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
- Sphingosine-1-phosphate (S1P) promotes tumor growth and dissemination. Chronic positive feedback communication circuits between cancer and stromal cells involve S1P type-1-receptor (S1PR1) activating cell-type specific signaling networks. We hypothesized that such cell-type specific signaling components would be identifiable by rational, unbiased analysis of public oncogenomic and phosphoproteomic datasets. Guided by S1PR1 expression, we used data mining strategies applied to 32 cancer type datasets of the TCGA oncogenomics program, aiming to identify pan-cancer endothelial and immune S1PR1 signaling partners statistically correlated with patient survival. Gene ontology analysis and unbiased clustering of endothelial and immune S1PR1-signaling partners were used to reveal cell type-specific signaling components that individually and grouped, as transcriptional signatures, were statistically linked to patient survival. Furthermore, the breast cancer CPTAC dataset was analyzed focusing on the signaling phosphoproteome linked to S1PR1 expression. Oncogenic S1PR1 signaling companions included endothelial regulators of cell migration such as Ephexin5, a RhoGEF encoded by the ARHGEF15 gene, and RhoJ, a small Rho GTPase. The immune signaling repertoire linked to S1PR1 expression and patient survival included DOCK2, Vav1 and Rac2. Among the S1PR1 phospho-signaling partners, endothelial ARHGAP24, ARHGAP6, ARHGAP31, and TNS1, and immune ARHGAP25, known to be involved in cytoskeletal reorganization and cell mobilization, clustered as phosphoproteins within a subgroup of breast cancer patients. Given the pharmacological relevance of S1PR1 in endothelial and immune settings, revealing the identity of signaling molecules linked to S1PR1 expression provides useful information to further investigate therapeutic strategies targeting these pathways in the vascular and immune systems. - Source: PubMed
Publication date: 2026/06/20
Torres-Santos YazminBeltrán-Navarro Yarely MabellReyes-Cruz GuadalupeVázquez-Prado José - Cervical cancer (CC) is an alarming global health problem, with predominantly higher incidence, lethal progression, and mortality among women of African ancestry (AA) than women of European ancestry (EA). Although persistent high-risk human papillomavirus (HPV) integration and infection are the key etiological factors, currently available evidence implicates epigenetic reprogramming as a prime contributor to ancestry-associated differences in CC pathogenesis. To address these disparities, we performed genome-wide DNA methylation profiling of HPV-positive cervical intraepithelial neoplasia (CIN) lesions from AA ( = 15) and EA ( = 15) women. Differential methylation analysis identified a distinct epigenomic landscape in AA-CIN lesions, with widespread hypermethylation and hypomethylation at promoter-associated and regulatory CpG sites. Pathway enrichment analyses highlighted dysregulation of ECM-receptor interaction, focal adhesion, PI3K-Akt, MAPK, Ras, Rap1, and RUNX-dependent transcriptional networks. Comparative analysis across CIN grades (CIN1-CIN3) revealed progressive epigenetic reprogramming affecting cell cycles, cytoskeletal dynamics, signaling, and metabolic pathways. Among hypermethylated tumor suppressor genes, and showed significantly higher methylation in AA lesions, accompanied by concomitant loss of their protein expression. MBD1, a methylation-binding regulator, was upregulated in AA-CIN lesions, coinciding with global loss of 5-hydroxymethylcytosine (5hmC), suggesting enhanced transcriptional repression. In contrast, EA lesions retained protein expression and 5hmC levels. Collectively, these findings indicate that early, ancestry-specific epigenetic modifications target tumor suppressor pathways and converge on oncogenic signaling, cytoskeletal remodeling, and cell-cell adhesion. Our study provides mechanistic insight into CC health disparities, identifying and hypermethylation as potential biomarkers, and highlighting epigenetic regulation as a contributor to disparate CC progression in AA women. - Source: PubMed
Publication date: 2026/04/29
Masoud MohamedShastri CharuBanerjee RajarshiDasgupta SaanviChavarria-Bernal HectorSingh Karan PPierce Jennifer YDasgupta Santanu - Breast cancer is the most common malignant tumor in women all over the world, accounting for 15% of all female cancer-related mortality. Due to the limited sensitivity of current serum biomarkers (such as CA15-3, CEA) and the invasiveness of imaging/biopsy methods, early detection of breast cancer is still challenging. The purpose of this study is to use Olink proteomics to identify new diagnostic markers of breast cancer and integrate them into a multi-protein diagnostic model to improve the accuracy of early detection. - Source: PubMed
Publication date: 2026/05/04
Huang JingchunGao LixinGlazutdinova LiliiaJi XuyaoZhang JingLu YoumeiZhang SiyaoLiu Yu - - 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