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
- The biogenesis of small extracellular vesicles (sEVs) is only partially understood. Our recent findings provide evidence that a newly described sEV secretion pathway, the amphiectosome release followed by the sEV discharge by the 'torn bag mechanism' are present in all tested cell lines and mouse organs. Surprisingly, in in situ fixed steady-state cells, transmission electron microscopy did not reveal sEV release via exocytosis of multivesicular endosomes (MVEs). In the current study, we extended our previous analysis to additional mouse organs and confirmed the presence of secreted amphiectosomes in all of them. Furthermore, we investigated which parameters influence the activation of the distinct sEV release mechanisms in HEK cells. Our results show that under stress conditions (such as Ca ionophore-induced membrane stress or metabolic stress, induced by serum starvation), exocytosis of MVEs is activated, while this process is absent in steady-state conditions. By silencing ATG5 (a key regulator of autophagy) and RAB27a (an essential small GTPase for MVE exocytosis), we selectively modulated these two mechanisms, respectively. Amphiectosome release depended on both autophagy and ATG5, while exocytosis of MVE was autophagy-independent but RAB27a-dependent. Our findings suggest that sEV release via the 'torn bag mechanism' is a general and essential secretion pathway in non-stressed, steady-state mammalian cells, while stress conditions induce the sEV release via MVE exocytosis. - Source: PubMed
Lenzinger DorinaLankovics LillaDudás IstvánBárkai TündeSzász ZsófiaBalbisi MirjamWu Anthony Yan-TangVukman Krisztina VFletcher KelseyCsomos AttilaMucsi ZoltánBugyik EdinaCserép CsabaDénes ÁdámBősze SzilviaTuriák LillaLai Charles Pin-KuangBuzás Edit IVisnovitz Tamás - Accumulating data support the role of exosomes from virus-infected cells (especially RNA viruses) in the selective encapsulation of viral proteins, genomic material, and even whole virions, thereby mediating intercellular communication events and contributing to viral transmission. Tembusu virus (TMUV), a single-stranded RNA virus, has posed a threat to global public health since its emergence in 2010. However, whether exosomes can mediate TMUV intercellular transmission remains obscure. Here, we show that exosomes derived from TMUV-infected cells (TMUV-exosomes) contained viral genomic RNA and partial viral proteins (C, prM, E, NS1, NS2B, NS4B, and NS5). TMUV-exosomes enter HEK293 cells primarily via a dynamin-dependent, cholesterol-sensitive caveolae-mediated (CavME) endocytosis pathway, thereby suppressing the subsequent expression of key antiviral immune genes to create a proviral microenvironment that supports productive TMUV infection. Remarkably, central to this exosomal hijacking mechanism, the viral NS4A protein and host Rab27a protein form a critical regulatory axis. Specifically, NS4A upregulates Rab27a expression to potentiate the release of exosomes encapsulating viral nucleic acids and proteomic components. Overall, our study provides a mechanistic model for understanding the role of exosomes in TMUV intercellular transmission and identifies the NS4A-Rab27a axis as a critical regulatory node. Disrupting this interaction may represent a potential therapeutic strategy for TMUV infection, warranting further investigation. - Source: PubMed
Publication date: 2026/08/09
He DalinYang JingCui YitongWu BingrongWei FengZhu SimingDiao YouxiangTang Yi - To investigate the changes in synovial matrix stiffness in a mouse model of osteoarthritis (OA) and the expression of RAB27A, a key regulator of exosome biosynthesis, in synovial fibroblasts, and to validate the effect of matrix stiffness on RAB27A expression in vitro. - Source: PubMed
Publication date: 2026/08/05
Kaiyuan JinHanglin LiHong DengYilei DongBoyao HouYaxin Deng - Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social communication and repetitive behaviors, with genetic studies implicating widespread synaptic dysfunction. However, the contribution of presynaptic vesicle trafficking mechanisms to ASD pathogenesis remains incompletely understood. Here, we identify synaptotagmin-like protein 4 (SYTL4), a RAB27A effector previously characterized in secretory cells, as a regulator of presynaptic function in the mammalian brain. We report a recurrent hemizygous missense variant, R126H, located within the Rab-binding domain of in four unrelated male individuals, consistent with an X-linked recessive mode of ASD, and additionally identify a de novo missense variant in (T41A) in an independent ASD family that affects a domain mediating interactions with downstream effectors. Using a R126H knock-in mouse model, we show that R126H knock-in male mice exhibit ASD-relevant behavioral abnormalities accompanied by synaptic deficits in the medial prefrontal cortex. At the molecular level, ASD-associated and variants interfere with the interaction between SYTL4 and RAB27A, providing a mechanistic link between human genetic variation and synaptic dysfunction. Together, these findings implicate disrupted SYTL4-RAB27A-dependent vesicle trafficking in ASD pathogenesis and identify and as previously unrecognized contributors to autism-associated synaptic deficits and behavior. - Source: PubMed
Publication date: 2026/07/30
Liao YangZhang ShujuZhang XiaoleiTan SenweiLuo YuWan YingjieLyu YongqingXie BoyuanZhan RuiZhang YuChen GuodongJia XiangbinHu ZhengmaoZheng YuMao XiaoWang HuaTan JieqiongLi FaxiangPeng YuXia KunGuo Hui - : (Meisn.) H.Gross (PS) has anti-photoaging, anti-inflammatory, and antioxidant activities, but the anti-pigmentation potential of the PS flower absolute (PSFAb) remains largely unexplored. This study aimed to examine the chemical composition and anti-melanogenic and melanosome transport-inhibitory effects of PSFAb using B16BL6 murine melanoma cells. : PSFAb was extracted with hexane and analyzed by gas chromatography-mass spectrometry (GC-MS). The biological activities in B16BL6 murine melanoma cells were evaluated using water-soluble tetrazolium salt (WST) assays, 5-bromo-2'-deoxyuridine (BrdU) incorporation, enzyme-linked immunosorbent assays, and immunoblotting methods. : GC-MS analysis identified eight constituents in PSFAb. Cell viability was not significantly altered in B16BL6 cells at concentrations ≤ 100 μg/mL, which were used for additional tests. PSFAb inhibited serum-induced cell proliferation and suppressed α-melanocyte-stimulating hormone (α-MSH)-induced melanin synthesis and tyrosinase activity in B16BL6 cells. PSFAb also downregulated the α-MSH-induced expression of key melanogenic regulators, including microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein-1 (TRP-1), and TRP-2. PSFAb decreased extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase phosphorylation but enhanced JNK phosphorylation in α-MSH-stimulated B16BL6 cells. Furthermore, PSFAb reduced the α-MSH-induced expression of melanosome transport-related proteins (melanophilin and Rab27a) in B16BL6 cells. : Overall, these results suggest that PSFAb has the potential to exert anti-pigmentation effects by suppressing melanogenesis and downregulating melanosome transport-related proteins. Therefore, PSFAb may be a promising candidate for the development of natural agents targeting hyperpigmentation and skin pigmentation regulation. - Source: PubMed
Publication date: 2026/07/22
Won Kyung JongLee Hwan MyungKim Yoon YiBae Ji HyeYun Ji SeongKim Do Yoon