Ask about this productRelated genes to: RGS6 antibody
- Gene:
- RGS6 NIH gene
- Name:
- regulator of G protein signaling 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-17
- Date modifiied:
- 2017-04-13
Related products to: RGS6 antibody
Related articles to: RGS6 antibody
- Pruritus, commonly known as itch, is a protective somatosensory sensation whose dysregulation is a common feature of many pathologic conditions and can severely impact quality of life. Despite its clinical relevance, itch perception is among the least well known of all somatosensory modalities. G protein coupled receptors (GPCRs) in pruritic circuits are key modulators of itch, however the intracellular regulators of GPCR signaling in itch circuits remain largely unexplored. Regulators of G protein signaling (RGS) proteins are vital modulators of GPCR signaling and may influence itch processing in histaminergic and non-histaminergic circuits. Here we report that RGS6, a member of the R7 RGS protein family, modulates itch through both histaminergic and non-histaminergic mechanisms in female mice. Using global knockout mouse models, we show that this anti-pruritic phenotype is specific to RGS6, with no comparable effect in RGS7, highlighting functional specificity within the R7 RGS family. This study uncovers a regulatory role of RGS6 in modulating pruritus in females and provides critical insights into mechanisms fundamental to acute and pathological itch. - Source: PubMed
Publication date: 2026/09/05
P Blount AlysonGavagan SaraJawhar LeenSutton Laurie P - Heart failure is the leading cause of death in individuals with diabetes mellitus (DM), and no effective treatments exist to treat or prevent hyperglycemia-driven cardiomyopathy. Here, we demonstrate that high glucose triggers regulator of G protein signaling 6 (RGS6) up-regulation in both human and murine cardiomyocytes, the hearts of hyperglycemic mice, and cardiac tissue samples from individuals with heart failure and a history of diabetes. Modulation of RGS6 expression in isolated cardiomyocytes resulted in corresponding changes in the expression of the transcription factor Krüppel-like factor 4 (KLF4), a novel RGS6-interacting protein. Further, RGS6-dependent, KLF4-mediated suppression of microRNA 30e (miR-30e) increased expression of the pro-apoptotic miR-30e target Ca/calmodulin-dependent kinase II δ isoform (CaMKIIδ). Importantly, inhibition of either KLF4 or CaMKII or overexpression of miR-30e mitigated the deleterious impact of RGS6 overexpression on myocyte viability. Indeed, cardiac-specific RGS6 knockdown provided marked protection against hyperglycemia-driven oxidative stress, mitochondrial dysfunction, and activation of the intrinsic mitochondrial apoptosis pathway in the murine myocardium. Similarly, inhibition of KLF4 decreased cardiotoxicity resulting from viral overexpression of RGS6 in mouse heart. Thus, RGS6 is both necessary and sufficient to drive cardiac damage resulting from chronic elevations in blood glucose. Together, these data point to RGS6/KLF4 as key sources of pathogenic cardiac damage in individuals with DM. - Source: PubMed
Publication date: 2026/08/23
Sengar Abhishek SinghChakraborti SreemoyeeLye AnushreeVerma Sumit KumarKumar ManishKumar DineshKumar PraneshStewart AdeleMaity Biswanath - Gastrointestinal (GI) tract diseases cause symptoms that significantly affect the quality of life. A promising direction in the search for novel therapeutic options in this field is the investigation of G protein-coupled receptors (GPCRs), whose activity is modulated by their regulator proteins (RGS). In this study, we examined RGS6 involvement in GI inflammation and functional disorders and its effect on cannabinoid (CB), opioid, and serotonin receptor (5HTR)-targeting compounds, METHODS: Using quantitative PCR, western blot, and ELISA assays, we characterized RGS6 expression in the mouse GI tract and measured GPCR-related secondary messenger expression upon stimulation with GPCR agonists in vitro in Caco-2 cells, both wild type (WT) and RGS6 knock-out (KO). Then, in vivo in a dextran sulfate sodium (DSS) mouse model of colitis using WT, global and tissue-specific RGS6 KO mice, inflammation, antinociceptive effects, and GI motility were examined. - Source: PubMed
Publication date: 2026/08/13
Świerczyński MikołajMakaro AdamJaczyńska MariaSobalska-Kwapis MartaSeweryn MichałKasprzak ZuzannaTarasiuk-Zawadzka AleksandraSałaga Maciej - Osteoporosis (OP) and cognitive decline are highly prevalent comorbidities; however, the molecular mechanisms linking them remain unclear. We adopted a multimodal integrative strategy combining neuroimaging, transcriptomics, single-cell analysis, and in vivo validation to elucidate potential mechanisms. - Source: PubMed
Publication date: 2026/05/18
Fang MinLi NanXu WenyueXue YuanWang RuiZhou Jiaming - Epilepsy is one of the most common chronic neurological disorders. This study aimed to identify hippocampal neuronal subpopulations with the most prominent transcriptional alterations during the latent period following status epilepticus, thereby elucidating early molecular mechanisms of epileptogenesis in a pilocarpine-induced model. Status epilepticus (SE) was induced in male C57BL/6 N mice via intraperitoneal pilocarpine injection, and hippocampal tissue was collected on Day 7 post-SE (n = 3 per group) for single-nucleus RNA sequencing using a 10× Genomics platform. Data were processed using Seurat, clustered via UMAP, and analysed for differential gene expression and KEGG pathway enrichment. From 76,412 high-quality nuclei, we identified 45,584 excitatory neurons, 5,897 inhibitory neurons, and major glial subtypes. Dentate gyrus (DG) excitatory neurons exhibited the most profound transcriptional remodelling, segregating into control-enriched (DG1) and epilepsy-enriched (DG2) factions. The expression of Sorcs3, Rgs6, and Galntl6 was upregulated in DG2 neurons, whereas the expression of Trpc5, Itpr1, and Calb1 was upregulated in DG1 neurons. Among inhibitory neurons, Meis2-expressing interneurons showed the greatest change in relative abundance, with the Meis2-1 subtype tending to increase in relative abundance post-SE compared to controls (P = 0.0728, not significant) and selectively expressing the seizure-related genes Cpa6, Ano1, and Ano2. DG excitatory neurons and Meis2-positive inhibitory neurons represent the most prominently altered hippocampal cell types following seizures, highlighting their potential role in epileptogenic network reorganization. The identification of disease-specific molecular signatures within these populations provides a prioritised framework for investigating causal mechanisms and developing cell type-targeted therapeutic strategies for precision epilepsy treatment. - Source: PubMed
Publication date: 2026/05/29
Wang YuxuanWang LiLuo KangchengChen ZhibiaoXia Lu