Ask about this productRelated genes to: EYA2 antibody
- Gene:
- EYA2 NIH gene
- Name:
- EYA transcriptional coactivator and phosphatase 2
- Previous symbol:
- -
- Synonyms:
- EAB1
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-24
- Date modifiied:
- 2016-10-05
Related products to: EYA2 antibody
Related articles to: EYA2 antibody
- Seasonal morphological brain plasticity plays a key role in driving adaptive behavioural responses. Structural changes in the brain including the hippocampus and amygdala (nucleus taeniae in birds), across photoperiods are thought to underlie seasonal shifts in emotional state. For humans, this includes manifestations of short photoperiod seasonal affective disorder (SAD). While morphological brain changes are well documented, the associated transcriptomic dynamics remain poorly understood. Here, we examined the transcriptomes of the hippocampus and amygdala or nucleus taeniae in two highly photoperiodic species, the Siberian hamster (Phodopus sungorus) and the Japanese quail (Coturnix japonica), to identify transcriptomic changes which could underpin seasonal shifts in emotional state. Hamsters and quail exhibited robust physiological changes between long and short photoperiod treatment. Under short photoperiod, hamsters displayed anxiety-like behaviour (increased grooming) in the open field test. Transcriptomic analysis of the amygdala in hamsters identified 76 significantly differentially expressed (DE) transcripts (including transthyretin, TTR) and prolactin receptor, PRLR as differentially expressed, but not significantly. In the quail nucleus taeniae, we found 54 DE transcripts (including tenascin-C, TNC). In the hamster hippocampus, 14 DE transcripts were found, including mahogunin ring finger-1 (MGRN1), and 31 in the quail hippocampus, including eyes absent-2 (Eya2). These findings provide novel insights into the transcriptomic mechanisms underpinning seasonal affective states and suggest potential conserved roles for prolactin and thyroid hormone signalling in mediating seasonal changes in physiology and affective behaviour, particularly in the Siberian hamster. - Source: PubMed
Publication date: 2026/08/22
Liddle Timothy AStewart CalumPérez Jonathan HMeddle Simone LStevenson Tyler J - Post-Acute Sequelae of COVID-19 (PASC) is increasingly associated with long-term cardiovascular complications, yet the underlying molecular mechanisms, remain poorly understood. Host genetic susceptibility is likely to modulate post-viral cardiac vulnerability, but its interaction with persistent molecular remodelling after SARS-CoV-2 infection has not been systematically investigated. We employed an integrative multi-omics framework combining a pilot genome-wide association study (GWAS) of Indian PASC patients with post-acute cardiac transcriptomic profiling from a SARS-CoV-2-infected Golden Syrian hamster (GSH) model. GWAS signals were mapped to differentially expressed genes, followed by integrative stratification based on genetic risk and transcriptional perturbation. Consequences of genetic variations were quantified using structural bioinformatics approaches involving Molecular Dynamics. GWAS identified multiple loci associated with PASC, including genes implicated in arrhythmia, myocardial remodelling, vascular signaling, and cardiometabolic regulation. Integration with post-acute cardiac transcriptomics of GSH revealed 15 genes with convergent genetic and transcriptional evidence. Although no global monotonic correlation was observed between genetic risk and expression magnitude, genes segregated into distinct mechanistic classes, including genetically primed and virally activated drivers, inherited susceptibility genes with minimal post-viral expression change, and virus-driven transcriptional responses. Structural and molecular dynamics analyses of EYA2, TTN, VAV2, and KCNQ1 demonstrated variant-specific destabilization affecting myocardial stress adaptation, sarcomeric mechanics, vascular signalling, and cardiac electrical stability. These findings support a model where inherited genetic susceptibility interacts with persistent post-infectious cardiac remodelling to drive chronic cardiovascular dysfunction observed in PASC patients. Integrative host genomics provides a mechanistic framework for risk stratification and precision surveillance of post-COVID cardiovascular disease (CVD). - Source: PubMed
Publication date: 2026/07/21
Rao Rajas MKumar NarendraP Shaminth PrasadRao Manvitha JP Farooq HussainN S Chaitanya ShreeN HarithaAcharya ArpanByrareddy Siddappa NDas Ranajit - Branchio-oto-renal (BOR) syndrome is an autosomal dominant condition characterized by variable malformations including hearing loss and renal dysfunction. Variants in SIX1 or its activating co-factor EYA1 are causative in about 50% of patients. Some patients carrying BOR variants also present with craniosynostosis, indicating that cranial skeletal dysmorphologies could be an under-diagnosed feature. To date, most studies on the role of SIX1 have focused on its role in the cranial placode-based development of the inner ear, whereas its role in the neural crest cells of the mandibular arch, which will give rise to the jaws and middle ear ossicles, is less well characterized. Here, we present novel expression profiles of three putative SIX1 co-factors (PA2G4, MCRS1, and SOBP) in the developing mouse first pharyngeal arch and tooth. SIX1 colocalizes with PA2G4, MCRS1, and SOBP within the oral domain of the mandibular arch and during odontogenesis, although each exhibits a distinct expression pattern. Functional analyses revealed that SOBP binds SIX1, EYA1, and EYA2 and represses both SIX1 + EYA1 and SIX1 + EYA2 transcriptional activity, whereas MCRS1 binds only SIX1 and selectively represses SIX1 + EYA2 activity. In contrast, PA2G4 does not bind SIX1, yet modulates SIX1 + EYA2 activity. We further show that SIX1 is required for proper expression of Pa2g4, Mcrs1, and Sobp in the mouse mandibular arch. Collectively, these results demonstrate that regulation of SIX1 + EYA transcriptional activity is highly context dependent, occurs through both direct and indirect mechanisms, and differs between SIX1 + EYA1 and SIX1 + EYA2 complexes. These findings reveal species-specific differences and uncover a level of regulatory complexity not previously identified in Xenopus studies. - Source: PubMed
Publication date: 2026/07/16
Jourdeuil KarynChukwuocha KelechiGafurova JasminaBen-Mayor AshleyMoody Sally ATavares Andre L P - Cyclin-dependent kinase 6 (CDK6) has been reported to exert tumor-suppressive functions through its non-enzymatic activity and promotes the degradation of the oncogenic driver EYA2. This suggests a potential strategy for targeted protein degradation by exploiting endogenous protein-protein interactions. Here, we report the design and synthesis of a bifunctional small molecule, EC21, capable of simultaneously engaging CDK6 and EYA2. Structure-guided design based on the reported binding modes of palbociclib and the EYA2 inhibitor ETC-616 enabled the identification of EC21 as a lead compound. Biological studies demonstrated that EC21 effectively reduced EYA2 protein levels in breast cancer cells in a time- and concentration-dependent manner through a ubiquitin-proteasome-dependent process. Mechanistic investigations indicated that EC21 enhances the interaction between CDK6 and EYA2, thereby promoting EYA2 degradation. Functional analyses further revealed that EC21 disrupts DNA damage repair pathways and significantly suppresses breast cancer cell proliferation. Importantly, EC21 exhibited pronounced antitumor activity in a syngeneic breast cancer mouse model and reduced EYA2 protein levels in tumor tissues without apparent toxicity. Collectively, these findings demonstrate that pharmacological stabilization of the CDK6-EYA2 interaction represents a feasible strategy for inducing EYA2 degradation and provides a potential therapeutic approach for EYA2-driven breast cancer. - Source: PubMed
Publication date: 2026/06/18
Zhang YanhuiKan ChenchenAi JiaxinZhou RuiZhao QunGao JiahuiWang YuWu ZhaofengQin XiaoyuMa JuntingYuan BinLiu MingmingLuo Qichao - In humans, retinal-neuron death, optic-nerve injuries, and associated neurodegenerative diseases, such as glaucoma and age-related macular degeneration, often lead to permanent vision loss. While the capacity for regeneration is low in the human nervous system, including the retina, some non-mammalian vertebrate species, including zebrafish, are capable of endogenous neuronal regeneration after injury. Unlike mammals, zebrafish do not form a scar that inhibits axonal and neuronal regeneration after injury. Rather, they harbor neural progenitor and stem-cell populations allowing regeneration of entire parts of the nervous system and restoration of tissue integrity and function. In the zebrafish retina, cycling neural progenitor cells of the ciliary marginal zone and quiescent resident neural stem cells (the latter of which are also called Müller glial cells) participate in neuronal regeneration following different types of injury. In this study, we report the identification of a novel, additional cellular source participating in neuronal regeneration of neurons in the zebrafish retina after genetic ablation of retinal ganglion cells. Before injury, these progenitor cells express molecular markers of neural-crest-cell and/or fibroblast identity, such as , , and , while after neuronal ablation they also express proneural factors including the and genes. Combining genetic ablation of neurons with photoconversion or Cre/Lox-dependent genetic lineage tracing of -expressing cells, we demonstrated that these cells can differentiate into post-mitotic retinal neurons in the ganglion cell layer (GCL) in the absence of cell proliferation. We also showed, surprisingly, that this progenitor population locally produces mRNA, and that insulin signaling is involved in the accumulation of mesenchymal-derived neural progenitors in the GCL and in their subsequent transdifferentiation into RGCs. This work reveals an unexpected and novel cellular mechanism of transdifferentiation, dependent on a neural-crest-derived mesenchymal cell population, participating in neuronal regeneration in the zebrafish retina. The discovery of this plastic cell population could potentially lead to new strategies to promote the formation of new neurons in the mammalian retina. - Source: PubMed
Publication date: 2026/05/22
Diwedi BidhiNeog AninditaBaanannou AissetteDas PrithaMenard RomainHalluin CarolineMorse DexterEmmerich KevinThierer James HPatnaude MichaelBonnet FredericGraber Joel HMumm Jeff SMadelaine Romain