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Eyes absent homolog 2

Eya2, eyes absent 2
This gene encodes a member of the eyes absent (EYA) family of proteins. The encoded protein may be post-translationally modified and may play a role in eye development. A similar protein in mice can act as a transcriptional activator. Alternative splicing results in multiple transcript variants, but the full-length natures of all of these variants have not yet been determined. [provided by RefSeq, Jul 2009] (from NCBI)
Top mentioned proteins: Six1, BOP, CAN, PAX3, Pax6
Papers on Eya2
New transcription factors involved with postnatal ventral prostate gland development in male Wistar rats during the first week.
Carvalho et al., Campinas, Brazil. In Life Sci, Jan 2016
KEY FINDINGS: 16 TFs were studied and we found an increased expression of Eya2, Lhrh and Znf142, invariable levels of Znf703 and Dbp, and decreased expression of 11 others at postnatal development day 3 and 6 as compared to day zero.
Aberrant hypomethylation and overexpression of the eyes absent homologue 2 suppresses tumor cell growth of human lung adenocarcinoma cells.
Xiao et al., Kunming, China. In Oncol Rep, Nov 2015
The eyes absent homologue 2 (EYA2) is a dual-functional transcription factor/phosphatase that plays a critical role in neoplasia.
The SIX1-EYA transcriptional complex as a therapeutic target in cancer.
Ford et al., Aurora, United States. In Expert Opin Ther Targets, Feb 2015
Importantly, SIX1 and EYA are often co-overexpressed in tumors, and the SIX1-EYA2 interaction has been shown to be critical for metastasis in a breast cancer model.
Fgf-signaling-dependent Sox9a and Atoh1a regulate otic neural development in zebrafish.
Liu et al., Beijing, China. In J Neurosci, Feb 2015
Sox9a and Atoh1a coregulate numerous downstream factors identified through our ChIP-seq analyses, including Tlx2 and Eya2.
Transcriptome of Atoh7 retinal progenitor cells identifies new Atoh7-dependent regulatory genes for retinal ganglion cell formation.
Klein et al., Houston, United States. In Dev Neurobiol, 2014
Notably, many genes enriched in Atoh7-expressing RPCs encoded transcriptional regulators, and several were direct targets of ATOH7, including, and unexpectedly, Ebf3 and Eya2.
A phosphotyrosine switch determines the antitumor activity of ERβ.
Li et al., In J Clin Invest, 2014
Additionally, the c-ABL tyrosine kinase and EYA2 phosphatase directly and diametrically controlled the phosphorylation status of Y36 and subsequent ERβ function.
Foxi3 is necessary for the induction of the chick otic placode in response to FGF signaling.
Groves et al., Houston, United States. In Dev Biol, 2014
Mis-expression of Foxi3 was sufficient to induce markers of non-neural ectoderm such as Dlx5, and the PPR such as Six1 and Eya2.
Allosteric inhibitors of the Eya2 phosphatase are selective and inhibit Eya2-mediated cell migration.
Zhao et al., Aurora, United States. In J Biol Chem, 2014
We have previously identified a class of N-arylidenebenzohydrazide compounds that specifically inhibit the Eya2 phosphatase.
Epigenetic silencing of EYA2 in pancreatic adenocarcinomas promotes tumor growth.
Goggins et al., Baltimore, United States. In Oncotarget, 2014
To identify potentially important genes dysregulated in pancreatic cancer, we analyzed genome-wide transcriptional analysis of pancreatic cancers and normal pancreatic duct samples and identified the transcriptional coactivator, EYA2 (Drosophila Eyes Absent Homologue-2) as silenced in the majority of pancreatic cancers.
miR-30a suppresses breast cancer cell proliferation and migration by targeting Eya2.
Lv et al., Beijing, China. In Biochem Biophys Res Commun, 2014
Aberrant expression of Eya2 has been documented in a variety of cancers and correlates with clinical outcome.
Investigation of 305 patients with myelodysplastic syndromes and 20q deletion for associated cytogenetic and molecular genetic lesions and their prognostic impact.
Haferlach et al., München, Germany. In Br J Haematol, 2014
By aCGH (n = 30), the minimal common deleted region (CDR) was flanked by PTPRT (20q13·11) and EYA2 (20q13·12).
The role of SNP-loop diuretic interactions in hypertension across ethnic groups in HyperGEN.
Rao et al., Saint Louis, United States. In Front Genet, 2012
For EA, promising SNPs for SBP were identified in ESR1 and for DBP in SPATS2L and EYA2.
Transcription coactivator Eya2 is a critical regulator of physiological hypertrophy.
Park et al., Kwangju, South Korea. In J Mol Cell Cardiol, 2012
Eya2 in a physical complex with Six1 plays a critical role in physiological hypertrophy.
Eya2 is required to mediate the pro-metastatic functions of Six1 via the induction of TGF-β signaling, epithelial-mesenchymal transition, and cancer stem cell properties.
Ford et al., Aurora, United States. In Oncogene, 2012
Data implicate Eya2 as a necessary co-factor for many of the metastasis promoting functions of Six1.
Crystal structure of ED-Eya2: insight into dual roles as a protein tyrosine phosphatase and a transcription factor.
Kim et al., Taejŏn, South Korea. In Faseb J, 2010
Based on observation that the dachshund-binding site is located between the catalytic core & Sine Oculis binding sites within ED-Eya2, we propose that catalytic activity can be translated to SO binding through DAC, which acts as a transcriptional switch.
[Expression of EYA2 in non-small cell lang cancer].
Ye et al., Beijing, China. In Zhonghua Zhong Liu Za Zhi, 2009
Expression of EYA2 in lung adenocarcinoma is augmented.
Dephosphorylation of the C-terminal tyrosyl residue of the DNA damage-related histone H2A.X is mediated by the protein phosphatase eyes absent.
Tonks et al., New York City, United States. In J Biol Chem, 2009
EYA2 and EYA3 displayed specificity for Tyr-142 of H2A.X
Genome-wide analysis of survival in early-stage non-small-cell lung cancer.
Christiani et al., Boston, United States. In J Clin Oncol, 2009
and all five were located in known genes: STK39, PCDH7, A2BP1, and EYA2.
G(z) signaling: emerging divergence from G(i) signaling.
Wong et al., Hong Kong, Hong Kong. In Oncogene, 2001
Functional interactions of the alpha subunit of G(z) (Galpha(z)) with the NKR-P1 receptor, Galpha(z)-specific regulator of G protein signaling, p21-activated kinase, G protein-regulated inducers of neurite outgrowth, and the Eya2 transcription cofactor have been demonstrated.
A human homologue of the Drosophila eyes absent gene underlies branchio-oto-renal (BOR) syndrome and identifies a novel gene family.
Petit et al., Paris, France. In Nat Genet, 1997
A highly conserved 271-amino acid C-terminal region was also found in the products of two other human genes (EYA2 and EYA3), demonstrating the existence of a novel gene family.
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