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
- High-fat diet (HFD) exposure is a recognized risk factor for tendinopathy and impaired tendon healing in adults, yet its effects on baseline tendon properties following early-life exposure remain poorly understood. In this study, we investigated the structural, biomechanical, and transcriptomic characteristics of Achilles tendons in 12-week-old rat offspring born to dams fed an HFD or a normal diet during gestation. Compared with controls, HFD-exposed tendons exhibited a significant reduction in anteroposterior diameter on sagittal ultrasound imaging. However, histological assessment revealed comparable cellular density and collagen fiber organization between groups. Biomechanically, HFD exposure was associated with a significant increase in tendon stiffness, while the maximum tensile load was not significantly altered. Transcriptomic profiling identified 980 differentially expressed genes, including a marked downregulation of key tenogenic markers such as Scx and Eya2, along with an enrichment of pathways related to extracellular matrix remodeling and inflammation. Gene set enrichment further revealed an upregulation of inflammatory response, adipogenesis, and osteoblast differentiation signatures. Together, these findings demonstrate that early-life HFD exposure induces biomechanical and molecular alterations in intact Achilles tendons, suggesting compromised tendon quality that may increase susceptibility to mechanical overload and injury later in life. - Source: PubMed
Publication date: 2026/04/19
Yin HeyongYuan ZiyangJiang WenliGuo Ai - Diabetic retinopathy (DR) is a complication of diabetes that affects the eyes. This study aims to identify the genetic variants associated with DR in type 2 diabetes (T2D) patients from the UK Biobank cohort (n = 16,988). - Source: PubMed
Publication date: 2026/02/25
Cai TengdaPan QiTao YiwenNangia CharviRajendrakumar Aravind LYe YunyanDottorini TaniaHaque MainulPalmer Colin NaShao YongqingMeng Weihua - Endometrial polyps (EPs) are benign overgrowths of the endometrium causing abnormal uterine bleeding and infertility. Despite their clinical significance, the molecular mechanisms underlying their development and recurrence remain poorly understood, warranting comprehensive transcriptomic investigation. We hypothesized that transcriptomic differences, particularly at the single-cell level as revealed through cellular trajectory analysis, distinguish EPs from adjacent endometrium. To investigate this, paired EP and adjacent endometrium (adEN) samples were collected from 12 women undergoing hysteroscopic polypectomy (proliferative phase, = 9; secretory phase, = 3) and analyzed using bulk and single-cell RNA sequencing (scRNA-seq). Bulk RNA-seq revealed high transcriptional similarity between EPs and adENs, with only a few differentially expressed genes (FDR < 0.05) in proliferative-phase EPs, including upregulation of and and downregulation of and , potentially reflecting epigenetic regulation and protective mechanisms against tumorigenesis. scRNA-seq identified eight major cell clusters namely stromal, epithelial, endothelial, immune, perivascular, macrophage, B cell, and ciliated populations in both tissues. Pseudotime analysis revealed a mid-transcriptional arrest and enrichment of -positive intermediate epithelial states in EPs, in contrast to the late, mature epithelial stage seen in the adENs. This aberrant epithelial maturation may be associated with impaired perivascular and endothelial differentiation, potentially contributing to defective vascular remodeling and polyp persistence. In conclusion, while EPs exhibit global transcriptomic similarity to adENs, single-cell and pseudotime analyses suggest subtle but significant disruptions in epithelial differentiation and vascular remodeling that might be involved in EPs development. Study limitations include scRNA-seq restricted to the proliferative phase, which may limit generalizability. Nevertheless, future functional studies using primary epithelial organoids derived from EPs may provide a physiologically relevant model to evaluate targeted therapeutic strategies including hormonal interventions with potential applications in infertility management. - Source: PubMed
Publication date: 2026/02/19
Pathare Amruta D SLawarde AnkitaTäär KatrinMoreno Sergio VelaApostolov ApostolModhukur VijayachitraTarassova DarjaSola-Leyva AlbertoSalumets AndresSaare MerliPeters Maire - Hernias, particularly umbilical hernias (UH), are prevalent anatomical anomalies in swine, leading to significant welfare issues and economic losses. Besides environmental factors also genetic components contribute to the development of UHs, though the exact mechanisms remain unclear. This study employed a multiple approaches integrating RNA-seq, DNA methylation analysis, Sanger sequencing, droplet digital PCR and western blot analysis to investigate the genetic and epigenetic underpinnings of UH in pigs. Muscle tissue from affected and control pigs was examined to identify differentially expressed genes (DEGs) and associated pathways. - Source: PubMed
Publication date: 2025/11/18
Wozniak JakubSzabelska-Beresewicz AlicjaZyprych-Walczak JoannaNiemyjski RafalDudek KlaudiaStachowiak MonikaNowacka-Woszuk Joanna - Self-assembly of short peptides induced by enzymes is an emerging pathway to overcome drug resistance in cancer. However, specific targeting requires optimal precursor design and understanding of subcellular interactions. In our study, we synthesized six short peptides by modifying the N-terminal motif with fluorenylmethyloxycarbonyl (Fmoc), diphenyalanine (FF), arginylglycylaspartic acid (RGD), naphthyl (Nap), and 4-nitrobenz-2-oxa-1,3-diazole (NBD) motifs and including C terminal activation groups of tyrosine phosphate (pTyr) and threonine phosphate (pThr). We utilized the tyrosine phosphatase activity of Eye Absent Enzyme (EYA) to induce self-assembly of short peptides in breast cancer cells. The subcellular interaction of P1-P6 on DNA, mitochondria, and the cell membrane were evaluated in MDA-MB-231 (receptor-negative), MCF-7 (receptor-positive), and MCF10 (nontumorigenic epithelial breast) cells. Being dephosphorylated by EYA, the peptide transformed from monomers to assembled, which was confirmed by UV absorption shift and released phosphate. Studying protein expression showed that EYA2 is expressed in breast cancer cells but is absent in normal epithelial breast cells. The peptide/assemblies first aggregate on the cell membrane, then enter the cells, and accumulate in nuclei. Fmoc-FF-pTyr and RGD-FF-pTyr demonstrated significant binding affinity for phosphatidylserine on the surface of apoptotic cells. Among these, Fmoc-FF-pTyr effectively induced DNA damage and triggered apoptosis in cancer cells while remaining nontoxic to normal cells at optimal concentrations (10 μM). Peptides containing Nap groups selectively accumulated in the mitochondria of MCF-7 and MDA-MB-231 cells, enhancing the effectiveness of the doxorubicin treatments. These results demonstrate the critical role of EISA precursor in modulating phosphatase induced pathways by EYA's in breast cancer and the importance of considering these properties in nanotherapeutic design. - Source: PubMed
Publication date: 2025/09/14
Carney EmilyPowell RobertKumar AnanyaHabibi Neda