This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Facts about Nuclear receptor coactivator 3.
Involved in the coactivation of different nuclear receptors, such as for steroids (GR and ER), retinoids (RARs and RXRs), thyroid gland (TRs), vitamin D3 (VDR) and prostanoids (PPARs). Displays histone acetyltransferase activity.
Human | |
---|---|
Gene Name: | NCOA3 |
Uniprot: | Q9Y6Q9 |
Entrez: | 8202 |
Belongs to: |
---|
SRC/p160 nuclear receptor coactivator family |
ACTR; ACTRCBP-interacting protein; AIB1; AIB1AIB-1; Amplified in breast cancer 1 protein; BHLHE42; bHLHe42p/CIP; CAGH16; Class E basic helix-loop-helix protein 42; CTG26; KAT13B; MGC141848; NCOA3; NCoA-3; nuclear receptor coactivator 3; pCIP ; pCIP; RAC3; RAC-3; RAC3pCIP; Receptor-associated coactivator 3; SRC-1; SRC3; SRC-3; SRC-3EC 2.3.1.48; Steroid receptor coactivator protein 3; Thyroid hormone receptor activator molecule 1; TNRC16; TRAM1; TRAM-1TNRC14
Mass (kDA):
155.293 kDA
Human | |
---|---|
Location: | 20q13.12 |
Sequence: | 20; NC_000020.11 (47501887..47656872) |
Widely expressed. High expression in heart, skeletal muscle, pancreas and placenta. Low expression in brain, and very low in lung, liver and kidney.
Cytoplasm. Nucleus. Mainly cytoplasmic and weakly nuclear. Upon TNF activation and subsequent phosphorylation, it translocates from the cytoplasm to the nucleus.
If you are trying to find out how to use the NCOA3 Marker, you have probably noticed that there are many options and flow procedures to choose from. This article will cover a few of these options and give you tips for optimizing your experiments and preparing biological samples. We'll also cover the best uses and applications of the NCOA3 mark in fibrosis.
The NCOA3 genome encodes a cell-cycle regulator that is upregulated in cancer cells. Targeting NCOA3 within tumor cells results is mitotic catastrophe. This causes apoptosis. Cancer research is currently investigating clinical applications of the NCOA3 genes. We discuss some of the promising applications for the NCOA3 genes. We will be discussing recent findings on the expression and function NCOA3.
Many aspects of melanoma growth are influenced by the NCOA3 gene. It plays a key role in directing the transcriptional cascade, promoting cell survival after UVR and cell cycle progression. It also inhibits DDR inhibitors. NCOA3 expression significantly reduced photoproduct excision. This suggests that NCOA3 activation might be an effective mechanism for reducing the long-term effects of UVR-induced DNA damages.
The NCOA3 gene plays an important role in cancer therapy. It plays an important role both in the development and progressionof breast cancer and in resistance to antihormonal therapy. Higher NCOA3 levels are strongly associated with a shorter survival time and lower rates of death from any cause. The NCOA3 gene is a promising candidate for drug development in cancer research. It has the potential of predicting the progression to melanoma.
NCOA3 can be used to diagnose ovarian and melanoma. The gene is overexpressed in 60% of primary ovarian tumours and amplified in 5%-10% of breast cancers. Studies with transgenic mice overexpressing NCOA3 show increased mammary epithelial cell proliferation and hyperplasia. Transgenic mice also show that NCOA3 can be ablationed to reduce mammary hyperplasia.
The downregulation NCOA3 expression was a factor in the inhibition of melanoma-cell proliferation. It also increased the UVR-sensitivity of melanoma-cells. Furthermore, pharmacological targeting of NCOA3 induced significant anti-tumor activity, similar to NCOA3 gene silencing. These results suggest that NCOA3 plays important role in the development melanoma.
NCOA3 is also known to inhibit UV-mediated cytotoxicity, and affect DDR. When overexpressed in melanoma cells, NCOA3 reduces UV sensitivity and increases DNA damage markers such as gH2AX. The NCOA3 genes could be useful as a prognostic marker or therapeutic target. It is currently being investigated to see if it plays a role in lung disease.
This study looked at the role of nuclear receiver coactivator 3 ("NCOA3") in fibrosis. It was shown that NCOA3 is a key contributor in the uncontrolled activation fibroblasts in fibrotic disorders, and that its knockdown improved dermal fibrosis. The knockdown resulted in a reduction of expression of the TGFb target genes COL1A1, ACTA2, CTGF. Knockdown of NCOA3 caused fibrosis to mice with constitutively activated TGF-b receptor Type I.
NCOA3 expression varies between PC and pancreatitis. Mutations in NCOA3 can cause altered mucin expression. Researchers used a cerulein-based model, wild-type and mutant K–ras backgrounds to determine the role of NCOA3 for PC. The K–rasG12D mutation increased NCOA3 expression. The K–ras mutation is associated to inflammation.
This NCOA3 candidate gene is a novel candidate for the explanation of autosomal dominating progressive hearing loss. NCOA3 is a known interaction with SMAD3 that promotes TGF-b/SMAD3 signals. The gene is also known to play an important role in the activation of fibroblasts and the hardening of desmoplasia. Researchers can use NCOA3-deficient cell lines to study a new variant of fibrosis.
After RA treatment KD cells had a lower active transcriptional marking of NCOA3. PCR was amplified using two sets primers that target MUC4's promoter region. The ShNCOA3 Clone had a higher level of PCR amplification than the NCOA3KD Clone. This may be due to the low accessibility of the MUC4 Promoter.
PMID: 9346901 by Takeshita A., et al. TRAM-1, a novel 160-kDa thyroid hormone receptor activator molecule, exhibits distinct properties from steroid receptor coactivator-1.
PMID: 9267036 by Chen H., et al. Nuclear receptor coactivator ACTR is a novel histone acetyltransferase and forms a multimeric activation complex with P/CAF and CBP/p300.