Ask about this productRelated genes to: RAB27A Blocking Peptide
- Gene:
- RAB27A NIH gene
- Name:
- RAB27A, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- RAB27, RAM, GS2, HsT18676
- Chromosome:
- 15q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2019-04-23
Related products to: RAB27A Blocking Peptide
Related articles to: RAB27A Blocking Peptide
- Background Dendritic cells (DCs) serve as pivotal modulators of immune tolerance, with interleukin-10 (IL-10) secretion acting as a core mechanism to sustain this regulatory function. Rab27a, a small GTPase involved in vesicular trafficking processes, is well recognized for its critical role in cellular secretion events. However, its specific function in governing IL-10 release from DCs remains unclarified. This study aimed to decipher the molecular mechanisms through which Rab27a regulates IL-10 secretion in DCs and explore the relevance of this pathway to immune dysregulation in food allergy (FA). Methods Bone marrow-derived dendritic cells (BMDCs) were isolated from C57BL/6 mice and purified using flow cytometry. Plasmacytoid DCs (pDCs) were obtained from the peripheral blood of FA patients and age-matched healthy control individuals for comparative analysis. Results Peripheral pDCs from FA patients exhibited notably reduced Rab27a activation levels compared to those from healthy controls. Concurrently, DCs from FA patients showed impaired immune tolerogenic function, as evidenced by their decreased ability to induce type 1 regulatory T (Tr1) cells. A strong positive correlation was observed between Rab27a activation and the induction of Tr1 cells by DCs. Mechanistically, activated Rab27a formed a complex with IL-10, facilitating the extracellular release of IL-10 from DCs. The guanine nucleotide exchange factor MADD (MAPK-activating death domain) was identified as a key regulator of Rab27a activation; knockdown of MADD in DCs eliminated Rab27a activation and IL-10 secretion. Conclusions Activated Rab27a is essential for IL-10 secretion by DCs, and MADD acts as a critical upstream regulator of Rab27a activation. Defects in the MADD-Rab27a-IL-10 signaling pathway contribute to impaired DC tolerogenicity in FA, suggesting that this pathway may serve as a potential therapeutic target for restoring immune balance in allergic diseases. - Source: PubMed
Publication date: 2026/06/25
Wu Yang-PengPeng Shu-WangBin Dong HuaWang Zhuo-YaLiu QiaoWu Yang-DongPeng Ke-PengTan Sheng-LanYang Ping-ChangTian Gui-Xiang - Atherosclerotic cardiovascular disease (ASCVD) is driven by dysregulated lipid metabolism and chronic inflammation. However, the mechanisms governing immune-liver crosstalk in this context remain poorly defined. Proline/serine-rich coiled-coil protein 1 (PSRC1) is a known regulator of cholesterol metabolism, but whether macrophage-derived PSRC1 influences hepatic functions via intercellular communication is unknown. - Source: PubMed
Publication date: 2026/06/09
Wu TongweiHuang HuiZhang XiaoqianFeng XinyiLuo WeimingLin LilongLiu DanPan HangyuWang ShaopengZhang JierongZhang XianyiGuo ZhigangYin MengzhuoCao ShipingZhang Yanan - During ischemia‒reperfusion injury (IRI), has been shown to alleviate inflammation and kidney damage. However, the function of the tubular epithelium-macrophage interaction mediated by in IRI-induced renal fibrosis is still unclear. - Source: PubMed
Publication date: 2026/05/18
Chen WuZhao ShengYang SongyuanYu WeiminRao TingZhou XiangjunRuan YuanZou FanCheng FanLi Wei - Genome-wide association studies (GWASs) have revealed the lung cancer susceptibility-associated non-coding SNP rs17728461 C/G. In this study, we demonstrated that rs17728461 is also associated with lung cancer outcome. The risk G allele increases the proliferative index and motility of cancer cells and promotes cancer metastasis in vivo in a xenograft mouse model. Mechanistically, rs17728461-G establishes a physical interchromosomal interaction between the rs17728461-bearing DNA fragment and the RAB27A gene locus and thereby increases RAB27A expression and promotes subsequent exosome secretion. eQTL analysis and immunostaining revealed an association between rs17728461-G and increased RAB27A expression in human lung cancers. These findings reveal a noncoding SNP-mediated interchromosomal regulatory mechanism underlying lung cancer progression. - Source: PubMed
Publication date: 2026/06/02
Jin YanTian XiaolingLiu WenxuGuo BingLei XinyueLiu XinhuaLi GuoliLiu XujingXiao ZengtuanZhang MengzheFan YuxinZhang ZhenfaMa ZhenyiLiu Zhe - Endoplasmic reticulum (ER) stress has been identified as a critical regulator of cholesterol metabolism and tumor-derived extracellular vesicles (tEVs) secretion in tumor cells, which significantly influences TME composition and impairs anti-tumor immune responses. Here, we develop a multifunctional immunomodulator (CPMR) that simultaneously targets cholesterol metabolism and tEVs secretion, thereby reprogramming the ER stress-mediated immunosuppression and enhancing anti-tumor immunotherapy. CPMR is constructed by co-loading cholesterol oxidase (ChOx) and Rab27a-shRNA plasmid into a copper-based metal-organic framework (MOF-199) coated with DSPE-PEG-RGD. In 4T1 tumor cells, CPMR demonstrates favorable glutathione peroxidase-mimicking, ChOx and peroxidase-like activities, initiating cascade catalytic reactions that disrupt the intracellular redox and metabolic homeostasis, further triggering acute ER stress. Simultaneously, silencing of Rab27a effectively inhibits tEVs-mediated cholesterol efflux. The resulting intracellular cholesterol accumulation serves as a substrate for subsequent ChOx-mediated oxidative reactions, forming a positive feedback loop that amplifies oxidative stress. These synergistic effects ultimately induce immunogenic cell death. Notably, the reduction in extracellular levels of cholesterol and tEVs effectively mitigates the ER stress-mediated immunosuppression, thereby potentiating immune responses. This study offers a promising strategy to harness and mitigate the subsequent effects of ER stress for the advancement of anti-tumor immunotherapy. - Source: PubMed
Publication date: 2026/05/28
Jin Xiao-KangPan TingXu Zi-HanZhang Shi-ManChen HongWang Yu-ZhangYan XiaoDai Jia-JingCheng Si-XueLiu Chuan-JunZhang Xian-Zheng