Ask about this productRelated genes to: RHOB antibody
- Gene:
- RHOB NIH gene
- Name:
- ras homolog family member B
- Previous symbol:
- ARH6, ARHB
- Synonyms:
- RhoB, RHOH6, MST081
- Chromosome:
- 2p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-16
- Date modifiied:
- 2016-10-05
Related products to: RHOB antibody
Related articles to: RHOB antibody
- Primary sclerosing cholangitis (PSC) is a chronic autoimmune cholestatic liver disease characterized by progressive inflammation and fibrosis, but the role of neutrophils in PSC remains poorly understood. To define neutrophil states in the PSC liver microenvironment, we performed single-cell RNA sequencing of leukocytes isolated from liver perfusate obtained from healthy donor grafts and explanted PSC livers. We identified a marked expansion of transcriptionally diverse neutrophil subclusters in PSC liver perfusate. Importantly, PSC livers were enriched for four neutrophil subclusters: RHOB-high, immediate early gene-high, heat shock protein-high, and CXCL8-high liver neutrophil-like subclusters. These PSC-associated neutrophil subclusters showed increased activity of the TNF and IL-17 signaling pathways, consistent with current views of PSC pathogenesis. They also displayed activation of inflammatory transcriptional regulators, including CEBPB, JUN, FOS, and RELA. Pseudotime analysis suggested that RHOB and immediate early gene subsets were derived from immature neutrophils, whereas liver neutrophil-like and heat shock protein-high subsets exhibited more mature and tissue-adapted features. Together, these data reveal previously unrecognized heterogeneity of liver neutrophils in PSC and identify inflammatory neutrophil programs that may contribute to sustained hepatic inflammation and represent potential therapeutic targets. - Source: PubMed
Publication date: 2026/08/11
Zreka LynnMorita HajimeMa ShuheBando ToshiakiKhan MounaMasuo YukiUno ShunsukeSato HirotakaMatsuyama JoeyOkumura ShinyaIto TakashiHatano EtsuroAlshemali SuzanneYoshitomi HiroyukiUeno Hideki - This study focuses on exploring the co-morbid mechanisms by which Bisphenol A (BPA) induces non-alcoholic fatty liver disease (NAFLD) and osteoarthritis (OA). - Source: PubMed
Publication date: 2026/07/20
Di JingkaiWang ShuangGuo ZijianDi YijingYang NanJuma TalanteLong YinqiQi LikunCao YongpingXiang Chuan - The objective of this study is to explore the expression patterns of angiogenesis-related genes in papillary thyroid cancer (PTC) to enhance understanding of the molecular mechanisms underlying angiogenesis in this malignancy. The findings provide valuable insights into the development of therapeutic strategies. - Source: PubMed
Publication date: 2026/07/19
Zhao JunQin Ya-XinZhao MinNiu HuiLiu Xiao-Qi - Intraocular pressure (IOP), a major risk factor for glaucoma, follows a circadian rhythm with nocturnal increases driven by norepinephrine (NE) from the superior cervical ganglion. This rhythm depends on aqueous humor (AH) dynamics, particularly the outflow through the trabecular meshwork (TM). Herein, we investigated its underlying regulatory mechanisms in the TM because disruption of IOP rhythm increases the risk of glaucoma. Comprehensive gene expression analysis of human TM cells and mouse eyes uncovered NE-upregulated 18 genes, including the small GTPase RHOB. Promoter assays revealed that RHOB is regulated via a cAMP-responsive element. RHOB deficiency enhanced TM phagocytosis and reversed NE-induced suppression of permeability, whereas RHOB overexpression had the opposite effect. In mice, RHO and ROCK inhibitors reduced both nocturnal and NE-induced IOP elevations. These findings suggest that NE elevates IOP by inhibiting TM phagocytosis via RHOB, identifying RHOB as a key regulator of IOP rhythm and a potential target for glaucoma treatment. - Source: PubMed
Publication date: 2026/07/16
Ikegami KeisukeTakahashi TakumiKatamoto YutoOishi AtsuroYoshimi AkihideNagase MikiMiki AtsuyaYasuo ShinobuMasubuchi Satoru - tRNA-derived fragments (tRFs) have arisen as critical regulators in cancer development, however, their functions in esophageal squamous cell carcinoma (ESCC) remain poorly understood. Here, we reported that tRF-17-9L5FZU3 was significantly upregulated in ESCC cells and tissues, and correlated with poor patient outcome. Through integrated small RNA sequencing and qRT-PCR validation in 40 paired clinical samples, functional analyses, including colony formation, CCK-8, Transwell migration/invasion assays, and xenograft mouse models, demonstrated that tRF-17-9L5FZU3-knockdown suppresses ESCC cell proliferation, invasion, migration, and tumor growth in vivo. Furthermore, tRF-17-9L5FZU3 was shown to directly bind the 3'UTR of RhoB (Ras Homolog Family Member B) mRNA via dual-luciferase reporter assays, RNA pull-down, and AGO2 co-immunoprecipitation, leading to repression of RhoB expression at both mRNA and protein levels. RhoB was consistently downregulated in ESCC tumors and exhibited a significant inverse correlation with tRF-17-9L5FZU3 expression. Rescue experiments confirmed that oncogenic effects of tRF-17-9L5FZU3 were dependent on RhoB suppression. Moreover, tRF-17-9L5FZU3-knockdown decreased TGF-β secretion, increased IL-2 production, and inhibited PI3K/AKT and NF-κB signaling, which were reversed by co-silencing of RhoB. Collectively, these findings found that tRF-17-9L5FZU3 promoted ESCC malignancy by directly repressing RhoB, thereby activating oncogenic signaling pathways, positioning the tRF-17-9L5FZU3-RhoB axis as a critical regulator and potential therapeutic target in ESCC. - Source: PubMed
Publication date: 2026/07/09
Feng PingRen JianfengWang JinWei ShuangqinLi SisiZhao YijinLi YiSun Xing