Ask about this productRelated genes to: RAB31 antibody
- Gene:
- RAB31 NIH gene
- Name:
- RAB31, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- Rab22B
- Chromosome:
- 18p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-20
- Date modifiied:
- 2015-09-02
Related products to: RAB31 antibody
Related articles to: RAB31 antibody
- Tumor-associated macrophages (TAMs) play pivotal roles in shaping the tumor-microenvironment (TME) through functional plasticity, which is regulated by extrinsic and intrinsic signals. However, the role of vesicular trafficking in TAMs remains poorly understood. RAB31, a small GTPase enriched in myeloid cells, was proposed as a potential regulator of TAM polarization through clathrin-mediated endocytosis (CME). We hypothesized that RAB31 modulates TAM education by tumor-derived signals and thereby shapes antitumor immunity. - Source: PubMed
Publication date: 2026/09/02
Liu JingjingWang ShanshanBao DengyiDong GeMa YunxiZhang GuorongLiu XinZhang DongliWang LuluXu ShuqianCai Zhigang - Ras-related protein in brain (Rab) guanosine triphosphatases regulate vesicular trafficking and membrane dynamics, processes essential for platelet activation. Although several Rab family members are expressed in platelets, the role of Rab31 remains undefined. - Source: PubMed
Publication date: 2026/07/24
Wang YixianLuo JiajiaLiu JingjingYang QingyuanWu XiaowenGuo YifanLiu QianLiu ChangranYan YanChen DongxingKunapuli Satya PCai ZhigangDing Zhongren - Vestibular schwannoma (VS) is a benign Schwann cell-derived tumor that frequently causes progressive hearing loss and vestibulocochlear dysfunction, substantially impacting quality of life. The molecular mechanisms underlying VS pathobiology remain poorly defined, and reliable biomarkers or targeted therapies are lacking. This study aimed to delineate the molecular landscape of VS through a transcriptome-wide meta-analysis. We performed a genome-wide random-effects meta-analysis of four independent Affymetrix microarray datasets from the Gene Expression Omnibus (GEO) database. Differential expression analyses were conducted with and without covariate adjustment. Gene Ontology enrichment and DrugBank-based drug-gene interaction analyses were subsequently applied to characterize biological pathways and assess translational potential. Across the meta-analysis, more than 3,200 differentially expressed genes were identified in the covariate-free model. After applying a more stringent threshold (|metaLFC| > 1 and FDR < 0.05), 1,095 genes remained differentially expressed, with high concordance between the covariate-free and covariate-adjusted models. Downregulated genes included extracellular matrix and stromal components (MFAP5, FABP4, DCN), and sensory- and synapse-related transcripts (SLC22A3, LGI1). Upregulated genes included immune- and inflammation-associated genes (TREM2, CCL3, CCL4, L1CAM) and proliferative regulators (CCND1, RAB31, MOXD1). Functional enrichment highlighted extracellular matrix remodeling, immune modulation, sensory signaling, and cell cycle pathways. Notably, many of the most strongly dysregulated genes have not previously been associated with VS. Drug-gene interaction analysis identified multiple dysregulated genes with known pharmacological targets, suggesting potential translational relevance. This transcriptome-wide meta-analysis provides a comprehensive overview of gene expression patterns in VS, highlighting alterations related to extracellular matrix organization, sensory and synaptic processes, immune-associated signaling, and cell cycle-related pathways. The study highlights novel disease-associated genes and pathways and may help prioritize candidates for further investigation, including those with potential relevance for therapeutic targeting. - Source: PubMed
Publication date: 2026/07/10
