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
- Myocardial ischemia-reperfusion injury (MIRI) remains a critical complication associated with cardiopulmonary bypass (CPB). This study investigated whether p38 mitogen-activated protein kinase (p38MAPK) sustains myocardial glucose uptake by controlling glucose transporter-4 (GLUT4) expression and membrane translocation through distinct myocyte enhancer factor-2 (MEF2) isoforms. - Source: PubMed
Publication date: 2026/03/20
Gao WeilongZhang DanZhang BenfaSun PengCao YingYang SiyuanChen HongjinSong Yingnan - - Source: PubMed
Publication date: 2026/02/27
Schuelke SophieHaseeb SanaParmar Mayur S - Mutations in leucine-rich repeat kinase 2 (LRRK2) are among the most common genetic causes of Parkinson's disease (PD), yet substantial heterogeneity exists among pathogenic variants. How mutations in distinct functional domains of LRRK2 differentially perturb cellular homeostasis remains incompletely understood. Here, we compared two pathogenic LRRK2 mutations-G2019S in the kinase domain and I1371V in the GTPase domain-across multiple cellular models, including SH-SY5Y and U87 cells, and healthy human iPSC-derived floor plate cells. We demonstrate that the I1371V mutation induces markedly more severe cellular dysfunction than G2019S. I1371V-expressing cells exhibited elevated LRRK2 autophosphorylation at S1292 and robust hyperphosphorylation of Rab8A and Rab10, indicating enhanced downstream signaling. These alterations impaired sterol trafficking, leading to selective depletion of membrane cholesterol without changes in total cellular cholesterol. Consequently, I1371V cells displayed increased membrane fluidity, disrupted microdomain organization, altered membrane topology, reduced caveolin-1 expression, and impaired dopamine transporter surface expression and dopamine uptake. Lipidomic profiling further revealed a broad disruption of lipid homeostasis, including reductions in cholesteryl esters, sterols, sphingolipids, and glycerophospholipids, whereas G2019S cells showed comparatively modest changes. Pharmacological intervention revealed mutation-specific responses, with the non-selective LRRK2 modulator GW5074 outperforming the kinase-selective inhibitor MLi-2 in restoring Rab8A phosphorylation, membrane integrity, and dopaminergic function. Collectively, these findings identify membrane lipid dysregulation as a central cell biological mechanism in LRRK2-associated PD and underscore the importance of variant-specific therapeutic strategies. - Source: PubMed
Publication date: 2026/02/13
Singh KhushbooBanerjee RoonPotdar ChandrakantaShaw AnishaRakshith RakshithKamble NitishHolla VikramYadav RaviPal Pramod KumarDatta Indrani - Esophageal squamous cell carcinoma (ESCC) is a highly lethal cancer with limited therapeutic options and frequent relapse. RNA acetylation has emerged as a crucial regulator of tumor biology. In this study, we identify circTHBS1 as an oncogenic circRNA that promotes autophagy and drives ESCC progression. Mechanistically, circTHBS1 interacts with the N-acetyltransferase 10 (NAT10), preventing its ubiquitin-mediated proteasomal degradation and thereby increasing global N-acetylcytidine (acC) modification. Rab8a is identified as a key acC target, where acC modification at a conserved CGCCAG motif within the coding sequence facilitates NAT10 binding and enhances translation. Disruption of this modification impairs Rab8a-driven autophagy and suppresses tumor progression. Collectively, our findings reveal a circTHBS1/NAT10-acC/Rab8a axis that reprograms translational control and autophagy, providing new mechanistic insights and potential therapeutic targets for ESCC. - Source: PubMed
Publication date: 2026/02/19
Xie Shu-HuanXu Shui-DanMo Ao-TianTang YongWu Jun-HanZhuang Wei-TaoDuan Jin-LingHuang Ci-JunLi Si-WenQiao Gui-BinXie DanChen Ri-Xin - Ovarian cancer (OC) is the predominant gynecological cancer and is associated with severe morbidity and high mortality worldwide. Therefore, clarifying the molecular mechanisms underlying OC progression and exploring novel therapeutic targets are important. Here, using human OC samples, different OC cell lines, and xenograft nude mouse models in combination with multiple sequencings, we report that hnRPD, an RNA binding protein that modulates RNA stability, is highly expressed in OC tissues, and contributes to OC cell malignancy in human OC cells cultured in vitro and in OC cell-derived xenograft nude mouse models in vivo. Mechanistically, ectopically expressed GPR137 binds to hnRPD and enhances hnRPD protein stability, which reciprocally transactivates GPR137 through the transcription factor FLI1. On the other hand, elevated hnRPD upregulates RAB8A expression by interacting with RAB8A mRNA and promoting its stability, leading to activation of downstream cell signaling and thereby enhanced OC cell malignant behaviors including cell proliferation, cell invasion, cell migration, and colony formation ability as well as OC xenograft growth in nude mice. Moreover, cisplatin in combination with silencing of hnRPD expression, significantly induces apoptosis in cisplatin-resistant OC cells through regulation of OC cell metabolism. Therefore, our data provide evidence that hnRPD could represent an innovative prognostic indicator for OC and may be an attractive therapeutic target for improving clinical outcomes in OC treatment. - Source: PubMed
Publication date: 2026/02/09
Tang ChaoZhu ChongyingAn ZihaoCao BinXu QiangLi LinBao YiyaoLi Jiayong