Ask about this productRelated genes to: ARHGDIG Blocking Peptide
- Gene:
- ARHGDIG NIH gene
- Name:
- Rho GDP dissociation inhibitor gamma
- Previous symbol:
- -
- Synonyms:
- RHOGDI-3
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-04-01
Related products to: ARHGDIG Blocking Peptide
Related articles to: ARHGDIG Blocking Peptide
- BACKGROUND: Prostate adenocarcinoma (PRAD) has substantial recurrence after primary treatment, and reliable prediction is clinically needed. We integrated clinical, genomic, and transcriptomic data to identify recurrence-associated genes, characterize their tumor microenvironmental context, and develop a prognostic model. METHODS: Gene expression and clinical data were obtained from TCGA (training; n = 145) and the GEO dataset GSE54460 (validation; n = 106). Single-cell RNA-seq data were analyzed to resolve gene expression across cell types. Immune infiltration was estimated using ssGSEA and the ESTIMATE algorithm, and cell–cell communication was assessed with CellChat. Recurrence-associated genes were identified by univariate Cox regression, and a LASSO Cox model was used to construct and externally validate the risk score. RESULTS: Pathological T stage, N stage, Gleason score, and TP53 mutation were linked to higher recurrence risk. We identified six risk genes (AMH, CRYBA2, CTHRC1, EFNA2, BMP6, ARHGDIG) and two protective genes (CKMT2, IP6K3) and built a risk-score model that discriminated against PFS in the training and validation cohorts. Single-cell analysis localized CTHRC1 predominantly to a fibroblast subpopulation characterized by upregulated midkine (MDK) signaling and extensive intercellular communication. Drug–gene correlation screening nominated decitabine, tegafur, calusterone, EMD-1204831, and ARQ-680; expression of several risk genes positively correlated with CTLA4, suggesting testable sensitivity to checkpoint blockade. CONCLUSIONS: Clinical variables together with transcriptomic features—particularly a CTHRC1-high fibroblast program—associate with PRAD recurrence. The externally validated risk score and the stromal context of CTHRC1/MDK provide testable avenues for prognosis and therapeutic exploration. - Source: PubMed
Publication date: 2026/03/14
Ma YuanLin GaotengWang KeruoLiu ZihaoShao YuanYu WenyueZhao XiaoyiYu DanZhan FangfangWang XinghangDuan ShidaDuan KeFei - Hepatocellular carcinoma (HCC) is one of the most common as well as leading causes of mortality worldwide, and sorafenib is the first-line treatment in HCC patients. Unfortunately, drug resistance to sorafenib often develops. However, the underlying mechanism remains unclear. Here, we reveal the important role of macrophage extracellular traps (METs)-mediated crosstalk between macrophages and tumor cells in sorafenib resistance. - Source: PubMed
Publication date: 2024/11/11
Huang XiangboYi NanZhu PengfeiGao JianLv Jun - Dementia is a debilitating neurological disease affecting millions of people worldwide. The exact mechanisms underlying the initiation and progression of the disease remain to be fully defined. There is an increasing body of evidence for the role of immune dysregulation in the pathogenesis of dementia, where blood-borne autoimmune antibodies have been studied as potential markers associated with pathological mechanisms of dementia. - Source: PubMed
Publication date: 2023/11/30
Ehtewish HananMesleh AreejPonirakis GeorgiosLennard KatieAl Hamad HanadiChandran ManiParray AijazAbdesselem HouariWijten PatrickDecock JulieAlajez Nehad MRamadan MarwanKhan ShafiAyadathil RaheemOwn AhmedElsotouhy AhmedAlbagha OmarArredouani AbdelilahBlackburn Jonathan MMalik Rayaz AEl-Agnaf Omar M A - The pathological roles and mechanisms of Rho-specific guanine nucleotide dissociation inhibitor 3 (RhoGDI3) in vascular smooth muscle cell (VSMC) phenotypic modulation and neointima formation are currently unknown. This study aimed to investigate how RhoGDI3 regulates the Nod-like receptor protein 3 (NLRP3) inflammasome in platelet-derived growth factor-BB (PDGF-BB)-induced neointima formation. - Source: PubMed
Publication date: 2023/11/19
Sun JingwenZhu QingyuYu XiaoqiangLiang XiuyingGuan HaijingZhao HeyanYao Wenjuan - Biochemical recurrence (BCR) is considered as an early sign of prostate cancer (PCa) progression after initial treatment, such as radical prostatectomy and radiotherapy; hence, it is important to stratify patients at risk of BCR. In this study, we established a robust 8-gene signature (APOF, Clorf64, RPE65, SEMG1, ARHGDIG, COMP, MKI67 and PRAME) based on the PCa transcriptome profiles in the Cancer Genome Atlas (TCGA) for predicting BCR-free survival of PCa, which was further validated in the MSK-IMPACT Clinical Sequencing Cohort (MSKCC) PCa cohort. Moreover, we found that one risk-related gene (PRAME) was upregulated in tumor samples, particularly in high-risk group was well as in patients metastatic tumor and was correlated with chemotherapeutic drug response. In vitro experiments showed that knocking down PRAME reduced the proliferation, migration, and invasion of PCa cells. Therefore, our study established a new 8-gene signature that could accurately predict the BCR risk of PCa. Inhibition of PRAME attenuated the proliferation, invasion, and migration of PCa cells. These findings provide a novel tool for stratifying high-risk PCa patient and shed light on the mechanism of PCa progression. - Source: PubMed
Publication date: 2023/07/15
Kadeerhan GaohaerXue BoWu XiaolinHu XiaofengTian JunWang Dongwen