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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 ELISA Kits) synergistically activate TSHbeta (show TSHB ELISA Kits) expression and that this activation is further enhanced by Tef (show TEF ELISA Kits) and Hlf (show HLF ELISA Kits).
The phosphatase function of Eya switches the function of Six1 (show SIX1 ELISA Kits)-Dach (show DACH1 ELISA Kits) 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 ELISA Kits) activity and can autocatalytically dephosphorylate itself
Ski (show SKI ELISA Kits) is necessary for muscle terminal differentiation and that it exerts this role, at least in part, through its association with Six1 (show SIX1 ELISA Kits) and Eya3 to regulate the Myog (show MYOG ELISA Kits) 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 ELISA Kits) and EYA3 displayed specificity for Tyr (show TYR ELISA Kits)-142 of H2A.X (show H2AFX ELISA Kits)
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