Ask about this productRelated genes to: RASGRP3 antibody
- Gene:
- RASGRP3 NIH gene
- Name:
- RAS guanyl releasing protein 3
- Previous symbol:
- -
- Synonyms:
- KIAA0846, GRP3, CalDAG-GEFIII
- Chromosome:
- 2p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-05
- Date modifiied:
- 2016-10-05
Related products to: RASGRP3 antibody
Related articles to: RASGRP3 antibody
- Uveal melanoma, the most common eye cancer in adults, remains limited to surgical intervention and radiotherapy, with a dismal survival rate that has not improved in over 50 years. To address this therapeutic impasse, we systematically analyzed public gene expression and CRISPR knockout datasets, identifying as an essential gene specifically for uveal melanoma. RasGRP3 is uniquely overexpressed and essential for survival in uveal melanoma cells, but dispensable in healthy cells. However, RasGRP3 remains "undruggable" due to its intracellular localization and lack of targetable binding pockets. To overcome this, we developed a CRISPR-Cas13d RNA-targeting therapeutic against RasGRP3, which mediates potent yet selective uveal melanoma killing through two synergistic mechanisms: (1) on-target knockdown of the essential RasGRP3 mRNA, and (2) collateral RNA degradation triggered by the cleavage of overexpressed RasGRP3. When delivered via optimized lipid nanoparticles loaded with Cas13d mRNA and guide RNA, this strategy eliminated >97% of uveal melanoma cells while sparing healthy cells, including retinal pigment epithelial cells. This approach outperformed conventional Cas9 and siRNA methods in potency without inducing permanent genomic alterations. Our findings establish an RNA-targeting therapeutic for uveal melanoma and a framework for Cas13-based interventions against other "undruggable" cancers. - Source: PubMed
Publication date: 2026/02/10
Stauber DanielSosnick LucasMa YitongPimcharoen SopidaLawanprasert AtipMurthy NirenMyung DavidQi Lei S - Atherosclerosis (AS) is a cardiovascular disorder accompanied by endothelial dysfunction and vascular inflammation. We aim to investigate the effects of Ras guanine nucleotide-releasing protein 3 (RasGRP3), a guanine nucleotide exchange factor in AS. Decreased RasGRP3 protein expression was observed in the endothelium of high-fat diet-fed ApoE mice and oxidized low-density lipoprotein (ox-LDL)-induced human primary aortic endothelial cells. RasGRP3 overexpression decreased the mRNA expressions and productions of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α, VCAM-1 protein expression, and THP-1 cell adhesion in vitro. RasGRP3 overexpression inhibited NF-κB pathway activation and THP-1 cell adhesion in vitro by activating Ras-related protein 1 (RAP1) without altering its protein expression. In endothelial cell-specific RasGRP3 overexpression ApoE mice, the RAP1B activity was elevated. RasGRP3 overexpression inhibited atherosclerotic plaque formation in the aortic root and reduced lipid deposition in the entire aorta. Additionally, the concentration of IL-1β, IL-6, and TNF-α in vivo was reduced by the RasGRP3 overexpression. Ubiquitin-like containing PHD and RING finger domain 1 (UHRF1), a member of the E3 ubiquitin ligase family, is one of the RasGRP3 binding proteins. A previous study reported that UHRF1 inhibition alleviated ox-LDL-induced endothelial injury. We found that by inhibiting ubiquitination and degradation of RasGRP3, UHRF1 knockdown promoted RasGRP3 protein expression in vitro. In conclusion, RasGRP3 overexpression alleviated endothelial dysfunction and vascular inflammation in AS mice through activation of RAP1B, a process that may be mediated by UHRF1 regulation of RasGRP3 ubiquitination. - Source: PubMed
Publication date: 2026/02/14
Zhang BojianWei ZhengZou QingyunQiao Haiquan - Archaic introgression introduced functionally relevant variants into modern humans, yet small-scale insertions remain understudied. Here, we leverage 2519 modern human genomes and four high-coverage archaic hominin genomes to systematically characterize nuclear mitochondrial DNA segments (NUMTs). We uncover 483 polymorphic NUMTs across globally diverse human populations and 10 in archaic genomes. By combining overlap with Neanderthal-derived and Denisovan-derived haplotypes, phylogenetic analyses, insertion time estimates, and haplotype colocalization, we identify five NUMTs introduced into modern humans via archaic hominin introgression. Functional analyses reveal that introgressed NUMTs can modulate gene expression, including allele-specific up-regulation of the immune-related gene , and reshape three-dimensional chromatin structure at loci such as and . These findings highlight an underappreciated mechanism by which archaic mitochondrial fragments shape nuclear genome function and evolution. Our study reframes NUMTs not as passive genomic fossils but as dynamic elements influencing modern human diversity and adaptation. - Source: PubMed
Publication date: 2026/02/04
Zhu QiongZhang JinningZhou WeichenLiang Shen-AoWang ShengmiaoCai XinyuLi FuyuanLi JinZhang GuojieFeng HuijuanFu QiaomeiAkey Joshua MZhang FengJin LiXu ShuhuaZheng Hong-XiangChen Lu - The activation of dendritic cells, which is atypical, is vital for triggering the acquired immune response in people afflicted with chronic obstructive pulmonary disease (COPD). This research seeks to pinpoint significant genes linked to dendritic cells within the lung tissues of COPD patients by utilizing bioinformatics predictions and experimental validation. - Source: PubMed
Publication date: 2025/10/29
Huo ZengyuZou JiaweiOu SiyiXu CunlaiXiao LinlinChen FengYang YangChen SimingCen XiangyuanQin YiraoBai Jing - Melanoma is an aggressive skin cancer derived from melanocytes, known for its high metastatic potential and poor prognosis. Understanding the molecular mechanisms underlying melanoma progression could provide novel therapeutic targets for improving treatment outcomes. Our study aims to investigate the role of the RHO family GTPase RHOJ in melanoma progression and its regulation of cell adhesion, proliferation, and apoptosis through the Rap1 signaling pathway. - Source: PubMed
Publication date: 2025/08/21
He XiMa JieXia JialiGuan ZhiqiangJiang Guan