Ask about this productRelated genes to: RAB5C Blocking Peptide
- 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 Blocking Peptide
Related articles to: RAB5C Blocking Peptide
- Noncanonical conjugation of ATG8 proteins, including LC3, to single membranes implicates the autophagy machinery in cell functions unrelated to metabolic stress. One such pathway is LC3-associated phagocytosis (LAP), which aids in phagosome maturation and subsequent signaling upon cargo uptake mediated by certain innate immunity-associated receptors. Here, we show that a specific isoform of RAB5 GTPases, the molecular switches controlling early endosome traffic, is necessary for LAP. We demonstrate that RAB5c regulates phagosome recruitment and function of complexes required for phosphatidylinositol 3-phosphate [PI(3)P] and reactive oxygen species (ROS) generation by macrophages. RAB5c facilitates phagosome translocation of the V-ATPase transmembrane core, which is needed for ATG16L1 binding and consequent LC3 conjugation. RAB5c depletion impaired macrophage elimination of the fungal pathogen and disruption of the V-ATPase-ATG16L1 axis increased susceptibility in vivo. Thus, early endosome-to-phagosome trafficking can be selectively engaged to promote pathogen elimination by directing phagosomal maturation toward LAP. - Source: PubMed
Publication date: 2026/05/08
Freitas-Filho Edismauro GarciaZaidan IsabellaAlzamora-Terrel Daniel LeonardoBifano CarolinaFortes-Rocha Marlonde Castro Patrícia AlvesEugênio Araujo Piraine RenanPinzan Camila Figueiredode Rezende Caroline PatiniBoada-Romero EmilioWileman ThomasAlmeida FaustoGoldman Gustavo HenriqueFlorey OliverCunha Larissa Dias - We show continuous tumor exposure results in a loss of chimeric antigen receptor (CAR) T cell (CART) endocytic activity due to downregulation of Rab5. Loss of endocytic activity exacerbates the effects of trogocytosis, the bidirectional transfer of tumor target antigens and CARs between malignant cells and CARTs, resulting in CART dysfunction and fratricide. Constitutive expression of Rab5 within the CARTs reduced fratricide by reducing the amount of trogocytosed antigens on the cell surface, while simultaneously enhancing CAR availability through dissociation of CAR from target, recycling unbound CAR back to the plasma membrane, and limiting CAR capture by tumor cells. Rab5-expressing CARTs exhibited superior antitumor activity in both BCMA-CARTs isolated from the bone marrow of treated patients and mesothelin-specific CARTs in a solid tumor model. These studies uncover an unexpected relationship between endocytosis and CART function and suggest that pairing Rab5 with CAR expression could improve the clinical efficacy of CART therapy. - Source: PubMed
Publication date: 2026/05/05
Gu MeidiRead Kaitlin ABhardwaj VipinCarvalho Edmund JNardo DavidShayne Justin CShukla DivanshuLiu WeiSiegel Donald LSheppard Neil CMilone Michael CCohen Adam DGarfall Alfred LRiley James L - 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