Anti_Human, mab EphA1 Source Mouse
- Known as:
- Anti_Human, mab EphA1 Source Mouse
- Catalog number:
- 101-M390
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab EphA1 Source Mouse
Related genes to: Anti_Human, mab EphA1 Source Mouse
- 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: Anti_Human, mab EphA1 Source Mouse
Related articles to: Anti_Human, mab EphA1 Source Mouse
- 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 - Late-onset Alzheimer's disease is a devastating and complex neurodegenerative disorder with a multifactorial etiology. Over the past decade, advances in genetic research have identified novel risk genes, shedding light on the underlying pathogenic mechanisms of late-onset Alzheimer's disease. This review provides a comprehensive overview of several of these crucial genetic factors and their potential mechanisms in the pathogenesis of Alzheimer's disease. Genome-wide association studies, whole-genome sequencing, and multi-omics studies have played a crucial role in identifying key risk genes, particularly those involved in amyloid-β metabolism and clearance, such as CLU and APOE, which influence amyloid-β aggregation. Tau pathology, characterized by neurofibrillary tangles, is another hallmark of Alzheimer's disease, with genes such as BIN1 implicated in tau-mediated neurodegeneration. Additionally, immune regulatory genes, including CR1, MS4A6A, CD33, and TREM2, play crucial roles in microglial activation and neuroinflammation, thereby contributing to disease progression. Synaptic dysfunction is also a critical factor in Alzheimer's disease pathology, with genes such as IQCK, EPHA1, and CD2AP linked to synaptic function and plasticity, highlighting their potential impact on cognitive decline. Understanding these genetic risk factors provides valuable insights into the complex genetic landscape of Alzheimer's disease and its highly heterogeneous pathological mechanisms, including amyloid-β metabolism, tau pathology, immune response and neuroinflammation, and synaptic dysfunction. Future research should focus on elucidating the functional roles of these individual genes and their potential as therapeutic targets for altering the course of Alzheimer's disease. - Source: PubMed
Publication date: 2026/01/27
Akkaoui JulietDevadoss DineshRodriguez Melissa DiazArias Adriana YndartVashist ArtiMovila AlexandruLakshmana Madepalli K