Ask about this productRelated genes to: ARHGAP25 antibody
- Gene:
- ARHGAP25 NIH gene
- Name:
- Rho GTPase activating protein 25
- Previous symbol:
- -
- Synonyms:
- KIAA0053
- Chromosome:
- 2p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-06
- Date modifiied:
- 2016-04-25
Related products to: ARHGAP25 antibody
Related articles to: ARHGAP25 antibody
- - Source: PubMed
Publication date: 2026/02/26
- Bacterial infectious skin diseases are common dermatological conditions caused by various pathogenic bacteria. In recent years, their incidence has remained high due to factors such as climate change and the overuse of antibiotics, posing persistent challenges for clinical diagnosis and treatment. This study aimed to identify plasma proteins causally associated with cellulitis, erysipelas, cutaneous abscess, furuncle, and carbuncle through Mendelian randomization (MR) analysis. - Source: PubMed
Publication date: 2026/03/02
Yan ZhangrenShi ZiyangWang YeYin Hongwei - To investigate the genetic relationship between irritable bowel syndrome (IBS) and non-alcoholic fatty liver disease (NAFLD). - Source: PubMed
Publication date: 2025/12/15
Hong JundongJi RuiWang PeichengHuang FengmingZhang FanZhou YanlinLv Bin - Atherosclerosis (AS) is a common cardiovascular disease worldwide. The mitochondrial unfolded protein response (UPRmt) is a defense mechanism that enhances protein folding and degradation to maintain mitochondrial function and cellular homeostasis under stress. Research suggests a strong link between mitochondrial dysfunction and AS, particularly related to oxidative stress and inflammation. However, the exact relationship between UPRmt and AS is unclear. Identifying biomarkers associated with UPRmt is crucial for improving AS diagnosis and treatment. - Source: PubMed
Publication date: 2025/11/27
Wu ShuguangLiu YanhongLi YuLai JunyuWan QiangWu JianguangMa Yirong - Multiple sclerosis (MS) is an autoimmune disease characterised by neuroinflammation and neurodegeneration. This study investigates genetic and immunological factors in MS, focusing on microglial regulation. We analysed differentially expressed genes using RNA sequencing from MS lesions (GSE108000) and plaques (GSE227781), validated with cis-eQTL analysis, and integrated Mendelian randomisation (MR), SMR, co-localisation, methylation, and protein-protein interaction (PPI) analyses to assess causal effects on MS risk. We identified five genes-ARHGAP25, HLA-DRB1, MERTK, MS4A6A, and SYK-linked to MS susceptibility. MR revealed that elevated levels of ARHGAP25 (OR = 1.45), HLA-DRB1 (OR = 2.24), MERTK (OR = 1.10), MS4A6A (OR = 1.15), and SYK (OR = 1.13) increased MS risk. SMR confirmed a causal link between HLA-DRB1 and MS, while co-localisation analysis showed shared variants with MS for HLA-DRB1 (100%) and SYK (97.93%). Methylation analysis highlighted 10 sites within HLA-DRB1, and PPI and DrugBank analyses revealed interactions between these genes and multiple proteins or chemicals. This study demonstrates the value of integrating genomic and eQTL data through MR to identify novel MS therapeutic targets, particularly microglial genes, offering potential new avenues for treatment. - Source: PubMed
Yan WuWen JiangJianhong Wang