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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Ets variant 4

Top mentioned proteins: AP-1, ER81, ERM, CAN, NET
Papers on PEA3
The conserved genetic background for pluteus arm development in brittle stars and sea urchin.
Wada et al., Tsukuba, Japan. In Evol Dev, Feb 2016
Several genes are known to be involved in the development of pluteus arms in sea urchins, including fgfA, pax2/5/8, pea3, otp, wnt5, and tet.
β-Cell Insulin Secretion Requires the Ubiquitin Ligase COP1.
Dixit et al., San Francisco, United States. In Cell, Jan 2016
Here, we show that post-translational regulation of the transcription factors ETV1, ETV4, and ETV5 by the ubiquitin ligase COP1 (also called RFWD2) in β cells is critical for insulin secretion.
FGF-Regulated ETV Transcription Factors Control FGF-SHH Feedback Loop in Lung Branching.
Sun et al., Madison, United States. In Dev Cell, Dec 2015
Here we show that loss of FGF-activated transcription factor genes, Etv4 and Etv5 (collectively Etv), led to prolonged branch tip growth and delayed new branch formation.
ACLY and ACC1 Regulate Hypoxia-Induced Apoptosis by Modulating ETV4 via α-ketoglutarate.
Chi et al., Durham, United States. In Plos Genet, Oct 2015
Additionally, the loss of ACLY or ACC1 reduced levels and activities of the oncogenic transcription factor ETV4. Silencing ETV4 also protected cells from hypoxia-induced apoptosis and led to remarkably similar transcriptional responses as with silenced ACLY or ACC1, including an anti-apoptotic program.
C-kit signaling promotes proliferation and invasion of colorectal mucinous adenocarcinoma in a murine model.
Zhou et al., Beijing, China. In Oncotarget, Oct 2015
Significantly, c-kit strongly promoted tumor cell invasiveness by increasing ETV4, which induced MMP7 expression and epithelial-mesenchymal transition (EMT) via ERK pathway.
Unusual Clinical Presentation of Gastrointestinal Clear Cell Sarcoma.
Imyanitov et al., Saint Petersburg, Russia. In Gastrointest Tumors, Sep 2015
However, polymerase chain reaction testing for ES-specific rearrangements (EWSR1/FLI1, EWSR1/ERG, EWSR1/ETV1, EWSR1/ETV4, EWS/FEV) failed to confirm the ES origin of the neoplastic tissue.
Protein deregulation associated with breast cancer metastasis.
El-Tanani et al., Belfast, United Kingdom. In Cytokine Growth Factor Rev, Aug 2015
This review will focus on a select group of proteins, often deregulated in breast cancer metastasis, which have shown therapeutic promise, notably, EMT, E-cadherin, Osteopontin, PEA3, Transforming Growth Factor Beta (TGF-β) and Ran.
Genomic and molecular aberrations in malignant peripheral nerve sheath tumor and their roles in personalized target therapy.
Du et al., Tianjin, China. In Surg Oncol, 2013
The genomic and molecular aberrations of EGFR, IGF1R, SOX9, EYA4, TOP2A, ETV4, and BIRC5 exhibit great promise as personalized therapeutic targets for MPNST patients.
ETV1, 4 and 5: an oncogenic subfamily of ETS transcription factors.
Janknecht et al., Oklahoma City, United States. In Biochim Biophys Acta, 2012
The homologous ETV1, ETV4 and ETV5 proteins form the PEA3 subfamily of ETS transcription factors.
The coactivator activator CoAA regulates PEA3 group member transcriptional activity.
Monte et al., Lille, France. In Biochem J, 2011
Heterogeneous nuclear ribonucleoprotein-like protein CoAA interacts with PEA3 group member proteins and modulates their transcriptional activity.
PEA3 activates CXCR4 transcription in MDA-MB-231 and MCF7 breast cancer cells.
Wu et al., Shanghai, China. In Acta Biochim Biophys Sin (shanghai), 2011
These results indicated that PEA3 could activate CXCR4 promoter transcription and promote breast cancer metastasis.
The role of Pea3 group transcription factors in esophageal squamous cell carcinoma.
El-Tanani et al., Belfast, United Kingdom. In Am J Pathol, 2011
Pea3 and Erm, but not Er81, play an important role in the progression of esophageal squamous cell carcinoma
PEA3/ETV4-related transcription factors coupled with active ERK signalling are associated with poor prognosis in gastric adenocarcinoma.
Sharrocks et al., Manchester, United Kingdom. In Br J Cancer, 2011
High PEA3 expression is associated with gastric adenocarcinoma.
COP1 is a tumour suppressor that causes degradation of ETS transcription factors.
Dixit et al., San Francisco, United States. In Nature, 2011
The proto-oncogenes ETV1, ETV4 and ETV5 encode transcription factors in the E26 transformation-specific (ETS) family, which includes the most frequently rearranged and overexpressed genes in prostate cancer.
NOTCH-1 and NOTCH-4 are novel gene targets of PEA3 in breast cancer: novel therapeutic implications.
Osipo et al., Maywood, United States. In Breast Cancer Res, 2010
Notch-1 and Notch-4 are novel transcriptional targets of PEA3 in breast cancer cells.
Etv4 and Etv5 are required downstream of GDNF and Ret for kidney branching morphogenesis.
Costantini et al., New York City, United States. In Nat Genet, 2009
Etv4 is positively regulated by Ret signaling in the ureteric bud tips.
ETS gene fusions in prostate cancer.
Cooper et al., Male, Maldives. In Nat Rev Urol, 2009
Fusions involving ETV1, ETV4 and ETV5 occur less frequently but exhibit greater variability in fusion structure with 12 unique 5' fusion partners identified so far.
The roles and action mechanisms of p160/SRC coactivators and the ANCCA coregulator in cancer.
Chen et al., Sacramento, United States. In Prog Mol Biol Transl Sci, 2008
We summarize results that the SRCs may contribute to tumorigenesis and disease progression through transcription factors such as E2F, PEA3, and AP-1 and through an intimate control of signaling pathways of growth factors-Akt and the receptor tyrosine kinases.
Gene panel model predictive of outcome in men at high-risk of systemic progression and death from prostate cancer after radical retropubic prostatectomy.
Vasmatzis et al., Rochester, United States. In J Clin Oncol, 2008
RESULTS: A model incorporating gene expression of topoisomerase-2a, cadherin-10, the fusion status based on ERG, ETV1, and ETV4 expression, and the aneuploidy status resulted in a 0.81 area under the curve (AUC) in receiver operating characteristic statistical analysis for the identification of men with systemic progression and death from high grade prostate cancer.
Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer.
Chinnaiyan et al., Ann Arbor, United States. In Nature, 2007
Recently, we identified recurrent gene fusions involving the 5' untranslated region of the androgen-regulated gene TMPRSS2 and the ETS (E26 transformation-specific) family genes ERG, ETV1 or ETV4 in most prostate cancers.
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