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EYA1 encodes a member of the eyes absent (EYA) family of proteins. Additionally we are shipping EYA1 Proteins (3) and many more products for this protein.
Showing 10 out of 63 products:
Human Polyclonal EYA1 Primary Antibody for EIA, WB - ABIN952149
Drake, Ruteshouser, Natrajan, Harbor, Wegert, Gessler, Pritchard-Jones, Grundy, Dome, Huff, Jones, Aldred: Loss of heterozygosity at 2q37 in sporadic Wilms' tumor: putative role for miR-562. in Clinical cancer research : an official journal of the American Association for Cancer Research 2009
Show all 3 references for ABIN952149
Human Polyclonal EYA1 Primary Antibody for ELISA, WB - ABIN560818
El-Hashash, Al Alam, Turcatel, Bellusci, Warburton: Eyes absent 1 (Eya1) is a critical coordinator of epithelial, mesenchymal and vascular morphogenesis in the mammalian lung. in Developmental biology 2011
Show all 2 references for ABIN560818
Human Polyclonal EYA1 Primary Antibody for WB - ABIN2778550
Suzuki, Fujisawa, Ando, Niino, Ohsawa, Shimokata, Ohta: Alcohol dehydrogenase 2 variant is associated with cerebral infarction and lacunae. in Neurology 2004
Show all 2 references for ABIN2778550
Cow (Bovine) Polyclonal EYA1 Primary Antibody for EIA, WB - ABIN487975
Orten, Fischer, Sorensen, Radhakrishna, Cremers, Marres, Van Camp, Welch, Smith, Kimberling: Branchio-oto-renal syndrome (BOR): novel mutations in the EYA1 gene, and a review of the mutational genetics of BOR. in Human mutation 2008
Eya1 phosphatase promotes Shh (show SHH Antibodies) signaling during hindbrain development and oncogenesis
results reveal a functional link between Eya1, Six2 (show SIX2 Antibodies), and Myc (show MYC Antibodies) 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 Antibodies) and PI3K/Akt (show AKT1 Antibodies) signal pathways restrain the GSK3 (show GSK3b Antibodies)/Fbw7 (show FBXW7 Antibodies)-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 Antibodies) promoter.
These findings uncover novel functions for Six1 (show SIX1 Antibodies)-Eya1-SHH (show SHH Antibodies) pathway during the saccular phase of lung morphogenesis.
Eya1 is crucial for the maintenance of tight junction protein (show OCLN Antibodies) assembly in the lung epithelium.
EYA1 is efficiently degraded during mitotic exit in a ANAPC1 (show ANAPC1 Antibodies)-dependent manner and these two proteins physically interact.
EYA1 and SIX1 (show SIX1 Antibodies) drive the neuronal developmental program in cooperation with the SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) chromatin-remodeling complex and SOX2 (show SOX2 Antibodies) in the mammalian inner ear.
Deletion of either or both Six1 (show SIX1 Antibodies) 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 (show SHARPIN Antibodies)) and Rbck1 (RBCC protein interacting with PKC1 (show RBCK1 Antibodies)) 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 Antibodies)-renal syndrome.
Eya1 and Six1 (show SIX1 Antibodies) are required for both the regulation of placodal neuronal progenitor proliferation, through their effects on SoxB1 expression, and subsequent neuronal differentiation.
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 Antibodies), 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 Antibodies)/Akt (show AKT1 Antibodies) 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.
A novel EYA1 splice site mutation was found to be associated with Branchio-Oto (show PGAP1 Antibodies)-Renal Syndrome and focal glomerulosclerosis.
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