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Eyes absent 3 homolog

This gene encodes a member of the eyes absent (EYA) family of proteins. The encoded protein may act as a transcriptional activator and have a role during development. A similar protein in mice acts as a transcriptional activator. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Eya2, BOP, ACID, CAN, Six1
Papers on Eya3
The Eyes Absent Proteins in Developmental and Pathological Angiogenesis.
Hegde et al., Cincinnati, United States. In Am J Pathol, Feb 2016
We find that the ability of the EYA proteins to promote endothelial cell (EC) migration contributes to a delay in postnatal development of the retinal vasculature when Eya3 is deleted specifically in ECs.
Binary Switching of Calendar Cells in the Pituitary Defines the Phase of the Circannual Cycle in Mammals.
Loudon et al., Manchester, United Kingdom. In Curr Biol, Nov 2015
We show that individual PT thyrotrophs can be in one of two binary states reflecting either a long (EYA3(+)) or short (CHGA(+)) photoperiod, with the relative proportion in each state defining the phase of the circannual cycle.
Circadian synchronization determines critical day length for seasonal responses.
Kumar et al., Delhi, India. In Physiol Behav, Sep 2015
To investigate this, we measured expression levels of genes implicated in the photoperiod-induced changes in reproduction (EYA3, TSH beta, DIO2, DIO3, GNRH and GNIH) and metabolism (SIRT1, HMGCR, FASN and PPAR alpha) in photosensitive redheaded buntings subjected to light-dark cycles of varying period lengths (T-photocycles).
A photoperiodic molecular response in migratory redheaded bunting exposed to a single long day.
Kumar et al., Delhi, India. In Gen Comp Endocrinol, 2014
A long day response is triggered by the activation of EYA3 (eyes absent 3) and TSH-β (thyroid stimulating hormone beta subunit) genes in the pars tuberalis (PT).
Clocks for all seasons: unwinding the roles and mechanisms of circadian and interval timers in the hypothalamus and pituitary.
Loudon et al., Manchester, United Kingdom. In J Endocrinol, 2014
Summer-like melatonin signals activate a PT-expressed clock-regulated transcription regulator (EYA3), which in turn drives the expression of the TSHβ sub-unit, leading to a sustained increase in TSH expression.
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
Herein, we demonstrate that these compounds are reversible inhibitors that selectively inhibit the phosphatase activity of Eya2, but not Eya3.
t(6;9)(p22;q34)/DEK-NUP214-rearranged pediatric myeloid leukemia: an international study of 62 patients.
Hasle et al., In Haematologica, 2014
Gene expression profiling showed a unique signature characterized by significantly higher expression of EYA3, SESN1, PRDM2/RIZ, and HIST2H4 genes.
Transcript co-variance with Nestin in two mouse genetic reference populations identifies Lef1 as a novel candidate regulator of neural precursor cell proliferation in the adult hippocampus.
Badea et al., Wakefield, United States. In Front Neurosci, 2013
In conclusion, our combination of bioinformatics approaches identified six novel candidate genes involved in adult neurogenesis; Amer3, Eya3, Mtdh, Nr4a3, Polr2a, and Tbkbp1.
Structure-activity relationships of benzbromarone metabolites and derivatives as EYA inhibitory anti-angiogenic agents.
Hegde et al., Seattle, United States. In Plos One, 2012
Longer substituents at the 2 position of the benzofuran ring promoted EYA3 binding and inhibition, but were less effective in cellular assays, likely reflecting non-specific protein binding and a resulting reduction in free, bio-available inhibitor.
Dual recognition of phosphoserine and phosphotyrosine in histone variant H2A.X by DNA damage response protein MCPH1.
Mer et al., Rochester, United States. In Proc Natl Acad Sci U S A, 2012
In response to DNA double-strand breaks (DSBs), H2A.X is instantaneously phosphorylated at Ser139 by the kinases ATM and ATR and is progressively dephosphorylated at Tyr142 by the Eya1 and Eya3 tyrosine phosphatases, resulting in a temporal switch from a postulated diphosphorylated (pSer139, pTyr142) to monophosphorylated (pSer139) H2A.X state.
Six1 and Six1 cofactor expression is altered during early skeletal muscle overload in mice.
Kostek et al., Columbia, United States. In J Physiol Sci, 2012
Six1 is a transcription factor that, along with cofactors (Eya1, Eya3, and Dach2), regulates skeletal muscle fiber-type and development.
EWS/FLI1 regulates EYA3 in Ewing sarcoma via modulation of miRNA-708, resulting in increased cell survival and chemoresistance.
Ford et al., Aurora, United States. In Mol Cancer Res, 2012
Herein, we show that the DNA repair protein and transcriptional cofactor, EYA3, is highly expressed in Ewing sarcoma tumor samples and cell lines compared with mesenchymal stem cells, the presumed cell-of-origin of Ewing sarcoma, and that it is regulated by the EWS/FLI1 fusion protein transcription factor.
The EYA tyrosine phosphatase activity is pro-angiogenic and is inhibited by benzbromarone.
Hegde et al., Cincinnati, United States. In Plos One, 2011
Using RNA interference techniques we show that EYA3 depletion in human umbilical vein endothelial cells inhibits transwell migration as well as Matrigel-induced tube formation.
Characterization of the threonine-phosphatase of mouse eyes absent 3.
Nagata et al., Kyoto, Japan. In Febs Lett, 2011
Data showed that the 68-amino acid domain between positions 53 and 120 was necessary and sufficient for its threonine-phosphatase activity.
Acute induction of Eya3 by late-night light stimulation triggers TSHβ expression in photoperiodism.
Ueda et al., Kōbe, Japan. In Curr Biol, 2011
Data demonstrate that Eya3 and its partner Six1 synergistically activate TSHbeta expression and that this activation is further enhanced by Tef and Hlf.
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
Ski regulates muscle terminal differentiation by transcriptional activation of Myog in a complex with Six1 and Eya3.
Stavnezer et al., Cleveland, United States. In J Biol Chem, 2009
Ski is necessary for muscle terminal differentiation and that it exerts this role, at least in part, through its association with Six1 and Eya3 to regulate the Myog transcription
Pleiotropic effects in Eya3 knockout mice.
Graw et al., München, Germany. In Bmc Dev Biol, 2007
There was no obvious defect in the eyes, ears and kidneys of Eya3 mutant mice. Homozygous mutants displayed decreased bone mineral content and shorter body length.
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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