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results implicate Eya4/Six1 regulates normal cardiac function via p27/casein kinase-2alpha/histone deacetylase 2 and indicate that mutations within this transcriptional complex and signaling cascade lead to the development of cardiomyopathy.
constructs of the homologous region ( Eya1HR and Eya4HR) interact with Six1 prey constructs, although no interaction with Dach1 prey was demonstrable
Eya4(-/-) mice developed otitis media with effusion; anatomic studies revealed abnormal middle ear cavity and eustachian tube dysmorphology.
that Eyes absent 4 (EYA4), originally identified as a co-transcription factor, stimulates the expression of IFN-beta and CXCL10 in response to the undigested DNA of apoptotic cells
the novel missense mutation c.1855T>G (p.W619G) in EYA4 causing autosomal dominant non-syndromic hearing impairment in the selected Chinese family, was identified.
Findings identified eyes absent homolog 4 (EYA4) as a tumor suppressor that disrupts aberrant activation of the nuclear factor kappa B (NF-kappaB)/RAP1 protein signaling pathway and thus orchestrates a physiological impediment to hepatocellular carcinoma (HCC) growth and invasion.
Overexpression of EYA4 enhanced glioma cell proliferation, and EYA4 suppressed the expression of p27Kip1 directly in these cells.
Although the clinical patient outcome of our 38 Colorectal Cancer patients was not associated with EYA4 promoter hypermethylation, the high frequency of this methylation and its high sensitivity and specificity to neoplastic cells may qualify EYA4 promoter methylation as a potential candidate screening marker in Iranian population and may help to improve early detection of CRC.
Eyes absent homolog 4 (Drosophila) protein (EYA4) is frequently hypermethylated in esophageal squamous cell carcinoma (ESCC) and may function as a tumor suppressor gene in the development of ESCC.
identified novel EYA4 mutation can be considered responsible of the hearing loss observed in the proband and her father, while a dual molecular diagnosis was reached in the relatives co-segregating the EYA4 and the PAX3 mutations
EYA4 hypermethylation is associated with colorectal cancer.
EYA4 functions as tumor suppressor gene in pancreatic ductal adenocarcinoma via repressing beta-catenin/ID2 activation, and was an independent prognostic factor in PDAC.
Low expression of EYA4 is associated with oral cancer.
We discovered two genome-wide significant SNPs. The first was novel and near ISG20. The second was in TRIOBP, a gene previously associated with prelingual nonsyndromic hearing loss. Motivated by our TRIOBP results, we also looked at exons in known hearing loss genes, and identified two additional SNPs, rs2877561 in ILDR1 and rs9493672 in EYA4 (at a significance threshold adjusted for number of SNPs in those regions).
Locus polymorphism of rs3813346 was associated with the risk of developing noise-induced hearing loss in the dominance model, the codominance model and the addictive model. Generalized multiple dimensionality reduction indicated that the combined interaction of the 2 loci-rs3813346 and rs9493627-significantly affected the incidence of noise-induced hearing loss.
Up to now, merely 7 loci have been linked to mid-frequency hearing loss. Only four genetic mid-frequency deafness genes, namely, DFNA10 (EYA4), DFNA8/12 (TECTA), DFNA13 (COL11A2), DFNA44 (CCDC50), have been reported to date. [review]
study identified EYA4 gene as targets for AML1-ETO and indicated it as a novel tumor suppressor gene. In addition, we provided evidence that EYA4 gene might be a novel therapeutic target and a potential candidate for treating AML1-ETO+ t (8;21) AML.
Loss of EYA4 expression is associated with intrahepatic cholangiocarcinoma.
The identification of a novel EYA4 truncation mutation associated with DFNA10, rather than syndromic hearing loss, supports a previously reported genotype-phenotype correlation in this gene.
In a Dutch family with c.464del EYA4 mutation, hearing impairment begins as a mid-frequency hearing impairment in childhood and develops into a high-frequency, moderate hearing impairment later in life.
Genetic variations in the EYA4, GRHL2 and DFNA5 genes and their interactions with occupational noise exposure may play an important role in the incidence of noise-induced hearing loss (NIHL).
analysis of an EYA4 mutation causing hearing loss in a Chinese DFNA family
A novel missense mutation c.1643C>G (p.T548R) in EYA4 may cause autosomal dominant non-syndromic hearing impairment.
This gene encodes a member of the eyes absent (EYA) family of proteins. The encoded protein may act as a transcriptional activator through its protein phosphatase activity, and it may be important for eye development, and for continued function of the mature organ of Corti. Mutations in this gene are associated with postlingual, progressive, autosomal dominant hearing loss at the deafness, autosomal dominant nonsyndromic sensorineural 10 locus. Defects in this gene are also associated with dilated cardiomyopathy 1J. Three transcript variants encoding distinct isoforms have been identified for this gene.
eyes absent homolog 4
, dJ78N10.1 (eyes absent)
, eyes absent 4