Ask about this productRelated genes to: RAB3C antibody
- Gene:
- RAB3C NIH gene
- Name:
- RAB3C, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-29
- Date modifiied:
- 2016-10-05
Related products to: RAB3C antibody
Related articles to: RAB3C antibody
- Endometrial polyps (EPs) are benign overgrowths of the endometrium causing abnormal uterine bleeding and infertility. Despite their clinical significance, the molecular mechanisms underlying their development and recurrence remain poorly understood, warranting comprehensive transcriptomic investigation. We hypothesized that transcriptomic differences, particularly at the single-cell level as revealed through cellular trajectory analysis, distinguish EPs from adjacent endometrium. To investigate this, paired EP and adjacent endometrium (adEN) samples were collected from 12 women undergoing hysteroscopic polypectomy (proliferative phase, = 9; secretory phase, = 3) and analyzed using bulk and single-cell RNA sequencing (scRNA-seq). Bulk RNA-seq revealed high transcriptional similarity between EPs and adENs, with only a few differentially expressed genes (FDR < 0.05) in proliferative-phase EPs, including upregulation of and and downregulation of and , potentially reflecting epigenetic regulation and protective mechanisms against tumorigenesis. scRNA-seq identified eight major cell clusters namely stromal, epithelial, endothelial, immune, perivascular, macrophage, B cell, and ciliated populations in both tissues. Pseudotime analysis revealed a mid-transcriptional arrest and enrichment of -positive intermediate epithelial states in EPs, in contrast to the late, mature epithelial stage seen in the adENs. This aberrant epithelial maturation may be associated with impaired perivascular and endothelial differentiation, potentially contributing to defective vascular remodeling and polyp persistence. In conclusion, while EPs exhibit global transcriptomic similarity to adENs, single-cell and pseudotime analyses suggest subtle but significant disruptions in epithelial differentiation and vascular remodeling that might be involved in EPs development. Study limitations include scRNA-seq restricted to the proliferative phase, which may limit generalizability. Nevertheless, future functional studies using primary epithelial organoids derived from EPs may provide a physiologically relevant model to evaluate targeted therapeutic strategies including hormonal interventions with potential applications in infertility management. - Source: PubMed
Publication date: 2026/02/19
Pathare Amruta D SLawarde AnkitaTäär KatrinMoreno Sergio VelaApostolov ApostolModhukur VijayachitraTarassova DarjaSola-Leyva AlbertoSalumets AndresSaare MerliPeters Maire - DENN/MADD (mitogen-activated protein kinase-activating death domain), a differentially expressed in normal and neoplastic cells (DENN) domain-containing protein functions in membrane trafficking. DENN domain-bearing proteins have guanine nucleotide exchange factor activity toward Rab GTPases. Here, we identify Rab GTPase substrates for DENN/MADD using a cell-based assay involving DENN domain-mediated recruitment of Rab substrates to mitochondria. We confirmed known interactions of DENN/MADD with Rab3A, Rab3B, Rab3C, Rab3D, and Rab27B and identified four new potential substrates, Rab8B, Rab15, Rab26, and Rab37, results confirmed with biochemical experiments. Mutations in the DENN domain of DENN/MADD result in diverse pathophysiological manifestations, ranging from predominant neurological dysfunction to a multisystem disorder. Structural analysis using AlphaFold suggested that these mutations affect DENN/MADD's interaction with Rab GTPases. Introducing such mutations into DENN/MADD's DENN domain influenced the mitochondrial recruitment of Rabs. This study identifies new DENN/MADD protein interactions and cellular pathways, the disruption of which results in human disorders. - Source: PubMed
Publication date: 2025/08/12
Khan MaleehaKumar RahulTrempe Jean-FrançoisFrancis VincentBanks EmilyAyoubi RihamLuna Luis AguileraMcPherson Peter S - The Rab3 protein family is composed of a series of small GTP-binding proteins, including Rab3a, Rab3b, Rab3c, and Rab3d, termed Rab3s. They play crucial roles in health, including in brain function, such as through the regulation of synaptic transmission and neuronal activities. In the high-energy-demanding and high-traffic neurons, the Rab3s regulate essential cellular processes, including trafficking of synaptic vesicles and lysosomal positioning, which are pivotal for the maintenance of synaptic integrity and neuronal physiology. Emerging findings suggest that alterations in Rab3s expression are associated with age-related neurodegenerative pathologies, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, among others. Here, we provide an overview of how Rab3s dysregulation disrupts neuronal homeostasis, contributing to impaired autophagy, synaptic dysfunction, and eventually leading to neuronal death. We highlight emerging questions on how Rab3s safeguards the brain and how their dysfunction contributes to the different neurodegenerative diseases. We propose fine-tuning the Rab3s signaling directly or indirectly, such as via targeting their upstream protein AMPK, holding therapeutic potential. - Source: PubMed
Publication date: 2025/07/14
He HaijunAi RuixueFang Evandro FeiPalikaras Konstantinos - Marfan syndrome (MFS) is a hereditary disorder primarily caused by mutations in the FBN1 gene. Its critical cardiovascular manifestation is thoracic aortic aneurysm (TAA), which poses life-threatening risks. Owing to the lack of effective pharmacological therapies, surgical intervention continues to be the current definitive treatment. In this study, the role of Piezo-type mechanosensitive ion channel component 1 (Piezo1) in MFS was investigated and the activation of PIEZO1 was identified as a potential treatment for MFS. - Source: PubMed
Yang PeiwenLiu HaoWang ShilinXiao XiaoyueJiang LangLe ShengChen ShanshanYe PingXia Jiahong - Lung cancer (LC) is one of the major malignant diseases threatening human health. The study aimed to identify the effect of citrulline on the malignant phenotype of LC cells and to further disclose the potential molecular mechanism of citrulline in regulating the development of LC, providing a novel molecular biological basis for the clinical treatment of LC. The effects of citrulline on the viability, proliferation, migration, and invasion of LC cells (A549, H1299) were validated by CCK-8, colony formation, EdU, and transwell assays. The cell glycolysis was assessed via determining the glucose uptake, lactate production, ATP levels, extracellular acidification rate (ECAR), and oxygen consumption rate (OCR). RNA-seq and molecular docking were performed to screen for citrulline-binding target proteins. Western blotting experiments were conducted to examine the expression of related signaling pathway molecules. In addition, the impacts of citrulline on LC growth in vivo were investigated by constructing mouse models. Citrulline augmented the viability of LC cells in a concentration and time-dependent manner. The proliferation, migration, invasion, glycolysis, and EMT processes of LC cells were substantially enhanced after citrulline treatment. Bioinformatics analysis indicated that citrulline could bind to RAB3C protein. Western blotting results indicated that citrulline activated the IL-6/STAT3 pathway by binding to RAB3C. In addition, animal experiments disclosed that citrulline promoted tumor growth in mice. Citrulline accelerated the glycolysis and activated the IL6/STAT3 pathway through the RAB3C protein, consequently facilitating the development of LC. - Source: PubMed
Publication date: 2024/05/21
Meng QingjunLi YanguangSun ZhenLiu Junfeng