Ask about this productRelated genes to: RAB7B antibody
- Gene:
- RAB7B NIH gene
- Name:
- RAB7B, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- MGC9726, MGC16212
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-28
- Date modifiied:
- 2015-08-25
Related products to: RAB7B antibody
Related articles to: RAB7B antibody
- Intranasal vaccines specifically eliciting mucosal immunity in the upper respiratory tract have shown advantages in protecting against respiratory virus invasion. Yet, no clinically licensed intranasal adjuvant remains a major hurdle for the development of intranasal vaccines with low immunogenic antigens like subunit vaccines. Here, we show that liposomes loading simvastatin (Lipo-SV) serve as potent mucosal adjuvants for the intranasal liposomal subunit vaccine encapsulating the hemagglutinin 1 (HA1) glycoprotein of A/PR/8/34 (PR8) H1N1 influenza (Lipo-HA1), providing robust protection against the lethal PR8 H1N1 infection. Compared to cholera toxin subunit B (CTB), the only mucosal adjuvant used in humans, the Lipo-SV substantiate intranasal Lipo-HA1 vaccines to elicit robust systemic and local mucosal immune responses. The underlying mechanism of the adjuvanticity of Lipo-SV involves the increased transcytosis of antigens by inhibiting the geranylgeranylation of RAB5 and RAB7B GTPases in nasal epithelial cells. Moreover, Lipo-SV enhance the submucosal recruitment of dendritic cell for antigen uptake the Toll-like receptor 4-dependent pathway. Unlike CTB, intranasal Lipo-SV do not induce inflammation in the lung or the inflammatory cytokines in the central nervous system. Our results present a paradigm of design of mucosal adjuvant to target the mucosal epithelial cells in addition to the antigen-presenting cells. - Source: PubMed
Publication date: 2026/01/05
Yang AfengZhang ChenWu AihuaXu JiaojiaoLin HongzhengLi ZheLi TingtingLi YunluXia NingshaoShi XunlongZhang TianyingLu Wei - Late endosomes and lysosomes (LE/Lys) are dynamic organelles primarily involved in the degradation of macromolecules within cells. Beyond this role, they are crucial for nutrient sensing, calcium signalling, cell proliferation and migration. The cytoskeleton is essential for the proper trafficking and function of LE/Lys. However, while the role of microtubules is well-established, the function of the actin cytoskeleton at LE/Lys is less understood. In this work, we performed an siRNA screen to identify actin regulators that play a role at LE/Lys. The screen revealed that the F-actin-binding protein nexilin regulates LE/Lys size as its depletion leads to their enlargement. We show that this is a consequence of inhibited LE/Lys fission and affects the retrograde transport from late endosomes to Golgi. Moreover, our data demonstrate that nexilin interacts with the small GTPase Rab7b and the lysosomal calcium channel TRPML1, and that TRPML1 activation rescues the LE/Lys enlargement caused by nexilin depletion. Taken together, our results indicate that nexilin mediates the interaction between LE/Lys and the acto-myosin cytoskeleton required for the calcium-dependent fission of these organelles. - Source: PubMed
Publication date: 2026/01/09
Bergundhaugen MarieSneeggen MarteProgida Cinzia - Liver cirrhosis remains a major global health challenge, with liver transplantation currently representing the most effective treatment. Elucidating its molecular pathogenesis is therefore critical for the development of novel therapeutic strategies. Emerging evidence indicates that mitophagy plays a pivotal role in cirrhosis progression. In this study, we employed integrative bioinformatics to explore the association between mitophagy and liver cirrhosis, aiming to identify potential therapeutic targets. Differentially expressed genes (DEGs) were obtained from GSE77627 and GSE139602 data sets, followed by functional enrichment analysis. Mitophagy-related differentially expressed genes (mito-DEGs) were screened and assessed through receiver operating characteristic (ROC) analysis, immune cell infiltration profiling, and protein-protein interaction (PPI). Weighted gene coexpression network analysis (WGCNA) identified key modules, and intersecting genes with mito-DEGs highlighted RAB7B as a candidate hub gene, which was validated in external data sets. Experimental verification confirmed elevated RAB7B expression in activated hepatic stellate cells (HSCs) and a mouse model of liver cirrhosis. Functional assays demonstrated that RAB7B inhibition attenuated HSC activation, and molecular docking revealed strong binding affinity between RAB7B and predicted anticirrhosis compounds. We found that RAB7B knockdown restored TGF-β-induced mitophagy inhibition, enhanced mitochondria-lysosome colocalization, and showed dynamic regulation by mitophagy status, indicating its role as a negative and responsive regulator of mitochondrial clearance. Collectively, our findings identify RAB7B as a mitophagy-related hub gene driving liver cirrhosis progression and provide novel insights into its therapeutic potential. - Source: PubMed
Publication date: 2025/12/01
Dai JinyaoYing ShuaibingLin JiePan YongZhang QiudanLiu JingLou YanQiu Yunqing - Public neoantigens, including KRAS, TP53, and PIK3CA mutations, which are shared across various tumor types, have demonstrated significant immunogenicity and offer great promise for cancer immunotherapy. Clinical trials targeting these public neoantigens have yielded encouraging results, including tumor regression and prolonged relapse-free survival. This study evaluates the human leukocyte antigen (HLA) binding properties of T-cell epitopes derived from these public neoantigens to identify optimal T-cell target and further develops T-cell receptor (TCR)-based therapeutics. - Source: PubMed
Publication date: 2025/07/18
Shen MeiyingHao YananHan XiaxiaWang BozhiLi LuoChen TongChen SiyinZou LinHuang JingjingWang WangLiu ShengchunHan XiaojianJin Aishun - The Rab family of small guanosine triphosphatases (GTPases) are nucleotide-dependent switches. Mutations in Rabs can result in human diseases. Rab7a and Rab7b transition from early endosomes to lysosomes and are presumed to function similarly. Most studies look at Rab7a, less on Rab7b, with the underlying assumption they function similarly. There have yet to be articles comparing them side by side. Whilst cloning Rab7 homologues, we identified splice isoforms for Rab7b only. These splice isoforms, Rab7b2 and Rab7bx8 lacking different exons, have not been previously characterized but suggest alternative function(s) for Rab7b. Thus, we hypothesize that Rab7 homologues have distinct functions. Here, we compare Rab7a and Rab7b nucleotide mutants locked in GDP-bound (Rab7T22N), GTP-bound (Rab7Q67L), nucleotide-free (Rab7aN125I/Rab7bN124I) states and characterized localization of the Rab7b splice isoforms. HeLa cells were transiently transfected with fluorescently tagged Rab7 reporters. Confocal images were processed with ImageJ and analyzed with SPSS. Rab7a and Rab7b nucleotide mutants were significantly different to one another. Approximately 50% of Rab7b splice isoform-expressing cells had aggregated vesicles, which were phenotypically different from Rab7b vesicles. Rab7a and Rab7b vesicles shared approximately 60% colocalization with each other, while Rab7b vesicles preferentially localized to the Trans Golgi Network. Our results suggest Rab7b is distinct from Rab7a, and Rab7b splice isoforms have different biological functions. - Source: PubMed
Publication date: 2025/03/14
Wong Wing HeiLiu Stephanie ZLi Annie Shi RuLiu XingyouManolson Morris FZirngibl Ralph A