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Notch is regulated by the threonine phosphatase activity of Eya1. Eya1 dephosphorylates p-threonine-2122 of the Notch1 intracellular domain (Notch1 ICD), which increases the stability of Notch1 ICD and maintains Notch signaling activity in the non-neuronal epibranchial placodal cells.
data support a model where Eya-Six may form a complex to regulate nephron progenitor cell development before metanephric specification and are critical mesenchymal factors for inducing nephric duct development.
Eya1 phosphatase promotes Shh signaling during hindbrain development and oncogenesis
results reveal a functional link between Eya1, Six2, and Myc 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 and PI3K/Akt signal pathways restrain the GSK3/Fbw7-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 promoter.
These findings uncover novel functions for Six1-Eya1-SHH 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 drive the neuronal developmental program in cooperation with the SWI/SNF chromatin-remodeling complex and SOX2 in the mammalian inner ear.
Deletion of either or both Six1 and Eya1 genes results in genitourinary tract defects including persistent cloaca; hypospadias; and hypoplastic genitalia.
Six1 and Eya1 genetically interacted with Fgf8 and the Tbx1 pathway that is crucial for cardiovascular and craniofacial morphogenesis
Eya1 function is critical for proper coordination of lung epithelial, mesenchymal and vascular development.
Data report the identification of the related proteins Sipl1 (Shank-interacting protein-like 1) and Rbck1 (RBCC protein interacting with PKC1) as novel interaction partners of Eya1.
Eya1 IS required for normal ear develoPMENT
Impaired interactions between mouse Eyal harboring mutations found in patients with branchio-oto-renal syndrome and Six, Dach, and G proteins
Eya1 is required for the morphogenesis of mouse thymus, parathyroid and thyroid.
The phosphatase function of Eya switches the function of Six1-Dach from repression to activation, causing transcriptional activation through recruitment of co-activators
Data identify Six1 and Eya1 as the first transcriptional complex that is able to reprogram adult slow-twitch oxidative fibers toward a fast-twitch glycolytic phenotype.
constructs of the homologous region ( Eya1HR and Eya4HR) interact with Six1 prey constructs, although no interaction with Dach1 prey was demonstrable
First report of an essential role of Eya1, which is required for lineage-specific differentiation of adenohypophyseal cells, but not for their survival.
Six1 and Eya1 can both promote and arrest neuronal differentiation by activating the Notch 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-renal syndrome.
Eya1 and Six1 are required for both the regulation of placodal neuronal progenitor proliferation, through their effects on SoxB1 expression, and subsequent neuronal differentiation.
SIX1/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-Myc binding to regulate the FBW7-mediated Myc degradation machinery in breast cancer cells.
miR-101 is downregulated in breast cancer, and can inhibit cell proliferation and promote apoptosis by targeting EYA1 through the Notch 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, 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/Akt 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-Renal Syndrome and focal glomerulosclerosis.
Two novel EYA1 mutations (c.466C>T and c.1735delG) were identified in two families with BOR syndrome.
A 23 year old woman with Branchio-oto-renal syndrome presented with a novel heterozygous mutation 1420-1421delCC in exon 14 of EYA-1 gene.
Study reports a screening of 140 patients from 124 families with Branchio-oto-renal and identified 36 EYA1 mutations in 42 unrelated patients, 2 mutations, and 1 change of unknown significance in SIX1 in 3 unrelated patients, but no mutation in SIX5.
This report describes the expanded phenotype of individuals, resulting from contiguous gene deletion involving the EYA1 gene and provides a molecular description of the genomic rearrangements involving this gene in branchio-oto-renal syndrome.
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