/CBP and CARM1 to regulate genetic transcription.
we identify a positive feedback regulatory loop consisting of XBP1 and NCOA3 that maintains high levels of NCOA3 and XBP1 expression in breast cancer tissues.
loss of miR-17 and miR-20b enhanced breast cancer resistance to taxol by upregulating NCOA3 levels.
Data (including data from studies of hydrogen-deuterium exchange coupled to mass spectrometry in presence of denaturants) suggest that, for peptide fragments of human ACTR and mouse Crebbp representing disordered interaction domains, exchange rates are changed dramatically by high concentrations of denaturants guanidinium chloride or urea. (ACTR = activator of thyroid and retinoid receptor; Crebbp = CREB binding protein)
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]
differential expression of NCOA3 in pig intramuscular and subcutaneous adipose tissue is regulated by miR-17-5p.
findings show that SRC-3 contributes to host defense against enteric bacteria, at least in part via upregulating CXCL2 expression to recruit neutrophils
Findings indicate that the Gata6 promoter is activated by Esrrb in association with Ncoa3, and Dax1 inhibited activities of Esrrb and Ncoa3, resulting maintenance of the undifferentiated status of embryonic stem (ES) cells.
SRC-1/3 are required for cardiomyocyte proliferation and differentiation at earlier developmental stages, and their dysfunction causes NCC-like abnormalities in the hearts of newborn and adult mice.
AIB1 promotes gastric cancer cell proliferation, survival and invasiveness through modulating major signaling pathways such as ErbB and Wnt/beta-catenin pathways. Findings suggest that AIB1 plays an important role in the pathogenesis of gastric cancer.
SRC-3 is a target for inhibiting aggressive prostate cancer containing neuroendocrine tumor cells.
Impaired hematopoiesis and delayed thrombopoietic recovery following sublethal irradiation in SRC3 knockout mice.
The p/CIP gene regulatory network identifies various feed-forward modules including one in which p/CIP activates members of the extended pluripotency network, demonstrating that p/CIP is a component of this extended network.
Loss of SRC3 also shows sex differences in anxiety and exploratory behaviors.
IRS1 levels are significantly increased in mouse cell lines representing fat and muscle lineages with p/CIP and SRC-1 deletions and in white adipose tissue and skeletal muscle of knockout mice.
Data show that knockdown of nuclear receptor coactivator 3 (Ncoa3) not only compromises the expression of pluripotency markers but also impairs in vitro and in vivo differentiation potential of embryonic stem cells.
Ncoa3, an essential coactivator, is required to mediate Esrrb function in embryonic stem cells.
A previously unknown function of SRC-3 in the control of endothelial cell phenotypes in vitro and neogenesis and physiologic wound healing in vivo is shown.
SRC-3 is the predominant transcriptional co-activator among the three SRC family members for CAR activation to promote hepatocyte proliferation and drug metabolism.
crucial role for SRC-3 in regulating hepatic lipid metabolism
the level of interaction of AIB1 with ERbeta domains in young and old male was significantly higher than female of same age, whereas the expression of AIB1 in adult and old female was significantly higher than male of same age
a model whereby the transcriptional activity of AIB1 is squelched by a repressive mechanism utilizing the N-terminal domain and that the increased coactivator function of AIB1-Delta4 is due to the loss of this inhibitory domain
Both AIB1 and AIB1delta3 overexpression increased prevalence of mammary hyperplasia and resulted in a significant increase in stromal collagen.
SRC-3 deficiency could lead to visceral/subcutaneous fat redistribution under high fat diets
Results demonstrate that NCOA1 and NCOA3 cooperatively regulate placental morphogenesis and embryo survival.
our data highlight a pivotal role of SRC-3 in the host defense system against bacterial infection.
The protein encoded by this gene is a nuclear receptor coactivator that interacts with nuclear hormone receptors to enhance their transcriptional activator functions. The encoded protein has histone acetyltransferase activity and recruits p300/CBP-associated factor and CREB binding protein as part of a multisubunit coactivation complex. This protein is initially found in the cytoplasm but is translocated into the nucleus upon phosphorylation. Several transcript variants encoding different isoforms have been found for this gene. In addition, a polymorphic repeat region is found in the C-terminus of the encoded protein.
nuclear receptor coactivator 3
, CBP-interacting protein
, amplified in breast cancer 1 protein
, class E basic helix-loop-helix protein 42
, receptor-associated coactivator 3
, steroid receptor coactivator protein 3
, thyroid hormone receptor activator molecule 1
, steroid receptor coactivator 3
, amplified in breast cancer-1 protein homolog
, retinoid X receptor-interacting coactivator xSRC-3