Ask about this productRelated genes to: RAB8A antibody
- Gene:
- RAB8A NIH gene
- Name:
- RAB8A, member RAS oncogene family
- Previous symbol:
- MEL
- Synonyms:
- RAB8
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-01-15
Related products to: RAB8A antibody
Related articles to: RAB8A antibody
- Chronic stress activates the hypothalamic-pituitary-adrenal (HPA) axis and induces systemic physiological changes. This study aimed to identify stress-associated serum biomarker candidates in chronically stressed beagle dogs and to evaluate the anti-stress effects of var. (Maxim.) Kitam. extract (CZE). Beagle dogs were subjected to movement restriction-induced chronic stress for 42 days, with or without repeated oral administration of CZE. Serum cortisol and corticosterone concentrations were measured using ELISA, and hematological and serum biochemical parameters were analyzed. Serum samples collected at day 0 and day 42 of the 84-day chronic stress model were subjected to LC-MS/MS-based proteomic analysis. Chronic stress increased serum cortisol and corticosterone concentrations and induced alterations in hematological and serum biochemical parameters, whereas CZE administration tended to attenuate or stabilize these stress-associated changes. Proteomic analysis identified 380 serum proteins, of which 348 quantified proteins were subjected to differential expression analysis. The differentially expressed proteins were primarily associated with immune response, inflammatory response, extracellular matrix organization, angiogenesis, neurogenesis, and secretion. TIMP1, TREM2, RAB8A, KRT9, PPBP, THBS1, and HSPB1 were identified as candidate stress-associated serum biomarkers. These findings indicate that chronic stress induces endocrine, hematological, biochemical, and serum proteomic alterations in beagle dogs. Changes in proteins related to immune-inflammatory regulation and extracellular matrix organization suggest that prolonged stress may affect systemic immune responses and tissue remodeling. CZE may contribute to the maintenance of physiological homeostasis under chronic stress conditions and may have potential as a functional anti-stress material, while the identified serum proteins may provide a basis for the development of biomarkers for chronic stress. - Source: PubMed
Publication date: 2026/08/26
Yang Ye JinKim Min JungKim Hee HoHeo Ji WoongChun Ju LanShin Eui-CheolKim Kyeong SooKim Hyun-WookJeong Eun JuLee DongbinPark Kwang Il - Ulcerative colitis (UC) is a type of inflammatory bowel disease. Macrophage polarization is crucial in the development of UC. Oxypalmatine (OPAL) is an isoquinoline alkaloid that can be isolated from various plant, including Phellodendron amurense and Sinomenium acutum. It is also an oxidative metabolite derived from the hepatic biotransformation of palmatine (PAL), which is one of the active constituents of Coptis chinensis that demonstrates anti-inflammatory and antioxidant properties. - Source: PubMed
Publication date: 2026/08/27
Huang ZhuowenZhang XiaFang YilongWeng XiaoyaGuo KaiDeng YafengHuang JinhaoXian YanfangChen JianpingLi MuxiaSu ZirenXie YouliangSu JiyanHuang Xiaoqi - Ferroptosis is an iron-dependent form of regulated cell death driven by lipid peroxidation; however, how selective autophagy regulates ferroptotic sensitivity remains incompletely understood. Here, we identify RAB8A as a selective autophagic substrate and negative regulator of ferroptosis. Quantitative proteomic analyses reveal that ferroptotic stress induces ATG5- and ATG7-dependent degradation of RAB8A. Mechanistically, ferroptotic stimuli induce RNF126-dependent polyubiquitination of RAB8A and subsequent SQSTM1-mediated autophagic degradation. Functionally, loss of sensitizes cancer cells to ferroptosis, whereas expression of the degradation-resistant active mutant RAB8A suppresses ferroptotic cell death. RAB8A interacts with TFRC and facilitates stress-induced redistribution of TFRC from the plasma membrane toward endolysosomal compartments. deficiency impairs TFRC clearance, enhances transferrin-dependent iron uptake, and increases intracellular Fe accumulation and lipid peroxidation. In fibrosarcoma