Ask about this productRelated genes to: RHOJ Blocking Peptide
- 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 Blocking Peptide
Related articles to: RHOJ Blocking Peptide
- - 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
Patel MaulikkumarFeng WeiMckay Nicole SMillar Peter RLiu MenghanYang ChengranCetin ArdaJohnson MatthewBudde JohnWestern DanielMarsh Thomas WSaliu Ibrahim OGordon Brian AGuerra Jorge J LlibreMorris John CBateman Randall JMcDade EricHoltzman David MRyan Natalie SBenzinger Tammie L SRenton Alan EGoate Alison MIbanez LauraSung Yun JuZhao GuoyanCruchaga CarlosPottier Cyril - BACKGROUND: Medication overuse headache (MOH) causes substantial disability in suffering patients, significantly reducing the quality of life. It may lead to structural and functional brain changes detectable by neuroimaging. Successful and effective treatments can alleviate headache burden, reduce consumption of abused drugs and reverse the biological alterations. Therefore, improvement of therapeutic strategies and optimization of patient stratification to match the individuals who can benefit with certain approaches, is essential. This study investigates DNA methylation (DNAm) associated with response to MOH treatment. METHODS: This analysis was performed within the frame of Epimode project - prospective quantitative longitudinal observational study of genome-wide DNA methylation in neurological cohort. 18 MOH patients, in age range between 33 and 66 years, received treatment which included education on diagnosis, recommendation to stop overused drugs and eventually 5-day inpatient withdrawal program. The effectiveness of MOH therapy was evaluated based on (a) overuse outcome (remission or persistence of MOH diagnosis) and (b) mitigating effect (reversal from chronic to episodic headache attacks), both assessed after 5 months from the enrolment. Genome-wide DNA methylation assay was performed (Infinium Human MethylationEPIC BeadChip, Illumina) in whole blood samples collected at baseline and after 3, 5 and 9 months from enrolment. RESULTS: Performed DNAm differential analysis identified methylation signatures linked to MOH treatment and revealed genes involved in epigenetic regulation of response. Among the others, we found PTPRN2, RHOJ, PCDH-γs, CACNA family and SLC38A4 genes as associated with MOH overuse outcome; MUC4 and FKBP11 - as related to mitigating effect of the intervention; and FMOD or ZDHHC14 which resulted linked to both endpoints. We observed that differential methylation signal seemed to predominantly capture the changes associated to excessive use of acute medications. Pathway enrichment analysis demonstrated that the genes with differential methylation signal might be involved in pathways related to (i) metabolic detoxification and (ii) neuropsychiatric/behavioral regulation. CONCLUSIONS: Our findings describe methylation patterns, genes and pathways that may be associated with response to MOH intervention. - Source: PubMed
Publication date: 2026/04/02
Kwiatkowska Katarzyna MalgorzataFavoni ValentinaFerraresi FrancescaPirazzini ChiaraRavaioli FrancescoBacalini Maria GiuliaDall'Olio DanieleSala ClaudiaCastellani GastoneCalzari LucianoGentilini DavideTerlizzi RossanaPierangeli GiuliaCortelli PietroMascarella DavideGaragnani PaoloCevoli Sabina - BACKGROUND: Chemoresistance is a cause of chemotherapy failure in gastric cancer (GC) treatment. Recent studies have shown that the dysregulation of glutamine metabolism plays a pivotal role in promoting chemoresistance. While small-molecule inhibitors targeting glutamine metabolism have been investigated, peptide-based compounds have attracted increasing attention because of their high specificity and low toxicity. Endogenous or rationally designed peptides have shown potential for inducing apoptosis, disrupting cancer-related signaling pathways, and overcoming drug resistance in various cancers. However, the potential of functional peptides to target glutamine metabolism and reverse drug resistance in the context of GC has not been thoroughly explored. METHODS: We performed proteomic profiling to identify upregulated proteins in cisplatin-sensitive GC cells, from which peptides were derived for functional screening. A RHOJ-derived peptide (peptide 1) was identified and validated as a candidate chemosensitizer. Untargeted metabolomics, flow cytometry, molecular docking, molecular dynamics simulations, fluorescence imaging, and a subcutaneous xenograft model were used to investigate the mechanism through which peptide 1 modulates GLUL-mediated glutamine metabolism and reverses cisplatin resistance. RESULTS: In this study, we found that glutamine metabolism was enhanced in cisplatin-resistant GC cells and that a peptide which derived from RHOJ (peptide 1) increased the sensitivity of resistant cells to chemotherapy. Molecular docking revealed that this peptide could bind to glutamine synthetase (GLUL), a key enzyme in the glutamine metabolism pathway. Mechanistically, peptide 1 inhibited glutamine production, increased ROS levels, induced DNA damage, and promoted apoptosis in resistant cells, ultimately restoring cisplatin sensitivity both in vitro and in vivo. CONCLUSIONS: Our study demonstrated that glutamine metabolism plays a vital role in the chemoresistance of GC cells and that RHOJ-derived peptide 1 enhances the chemosensitivity of drug-resistant GC cells through targeting GLUL, depleting glutamine, inducing ROS accumulation, and promoting DNA damage. These mechanisms ultimately restores chemosensitivity in drug-resistant cells and highlight peptide 1 as a promising therapeutic strategy for overcoming chemoresistance in GC. - Source: PubMed
Publication date: 2026/01/28
Li JianLi HuanqingYe FangzhouWang JiayiLi FanBei SonghuaZhang XiaohongJiang JunFeng Li