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Nuclear receptor coactivator 4

This gene encodes an androgen receptor coactivator. The encoded protein interacts with the androgen receptor in a ligand-dependent manner to enhance its transcriptional activity. Chromosomal translocations between this gene and the ret tyrosine kinase gene, also located on chromosome 10, have been associated with papillary thyroid carcinoma. Alternatively spliced transcript variants have been described. Pseudogenes are present on chromosomes 4, 5, 10, and 14. [provided by RefSeq, Feb 2009] (from NCBI)
Top mentioned proteins: RET, CAN, HAD, BRAF, PTC2
Papers using PTC3 antibodies
Thyroid tumorigenesis
Franc B et al., In British Journal of Cancer, 1993
... RET/PTC3, E7 transgenic and C57Bl/6 wild-type mice ...
Papers on PTC3
NTRK fusion oncogenes in pediatric papillary thyroid carcinoma in northeast United States.
Nikiforov et al., Bologna, Italy. In Cancer, Feb 2016
Six of 27 PTCs (22%) had ret proto-oncogene (RET) fusions (RET/PTC1, n = 5; RET/PTC3, n = 1); 2 tumors measured >2 cm and diffusely involved the thyroid, and 5 had lymphatic invasion, with vascular invasion in 2. Thirteen PTCs had the B-Raf proto-oncogene, serine/threonine kinase (BRAF) valine-to-glutamic acid mutation at position 600 (BRAF(V) (600E) ) (13 of 27 tumors; 48%), 11 measured <2 cm, and 6 had lymphatic invasion (46%), with vascular invasion in 3. Fusion oncogene tumors, compared with BRAF(V) (600E) PTCs, were associated with large size (mean, 2.2 cm vs 1.5 cm, respectively; P = .05),
Genetic Alterations in Hungarian Patients with Papillary Thyroid Cancer.
Lakatos et al., Budapest, Hungary. In Pathol Oncol Res, Jan 2016
In tumorous samples, 86 BRAF (44.2 %), 5 NRAS (3.1 %), 2 HRAS (1.0 %) and 1 KRAS (0.5 %) mutations were found, as well as 9 RET/PTC1 (4.6 %) and 1 RET/PTC3 (0.5 %) translocations.
Molecular imaging with (99m)Tc-MIBI and molecular testing for mutations in differentiating benign from malignant follicular neoplasm: a prospective comparison.
Bongiovanni et al., Bellinzona, Switzerland. In Eur J Nucl Med Mol Imaging, Jan 2016
Mutations for KRAS, HRAS and NRAS and for BRAF and translocations of PAX8/PPARγ, RET/PTC1 and RET/PTC3 were investigated.
Genetic Alterations in Differentiated Thyroid Cancer Patients with Acromegaly.
Erbas et al., Ankara, Turkey. In Exp Clin Endocrinol Diabetes, Dec 2015
BRAF V600E and NRAS codon 61 point mutations, RET/PTC1, RET/PTC3, and PAX8/PPARγ gene rearrangements were analyzed in thyroidectomy specimens.
Diffuse sclerosing variant of papillary thyroid carcinoma:Major genetic alterations and prognostic implications.
Kim et al., Seoul, South Korea. In Histopathology, Dec 2015
We tested for a panel of genetic alterations including BRAF(V) (600E) , NRAS codon 61, HRAS codon 12/13/61, and KRAS codon 12/13 point mutations as well as RET/PTC1, RET/PTC3, and PAX8/PPARγ rearrangements using reverse transcription real-time PCR.
Modulation of thyroidal radioiodide uptake by oncological pipeline inhibitors and Apigenin.
Jhiang et al., Columbus, United States. In Oncotarget, Nov 2015
To identify inhibitors that can be readily translated into clinical care, we examined oncological pipeline inhibitors targeting Akt, MEK, PI3K, Hsp90 or BRAF in their ability to increase RAIU in thyroid cells expressing BRAFV600E or RET/PTC3 oncogene.
Molecular characterization of sporadic pediatric thyroid carcinoma with the DNA/RNA ThyroSeq v2 next-generation sequencing assay.
Nikiforov et al., Pittsburgh, United States. In Pediatr Dev Pathol, Oct 2015
Fifteen cases were previously tested by our standard 7-gene (BRAF, NRAS, HRAS, KRAS, RET/PTC1, RET/PTC3, PAX8/PPARg) mutation panel.
