Ask about this productRelated genes to: EPHA1 antibody
- Gene:
- EPHA1 NIH gene
- Name:
- EPH receptor A1
- Previous symbol:
- EPHT, EPHT1
- Synonyms:
- EPH
- Chromosome:
- 7q34-q35
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-16
- Date modifiied:
- 2018-02-13
Related products to: EPHA1 antibody
Related articles to: EPHA1 antibody
- -ε4 is the strongest common genetic risk factor for Alzheimer's disease (AD), yet many carriers remain cognitively unimpaired into late life. We tested whether a protected-ε4-first proteomic approach could identify plasma proteins associated with delayed clinical onset among ε4 carriers. - Source: PubMed
Publication date: 2026/05/01
Guen Yann LePark JunyoungPeña-Tauber AndrésGreicius Michael D - Ephrin type-A receptor 1 (EPHA1) has been identified as a potential contributor to the pathogenesis of Parkinson's disease (PD). The complex interactions between PD symptoms and the EPHA1 protein warrant further exploration. - Source: PubMed
Lin Yu-ChenTan Chun-HsiangHong Wei-PinYu Rwei-Ling - Dysregulation of the peripheral immune system may increase Alzheimer's disease (AD) risk, but the underlying cell type-specific mechanisms remain unclear. - Source: PubMed
Lindbohm Joni VStražar MartinLee Hang-MaoAshenberg OrrMars NinaSipilä Pyry NRipatti SamuliGraham DanKivimäki MikaXavier Ramnik J - Hepatocytes demonstrate significant heterogeneity between normal liver tissue and hepatocellular carcinoma (HCC), with malignant hepatocytes playing a crucial role in remodeling the tumor microenvironment through specific ligand-receptor interactions. However, the mechanisms by which hepatocytes drive HCC progression at the single-cell level remain poorly understood. - Source: PubMed
Publication date: 2026/03/10
Chen YuanhongTang YulianNing YufanYang YangTian RenshengMao YongjiaoFeng ZhiquanLin WenxianWang DecaiFeng Xueping - Fetal growth restriction (FGR) is a major contributor to perinatal morbidity and mortality, most commonly arising from placental dysfunction, with increasing evidence implicating aberrant DNA methylation in its pathogenesis. To identify robust epigenetic alterations associated with FGR, we analyzed placental chorionic villi from an in-house early-onset FGR cohort and compared them with a publicly available dataset (GSE100197). DNA methylation profiling was performed using Illumina EPIC (in-house) and 450K (public) arrays, processed with identical normalization and quality-control pipelines, including adjustment for gestational age and estimation of placental cell-type composition. Differentially methylated positions (DMPs) were identified using linear regression models, revealing 10,427 DMPs in the in-house cohort and 7467 in the public dataset, with 108 shared DMPs showing consistent direction of change across both cohorts. Promoter-associated DMPs were mapped to genes involved in angiogenesis, morphogenesis, immune regulation, and transcriptional control, including , , , , and , while additional novel candidates such as , , and family members were also identified. Functional annotation suggests that these methylation changes may influence pathways essential for placental vascular development and structural organization. Overall, this cross-cohort comparison highlights reproducible epigenetic signatures of FGR and underscores the need for standardized approaches to clarify the molecular mechanisms underlying placental insufficiency. - Source: PubMed
Publication date: 2026/01/31
Bednarek-Jędrzejek MagdalenaTaryma-Leśniak OlgaPoniatowska MałgorzataCejko MateuszMaksym KatarzynaDzidek SylwiaBlatkiewicz MałgorzataKwiatkowska EwaTorbé AndrzejKwiatkowski Sebastian