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Xeya3 is a key factor for the formation and size control of brain and eyes in vertebrates.
Data demonstrate that Eya3 and its partner Six1 (show SIX1 Proteins) synergistically activate TSHbeta (show TSHB Proteins) expression and that this activation is further enhanced by Tef (show TEF Proteins) and Hlf (show HLF Proteins).
The phosphatase function of Eya switches the function of Six1 (show SIX1 Proteins)-Dach (show DACH1 Proteins) from repression to activation, causing transcriptional activation through recruitment of co-activators
Experiments performed in cultured Drosophila cells and in vitro indicate that Eyes absent has intrinsic protein tyrosine phosphatase (show ACP1 Proteins) activity and can autocatalytically dephosphorylate itself
Ski (show SKI Proteins) is necessary for muscle terminal differentiation and that it exerts this role, at least in part, through its association with Six1 (show SIX1 Proteins) and Eya3 to regulate the Myog (show MYOG Proteins) transcription
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.
Benzbromarone metabolites and derivatives function as EYA3 inhibitory anti-angiogenic agents.
These studies identify EYA3 as a novel mediator of chemoresistance in Ewing sarcoma and define the molecular mechanisms of both EYA3 overexpression and of EYA3-mediated chemoresistance
EYA2 (show EYA2 Proteins) and EYA3 displayed specificity for Tyr (show TYR Proteins)-142 of H2A.X (show H2AFX Proteins)
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.
eyes absent homolog 3
, eyes absent 3
, eyes absent 3 homolog