Ask about this productRelated genes to: RAB5C antibody
- Gene:
- RAB5C NIH gene
- Name:
- RAB5C, member RAS oncogene family
- Previous symbol:
- RABL
- Synonyms:
- RAB5CL
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-04
- Date modifiied:
- 2013-02-15
Related products to: RAB5C antibody
Related articles to: RAB5C antibody
- Altered lipid metabolism and lipid droplet (LD) dynamics are features of certain hepatocellular carcinoma (HCC) subtypes, but the molecular mechanisms governing LD trafficking and catabolism in HCC cells remain unclear. The small GTPase Rab5, a key regulator of early endosomal dynamics, has been previously observed to localize to the surface of LDs and participate in LD degradation through microlipophagy. However, the regulation of Rab5-LD interactions and its functional consequences in HCC cell metabolism and proliferation have not been elucidated. In this study, we explored the role of Rab5 in governing LD homeostasis and its impact on HCC cell proliferation. We found that GTP-bound Rab5 mutants (Q79L) exhibited increased association with LDs compared with the GDP-bound mutants (S34N) and WT Rab5. Acute nutrient starvation enhanced Rab5 GTP loading and recruitment to LDs, indicating that Rab5's GTPase cycle regulates its LD localization. Importantly, inhibition of Rab5 GTP binding led to increased LD accumulation, reduced mitochondrial respiration, and impaired proliferation in HCC cell lines. Transcriptomic analyses and tissue microarray immunohistochemistry further revealed that Rab5 is significantly overexpressed in HCC patient samples. These findings suggest that Rab5 GTP binding is an important contributor to LD dynamics in HCC cells, helping to govern LD turnover to sustain mitochondrial energy production and support cancer cell proliferation. - Source: PubMed
Publication date: 2026/02/25
Otakhor Kelly OZaidi Mohd Ali AbbasOberley-Deegan Rebecca EPonnusamy Moorthy PFisher Kurt WSchott Micah B - Alzheimer's disease (AD) risk is strongly influenced by genetic variants that converge on pathways regulating endosomal homeostasis. Among these, and have emerged as susceptibility genes, yet their functional relationship in AD remains largely unknown. Here, we investigated how BIN1 and RIN3 interaction regulates RAB5 activity and endosomal pathology. RIN3 has been shown to bind BIN1, and we previously reported that this interaction modulates amyloid-β (Aβ) precursor protein (APP) trafficking and Aβ generation in vitro. To extend these findings, we used constitutive knockout () mice and CRISPR-Cas9-edited human induced pluripotent stem cell-derived neurons carrying either knockout or rare familial AD missense mutations within the BIN1-binding domain. We found that disruption of BIN1-RIN3 binding, through either genetic deletion or pathogenic RIN3 variants, resulted in RIN3-mediated RAB5 hyperactivation and enlargement of neuronal endosomes, a hallmark of early AD pathology. Transcriptomic profiling further revealed dysregulated expression of AD-related genes. Together, these findings establish BIN1 as a critical regulator of RIN3-driven RAB5 activation and neuronal endosomal homeostasis. - Source: PubMed
Publication date: 2026/01/28
Maaser-Hecker Anna KZellmer Jacob CKim MichelleBakiasi GrisildaMaiti Amit KCurtat Matea P CChoi Se HoonProkopenko DmitryTanzi Rudolph EBhattacharyya Raja - Abnormal levels of VWF (von Willebrand Factor) are a risk factor for venous thromboembolism (VTE) and bleeding. Genome-wide association studies for VWF have identified novel candidate genes that may regulate VWF levels in humans, including (RAS [rat sarcoma]-associated protein RAB5C). We hypothesized that RAB5C regulates VWF release from endothelial cells. - Source: PubMed
Publication date: 2026/01/15
Reventun PaulaToledano-Sanz PabloDelgado-Marin MariaViskadourou MariaFoster D Briande Vries Paul SSabater-Lleal MariaAlcharani NunzioGonzalez-Cucharero ClaudiaOsburn William OMorrison Alanna CWolberg Alisa SSmith Nicholas LArvanitis Marios Lowenstein Charles J - Environmental light significantly influences neural development, yet the specific mechanisms underlying the effects of prolonged visual experience on homeostatic synaptic scaling remain unclear. Using manipulated ambient light conditions, we observed reduced mEPSC amplitudes and visually evoked responses in 20 hr light/4 hr dark (20LE) compared to a standard 12 hr light/12 hr dark (12LE) reared Xenopus laevis tadpoles. Prolonged light exposure accelerates the developmental decline of glutamatergic synaptic transmission via Rab5c-dependent endocytosis of AMPA receptor (AMPAR) subunits GluA1 and GluA2. The synaptic changes were accompanied by increased intrinsic neuronal excitability, but unchanged presynaptic release probability, and coincided with altered dendritic architecture. Notably, synaptic transmission and AMPAR expression were reversible upon re-exposure to standard 12LE conditions. Class I HDAC-mediated histone acetylation links epigenetic regulation to sustained AMPAR downregulation, revealing a two-stage process in which prolonged visual experience drives homeostatic synaptic downscaling through coordinated transcriptional/epigenetic mechanism and Rab5c-mediated trafficking. - Source: PubMed
Publication date: 2026/01/09
Zheng LijunDuan XinyiHuang WenyiLuo YuhaoWu YufeiLin QihuiWu XiaohuaHan LuShen Wanhua - This study aimed to screen the specific modules and hub genes of hyperlipidemia. - Source: PubMed
Publication date: 2025/12/10
Zhao ZhiyiCao YinGu AnnaYao Hanxin