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
- 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 - Regulator of G protein Signaling 6 (RGS6), heavily implicated in neurological and neuropsychiatric disorders, is enriched in mouse and human brain. Our initial cloning effort identified 36 RGS6 mRNAs in human brain. However, we recently identified an additional RGS6 protein isoform that is larger (∼69kDa) than the ubiquitously expressed ∼56kDa RGS6L(+GGL) isoforms. Notably, this isoform, named "RGS6B" for "brain-specific", is selectively expressed in the nervous system of mice and humans. Here, we report the cloning of a new RGS6-encoding mRNA, which resembles the RGS6Lα1(+GGL) transcript identified in our initial cloning effort but includes a highly conserved novel exon (Alternative 3, A3) that alters the reading frame of terminal exon α resulting in an extension of the protein C-terminus. When expressed in cells, RGS6LA3α1(+GGL) co-migrates with RGS6B, and, importantly, interfering RNA targeting exon A3 results in selective depletion of RGS6B in isolated primary cortical astrocytes. RGS6B is capable of stabilizing RGS6 binding partners R7BP and Gβ and, in fact, exhibits an increased protein half-life relative to RGS6L. Both RGS6L and RGS6B are downregulated in human gliomas and share the ability to kill U87MG glioblastoma cells when overexpressed indicating conservation of non-canonical cytotoxic activity between RGS6L and RGS6B species. However, RGS6B lacks the ability to counteract Gα -dependent suppression of cAMP signaling, indicating a lack of functional GTPase activating protein (GAP) activity. Instead, RGS6B functions in a dominant negative manner to block Gα regulation by RGS6L. RGSB is the first identified RGS protein member that functions to promote, rather than inhibit, G protein signaling. The discovery of the molecular identity of RGS6B will now allow for delineation of unique functions for RGS6 protein isoforms in both physiological and pathophysiological brain states. - Source: PubMed
Publication date: 2026/05/12
Ahlers-Dannen K EYang JBernholtz JGlebov-Mccloud AlexanderStrack StefanKoland J GFisher R AStewart A