and pancreatic cancer xenograft models, depletion enhances the antitumor efficacy of ferroptosis-inducing therapy. Clinically, RAB8A is upregulated and associated with poor prognosis and ferroptosis resistance in pancreatic cancer. Collectively, these findings establish an autophagy-RAB8A-TFRC axis that regulates ferroptotic sensitivity. BCA: bicinchoninic acid; BSA: bovine serum albumin; CCK-8: cellcounting kit-8; Co-IP: co-immunoprecipitation; DMSO: dimethylsulfoxide; ELISA: enzyme-linked immunosorbent assay; FBS: fetalbovine serum; HRP: horseradish peroxidase; IP: immunoprecipitation;LC-MS/MS: liquid chromatography-tandem mass spectrometry; MDA:malondialdehyde; MEF: mouse embryonic fibroblast; PBS:phosphate-buffered saline; PBS-T: PBS containing Tween-20; PI:propidium iodide; PVDF: polyvinylidene difluoride; qPCR: quantitativereal-time polymerase chain reaction; SDS: sodium dodecyl sulfate;STR: short tandem repeat; TBA: thiobarbituric acid; TBST:Tris-buffered saline containing Tween-20; TMT: tandem mass tag; WT:wild type. - Source: PubMed
Publication date: 2026/09/16
Li JingboZhou QileLiu JiaoChen XinYu ChunhuaKang RuiTang Daolin - Despite advances in percutaneous coronary intervention, ischemia-reperfusion (IR) injury remains a major cause of morbidity and mortality. Adiponectin confers broad cardioprotective effects, motivating the development of adiponectin receptor agonists. Here, we investigated the cardioprotective efficacy and mechanisms of ALY688, a synthetic adiponectin receptor agonist peptide, in myocardial IR injury. In a clinically translatable rat IR model, intravenous administration of ALY688 during ischemia together with subcutaneous dosing that continued for 28 days reduced troponin-I levels, cardiomyocyte death, and infarct size, while preserving cardiac function. ALY688 restored autophagic flux, mitigated reactive oxygen species accumulation, and suppressed apoptosis in both IR hearts and hypoxia-reoxygenation (HR)-treated cardiomyocytes. Proteomic profiling revealed that Rab8a, downregulated by IR, was maintained with ALY688 treatment. Notably, ALY688 increased extracellular vesicle (EV) abundance in myocardium and plasma, and EVs from treated animals displayed distinct proteomic signatures enriched in glycolytic and oxidative stress-related proteins. These EVs conferred protection against HR-induced injury in H9c2 and human iPSC-derived cardiomyocytes. CRISPR-mediated Rab8a knockout impaired ALY688-induced EV biogenesis and attenuated the cytoprotective effects of these EVs. Collectively, these findings identify ALY688 as a promising therapeutic that mitigates IR injury via both direct myocardial protection and Rab8a-dependent EV-mediated cardioprotective signalling. - Source: PubMed
Sung Hye KyoungTang JialingLei YubinNguyen KhangTam EddieWu JunLi Ren-KeRichard VincentBorchers Christoph HAntounians LinaBurger DylanZani AugustoSweeney Gary - LRRK2, the Parkinson's disease-associated kinase, phosphorylates a subset of Rab GTPases and regulates membrane dynamics. We previously reported that lysosomal stress activates LRRK2 and thereby induces the exocytic secretion of lysosomal contents, but the detailed secretion mechanism remained unclear. Here we found that, under lysosomal stress, endolysosomal luminal and membrane components were secreted with extracellular vesicles (EVs) via LRRK2. Bis(monoacylglycerol)phosphate, an endolysosomal lipid and a urinary marker of LRRK2 activity, was similarly secreted via LRRK2, whereas CD9-positive EVs were not involved. Further dissection of the secreted EVs revealed that Alix-positive EVs were secreted via Rab8a as well as the ESCRT component VPS4, whereas LAMP1/cathepsin B-positive EVs were secreted via Rab10/Rab35, and SNARE proteins syntaxin 2 and VAMP8 regulated the secretion of both EV subtypes. These findings suggest a distinctive stress-induced secretory mechanism whereby LRRK2 facilitates the secretion of multiple EV subtypes by controlling Rab GTPases involved in each pathway. - Source: PubMed
Publication date: 2026/08/13
Sakurai MariaKuwahara TomokiSuenaga ShoichiTakatori ShoTomita TaisukeShalit TammyTengstrand ElizabethHsieh FrankIwatsubo Takeshi