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Notch (show NOTCH1 Proteins) is regulated by the threonine phosphatase activity of Eya1. Eya1 dephosphorylates p-threonine-2122 of the Notch1 (show NOTCH1 Proteins) intracellular domain (Notch1 (show NOTCH1 Proteins) ICD), which increases the stability of Notch1 (show NOTCH1 Proteins) ICD and maintains Notch (show NOTCH1 Proteins) signaling activity in the non-neuronal epibranchial placodal cells.
Eya1 phosphatase promotes Shh (show SHH Proteins) signaling during hindbrain development and oncogenesis
results reveal a functional link between Eya1, Six2 (show SIX2 Proteins), and Myc (show MYC Proteins) in driving the expansion and maintenance of the multipotent progenitors during nephrogenesis
BOR syndrome-associated Eya1 missense mutations S454P, L472R, and L550P lead to enhanced proteasomal degradation of the Eya1 protein.
these findings reveal that the canonical Wnt (show WNT2 Proteins) and PI3K/Akt (show AKT1 Proteins) signal pathways restrain the GSK3/Fbw7 (show FBXW7 Proteins)-dependent Eya1 ubiquitination, and they further suggest that dysregulation of this novel axis contributes to tumorigenesis.
The EYA1 phosphatase regulates cell-cycle control via transcriptional complex formation at the cyclin D1 (show CCND1 Proteins) promoter.
These findings uncover novel functions for Six1 (show SIX1 Proteins)-Eya1-SHH (show SHH Proteins) pathway during the saccular phase of lung morphogenesis.
EYA1 is efficiently degraded during mitotic exit in a ANAPC1-dependent manner and these two proteins physically interact.
EYA1 and SIX1 (show SIX1 Proteins) drive the neuronal developmental program in cooperation with the SWI (show SMARCA1 Proteins)/SNF (show SNRPA Proteins) chromatin-remodeling complex and SOX2 (show SOX2 Proteins) in the mammalian inner ear.
Deletion of either or both Six1 (show SIX1 Proteins) and Eya1 genes results in genitourinary tract defects including persistent cloaca; hypospadias; and hypoplastic genitalia.
Data report the identification of the related proteins Sipl1 (Shank-interacting protein-like 1) and Rbck1 (RBCC protein interacting with PKC1 (show RBCK1 Proteins)) as novel interaction partners of Eya1.
First report of an essential role of Eya1, which is required for lineage-specific differentiation of adenohypophyseal cells, but not for their survival.
Six1 (show SIX1 Proteins) and Eya1 can both promote and arrest neuronal differentiation by activating the Notch (show NOTCH1 Proteins) pathway genes.
These studies lend support to the hypothesis that dominant-negative effects of EYA1 mutations may have a role in the pathogenesis of branchio-oto (show PGAP1 Proteins)-renal syndrome.
Eya1 and Six1 (show SIX1 Proteins) are required for both the regulation of placodal neuronal progenitor proliferation, through their effects on SoxB1 expression, and subsequent neuronal differentiation.
SIX1 (show SIX1 Proteins)/EYA1 mutations might be partially responsible for conotruncal heart defects.
These results identify the conserved arginine residues of EYA1 that play an important role for its activity, thus implicating arginine methylation as a novel regulatory mechanism of EYA function.
A variety of DNA changes including large deletions underlie BOR syndrome in different populations, which can be detected with comprehensive genetic testing
Results found that EYA1 affects FBW7 (show FBXW7 Proteins)-Myc (show MYC Proteins) binding to regulate the FBW7 (show FBXW7 Proteins)-mediated Myc (show MYC Proteins) degradation machinery in breast cancer cells.
miR (show MLXIP Proteins)-101 is downregulated in breast cancer, and can inhibit cell proliferation and promote apoptosis by targeting EYA1 through the Notch (show NOTCH1 Proteins) signaling pathway.
Association between EYA1 three SNPs and NSOCs and suggested that maternal environmental tobacco smoke, common cold history, and alcohol consumption.
Our findings implicate this EYA1 partial duplication segregating with branchiootic phenotype in a Brazilian pedigree and is the first description of a large duplication leading to the Branchiootorenal syndrome/BO syndrom
Three causative genes for BOR syndrome have been reported thus far: EYA1, SIX1 (show SIX1 Proteins), and SIX5, but the causative genes for approximately half of all BOR patients remain unknown.[review]
we proved that the branchiooto (BO) syndrome in these cases was caused by germinal mosaicism of the EYA1 gene in either the mother or father.
PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) signaling enhances Eya1 transcription activity, which largely attributes to the phosphorylation-induced reduction of Eya1 SUMOylation.
This gene encodes a member of the eyes absent (EYA) family of proteins. The encoded protein may play a role in the developing kidney, branchial arches, eye, and ear. Mutations of this gene have been associated with branchiootorenal dysplasia syndrome, branchiootic syndrome, and sporadic cases of congenital cataracts and ocular anterior segment anomalies. A similar protein in mice can act as a transcriptional activator. Four transcript variants encoding three distinct isoforms have been identified for this gene.
eyes absent 1
, eyes absent homolog 1 (Drosophila)
, eyes absent homolog 1
, eyes absent-1
, dog eared
, eyes absent-1 beta
, eyes absent 1 homolog