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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 crucial for the maintenance of tight junction protein (show OCLN Proteins) assembly in the lung epithelium.
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.
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.
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.
Low EYA1 expression is associated with gastric carcinoma.
results showed evidence of weak association between the two SNPs of EYA1 (rs13260349 and rs2380716) and nonsyndromic orofacial clefts.
Novel EYA1 mutations may add to the genotypic and phenotypic spectrum of BOR syndrome in the East Asian population.
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