Ask about this productRelated genes to: RRAGD Blocking Peptide
- Gene:
- RRAGD NIH gene
- Name:
- Ras related GTP binding D
- Previous symbol:
- -
- Synonyms:
- DKFZP761H171, bA11D8.2.1
- Chromosome:
- 6q15
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-07
- Date modifiied:
- 2016-02-23
Related products to: RRAGD Blocking Peptide
Related articles to: RRAGD Blocking Peptide
- - Source: PubMed
Publication date: 2026/04/21
Zhang ZongyeWang HongboCheng XingboZhang ZhichangHou ZhenxingLiu ZhendongGao Yanzheng - This study aimed to identify autophagy-related genes with a causal role in ischemic stroke (IS) risk using a multi-omics Mendelian randomization (MR) approach. We integrated summary-level data for blood-derived DNA methylation (mQTLs), expression (eQTLs), and protein (pQTLs) quantitative trait loci for 594 autophagy-related genes with large-scale IS genome-wide association studies for discovery (GCST006908) and validation (FinnGen). Summary-data-based MR (SMR) with colocalization analysis was performed, supplemented by brain eQTL analysis, protein-protein interaction networking, and drug prediction. The analysis identified 113 mQTLs, 38 eQTLs, and 9 pQTLs associated with IS risk, with colocalization supporting shared causal variants for a subset. Validation in FinnGen confirmed 13 mQTLs and 2 eQTLs, notably involving genes like CDKN1A, RRAGD, and SLC35D3. Multi-omics integration revealed regulatory cascades - for example, methylation at cg17245862 influencing DYNLT1 expression and protein levels. Brain-specific eQTL analysis supported 10 genes, including DYNLT1. Protein-protein interaction network analysis highlighted hub genes such as CDKN1A, PARK7, and LEP. Drug prediction suggested N-Acetyl-L-cysteine and acetaminophen as potential modulators targeting these genes. This study provides evidence for a potential causal role of autophagy-related genes and molecular traits in IS development, notably DYNLT1. Further research focusing on robustly identified candidates is warranted. - Source: PubMed
Nie HaoZhang LiHei YunpengMa TaoXu XinZhang Maoxian - Metabolic dysregulation has been recognized as a crucial driver of tumorigenesis, particularly in metabolic dysfunction-associated steatotic liver disease (MASLD)-related hepatocellular carcinoma (HCC). However, the underlying mechanisms remain poorly understood. Here, we identify lysosome-localized insulin receptor tyrosine kinase substrate (IRTKS) as a key activator of the metabolic master regulator mTORC1 through phospho-antibody array screening. IRTKS forms membrane-associated condensates that selectively interact with the GTPase RRAGD, a key upstream regulator of mTORC1, thereby enhancing the sensitivity of mTORC1 to free amino acids. Notably, in hepatic knockin mice, Irtks-mediated mTORC1 hyperactivation promotes obesity, hepatic lipid accumulation, and the progression from MASLD to metabolic dysfunction-associated steatohepatitis and HCC. Conversely, pharmacological inhibition of mTORC1 or genetic ablation of Irtks ameliorates hepatic steatosis, inflammation, and metabolic dysfunction in mouse models. Our study establishes IRTKS as a central regulator of mTORC1-dependent metabolic reprogramming during hepatocarcinogenesis, providing potential therapeutic targets for MASLD-associated liver cancer. - Source: PubMed
Publication date: 2026/01/22
Xie ChenyiCui XiaofangWei WeiHong PeichengYou LujiaChen ZiyaoLi LinWang LanWang NaHan Ze-Guang - Type 2 diabetes (T2D) is a major cause of morbidity in developed countries and involves insulin resistance, a failure to correctly respond to insulin. Numerous studies in rodent T2D models suggested that the short-chain fatty acid butyrate, produced by gut microbiota species through fermentation of dietary fibers, improves T2D symptoms. Here, we explored the potential antidiabetic effects of butyrate by measuring the transcription of selected T2D-implicated genes in human B lymphocyte-derived lymphoblastoid cell lines (LCLs) from 17 unrelated adult healthy donors. Human LCLs were cultured with and without sodium butyrate (1 mM for 48 h), followed by RNA extraction and real-time PCR analysis of the selected T2D-related genes. Butyrate significantly upregulated the expression of MT2A, RRAGD, IGF1R, OXTR, and INSR, while no changes were observed in the expression of other selected genes implicated in insulin signaling. Our findings, which should be considered preliminary until demonstrated by in vivo T2D animal models, suggest that butyrate is a potential modulator of metabolic pathways relevant to insulin resistance. Future studies should explore the tentative therapeutic potential of butyrate and its upregulated genes using proteomics and metabolomics in relevant tissues of T2D animal models, possibly followed by controlled clinical trials. - Source: PubMed
Shapira EladVoinsky IrenaKlin HanaGurwitz David - Variants in the Ras-related GTPase D () gene have been associated with autosomal dominant kidney hypomagnesemia (ADKH) characterized by hypokalemia, nephrocalcinosis, and dilated cardiomyopathy (DCM). , which encodes for the RagD protein, is involved in the activation of the mechanistic target of rapamycin complex 1 (mTORC1). Owing to the limited characterization of patients' phenotypes, the understanding of associated ADKH (ADKH-RRAGD) remains incomplete. Consequently, available treatment strategies are primarily symptomatic and insufficient. - Source: PubMed
Publication date: 2025/07/29
Adella AnastasiaJouret FrançoisMadariaga LeireLeermakers Pieter AArango PedroAriceta GemaBeck Bodo BBjerre AnnaBockenhauer DetlefCoccia PaulaDhamija Radhikade Frutos FernandoGarcia-Castano Alejandrovan Katwijk Sara BLucas JesusMöller ThomasMüller DominikPinto E Vairo FilippoRaki MelindaRips JonathanSchlingmann Karl PeterVenselaar HankaMachado Bressan Wilke Matheus VernetNijenhuis TomHoenderop Joostde Baaij Jeroen