Altınalan EbrarPanina AleksandraFredriksson RobertŞakul Ayse ArzuSchiöth Helgi B - BACKGROUND: The interaction between tumour-associated neutrophils (TANs) and angiogenesis plays a crucial role in tumour progression. However, the specific regulatory mechanisms by which different TANs populations influence angiogenesis in colorectal cancer (CRC) remain poorly understood. METHODS: The study integrates our own dataset with publicly available single-cell RNA sequencing (scRNA-seq) data to analyze the infiltration of various single-cell types in colorectal cancer (CRC). Using in vitro experiments, immunofluorescence, and animal models treated with anti-VEGFR antibodies, we investigated the role of tumor-associated neutrophils (TANs) in CRC and angiogenesis. We conducted RAB31 knockdown cell line, RNA sequencing, Western blotting, quantitative PCR, ELISA, tube formation assays, CCK8, and clonogenic assays, combined with in vivo experiments, to elucidate the impact of RAB31 in the tumor microenvironment (TME) and the mechanism by which tumor-derived RAB1 regulates TANs recruitment. RESULTS: Single-cell analysis revealed a significant infiltration of myeloid cells, particularly TANs, in CRC tumour tissue compared to normal tissue. RAB31 was found to be involved in malignant cell pathways, promoting CRC progression. Depletion of TANs substantially suppressed tumour growth and angiogenesis, while VEGFR blockade inhibited tumour growth and altered TANs infiltration in response to angiogenesis status. In vitro, knockdown of RAB31 expression inhibited tumour cell proliferation, and CXCL2 protein secretion was significantly reduced in shRab31-transfected tumour cells. In vivo, tumour tissue from shRab31 models showed decreased angiogenesis and reduced Neutrophil Extracellular Traps (NET) production, alongside reduced TANs infiltration. Moreover, CXCR4 expression was significantly elevated in TANs, and tumour cells influenced TANs through the CXCL2–CXCR4 axis. RAB31 regulated the PI3K–Akt signalling pathway, which is linked to neutrophil recruitment in CRC. CONCLUSIONS: Our findings suggest that tumour-derived RAB31 regulates the CXCL2–CXCR4 signalling pathway in CRC. RAB31 promotes CXCL2 secretion through the PI3K-Akt signalling pathway, facilitating TANs recruitment and angiogenesis, thereby driving tumour growth. This work enhances our understanding of the complex role of TANs and RAB31 in CRC progression and provides new insights into potential therapeutic strategies targeting the tumour microenvironment. - Source: PubMed
Publication date: 2026/02/26
Zong ZhenNing Zhi-KunHu CeguiJiang ShihaoYi HaoTang YingLuo QiulingYuan ChenweiZhu XiaopingZhu Xingen - Connexin43 (Cx43) is recognized as a transmembrane protein; its precise expression profile and molecular mechanisms in triple-negative breast cancer (TNBC) remain unclear. We systematically analyzed Cx43 expression in over 60 breast cancer cell lines from the CCLE and HPA databases. Immunohistochemical evaluation compared Cx43 expression between TNBC tissues and adjacent normal tissues. Cx43 expression was assessed in normal breast epithelial cells (MCF-10A) and two TNBC cell lines (MDA-MB-231 and BT-549) using qRT-PCR and Western blot. Functional assays (CCK8, wound healing, transwell) evaluated TNBC progression following Cx43 interference or overexpression. Rab31, a Cx43-interacting protein, was identified via bioinformatics, immunofluorescence, and Co-IP. Autophagy-related proteins (ULK1, ATG5, LC3, and p62) were analyzed after Cx43 or Rab31 modulation. Finally, a nude mouse model validated Cx43's in vivo effects on tumor growth and associated molecular changes. Cx43 was upregulated in TNBC tissues and cell lines. Overexpression enhanced proliferation, migration, and invasion, while knockdown suppressed these effects. Cx43 co-expressed with Rab31, regulating its protein levels and autophagy. Rab31 interference reversed Cx43-mediated autophagy and oncogenic behaviors. In vivo, Cx43 promoted tumor growth and modulated Rab31/autophagy pathways. The Cx43/Rab31 axis drives autophagy to facilitate TNBC progression, highlighting Cx43 as a potential therapeutic target. Our findings provide mechanistic insights for improving TNBC treatment. - Source: PubMed
Publication date: 2025/12/08
Yang JiaoWu DieYang TingLin Zi-JingJiang Pei-YaoWang Ting-RuiLu Zheng-JiaWang LuMing Jia