Ask about this productRelated genes to: RHOJ antibody
- Gene:
- RHOJ NIH gene
- Name:
- ras homolog family member J
- Previous symbol:
- RASL7B, ARHJ
- Synonyms:
- FLJ14445, TCL
- Chromosome:
- 14q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: RHOJ antibody
Related articles to: RHOJ antibody
- Breast cancer is the most common form of cancer diagnosed in women. Breast cancer cells gain the expression of mesenchymal-specific genes in a process known as epithelial-mesenchymal transition (EMT). RhoJ, a small Rho GTPase, is a key regulator that promotes resistance to a wide range of chemotherapeutic agents in epithelial-mesenchymal transition tumor cells. - Source: PubMed
Publication date: 2026/08/05
Catteau XavierCharry ManonAllard JustineRorive SandrineSalmon IsabelleNoël Jean-Christophe - Osteoarthritis (OA) and osteoporosis (OP) are prevalent conditions with a complex relationship, yet their shared epigenetic mechanisms remain poorly understood. While genes like , , and have been implicated in both diseases, the specific role of individual CpG sites has not been fully characterized. We investigated CpG methylation in these genes using bisulfite pyrosequencing of peripheral blood DNA from n = 96 postmenopausal women: n = 24 with comorbid OA and OP, n = 34 with OA, and n = 38 healthy controls. Methylation differences were analyzed using statistical tests and logistic regression. Comorbid patients showed significant hypermethylation at two CpG sites compared to the OA-only group (p = 0.0007 and p = 0.042). Conversely, one site was hypomethylated in the OA-only group relative to controls (p = 0.03). A regression model combining three sites and one site demonstrated predictive value for comorbid disease, with an AUC of 0.696. These findings identify site-specific methylation of and as a molecular signature associated with comorbid OA and OP, offering new insights into their shared etiology. - Source: PubMed
Publication date: 2026/06/23
Tyurin Anton VYalaev Bulat IAkhiiarova Karina EGalina Ilmira ILi JieKhusainova Rita I - - Source: PubMed
Publication date: 2026/06/30
Kim ChanYang HanseulFukushima YokoEr Saw PheiLee JunyeopPark Jin-SungPark IntaeJung JinmyungKataoka HiroshiLee DoheonHeo Won DoKim InjuneJon SangyongAdams Ralf HNishikawa Shin-IchiUemura AkiyoshiKoh Gou Young - 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 - Individuals with autosomal dominant Alzheimer's disease (ADAD) arising from mutations in PSEN1, PSEN2, or APP exhibit variability in clinical presentation. Genetic studies of ADAD have shaped our understanding of the disease, and the discovery of genetic modifiers can inform therapeutic interventions and improve patient outcomes. We aimed to discover new genetic modifiers in individuals with mutations in the three ADAD genes. - Source: PubMed
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