[Pooled Analysis of RET/PTC Gene Rearrangement Rate in Sporadic and Radiogenic Thyroid Papillary Carcinoma].
Biryukov et al., In Radiats Biol Radioecol, Jul 2015
Based on this database a pooled analysis of data on the rates of RET/PTC1, RET/PTC3 and RET/PTC in total was conducted.
Contactin 1 as a potential biomarker promotes cell proliferation and invasion in thyroid cancer.
Fan et al., Hangzhou, China. In Int J Clin Exp Pathol, 2014
Here, we firstly find CNTN1 is a new gene which can be regulated by RET/PTC3 (Ret proto-oncogene and Ret-activating protein ELE1) rearrangement gene and the protein level of CNTN1 is increasing in thyroid cancer.
BRAF(V600E) mutation is highly prevalent in thyroid carcinomas in the young population in Fukushima: a different oncogenic profile from Chernobyl.
Yamashita et al., Nagasaki, Japan. In Sci Rep, 2014
RET/PTC3 in one (1.5%) and ETV6/NTRK3 in four (5.9%).
Androgen receptor coactivators that inhibit prostate cancer growth.
Lee et al., New York City, United States. In Am J Clin Exp Urol, 2013
In this review, we discuss the expression and function of several AR coactivators exhibiting growth suppressive function in PCa, including ARA70/ELE1/NCOA4, androgen receptor coactivator p44/MEP50/WDR77, TBLR1, and ART-27.
Expression and function of nuclear receptor co-activator 4: evidence of a potential role independent of co-activator activity.
Brown et al., Toronto, Canada. In Cell Mol Life Sci, 2012
Nuclear receptor coactivator 4 (NcoA4), also known as androgen receptor-associated protein 70 (ARA70), was initially discovered as a component of Ret-Fused Gene expressed in a subset of papillary thyroid carcinomas.
Promoter variants in the MSMB gene associated with prostate cancer regulate MSMB/NCOA4 fusion transcripts.
Dean et al., Frederick, United States. In Hum Genet, 2012
Computational network analysis reveals that the MSMB gene is functionally connected to NCOA4 and the androgen receptor signaling pathway. The data provide an example of how GWAS-associated variants may have multiple genetic and epigenetic effects
Distinct function of androgen receptor coactivator ARA70α and ARA70β in mammary gland development, and in breast cancer.
Lee et al., New York City, United States. In Breast Cancer Res Treat, 2011
High ARA70alpha inhibited cell proliferation, and that ARA70beta promotes proliferation in breast cancer.
Targeting of the actin cytoskeleton by insecticidal toxins from Photorhabdus luminescens.
Aktories et al., Freiburg, Germany. In Naunyn Schmiedebergs Arch Pharmacol, 2011
Recently, the molecular mechanisms of the toxin complexes PTC3 and PTC5 have been elucidated.
Analysis of the 10q11 cancer risk locus implicates MSMB and NCOA4 in human prostate tumorigenesis.
Freedman et al., Boston, United States. In Plos Genet, 2010
Suppression of MSMB expression or NCOA4 overexpression promotes anchorage-independent growth of prostate epithelial cells.
Variable expression of nuclear receptor coactivator 4 (NcoA4) during mouse embryonic development.
Brown et al., Toronto, Canada. In J Histochem Cytochem, 2010
Results demonstrate ubiquitous NcoA4 expression throughout development and suggest that this coactivator may play a role in modulating nuclear receptor activity, particularly that of the aryl hydrocarbon receptor, during development.
Tumor suppressor function of androgen receptor coactivator ARA70alpha in prostate cancer.
Lee et al., New York City, United States. In Am J Pathol, 2010
ARA70alpha functions as a tumor suppressor gene
[Oncogenes RET/PTC and mechanisms of their involvement in thyroid cancerogenesis].
Voskoboĭnyk, In Ukr Biokhim Zh (1999), 2009
The most common of them are RET/PTC1 and RET/PTC3 forms.
Radiation carcinogenesis: lessons from Chernobyl.
Williams, Cambridge, United Kingdom. In Oncogene, 2008
The subtype and molecular findings change with latency; most early cases were solid PTCs with RET-PTC3 rearrangements, later cases were classical PTCs with RET-PTC1 rearrangements.
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