RGS6 antibody - N-terminal region (ARP34042_P050)
- Known as:
- RGS6 (anti-) - N-terminal region (ARP34042_P050)
- Catalog number:
- arp34042_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RGS6 antibody - N-terminal region (ARP34042_P050)
Related genes to: RGS6 antibody - N-terminal region (ARP34042_P050)
- 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 - N-terminal region (ARP34042_P050)
Related articles to: RGS6 antibody - N-terminal region (ARP34042_P050)
- 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 - Targeting the kappa opioid receptor (KOR) system has emerged as a potential alternative to current analgesics, however, advancing the therapeutic development of KOR requires further elucidation of its intracellular signaling events and modulators. Among these intracellular modulators, Regulators of G protein Signaling (RGS) proteins act as key modulators of GPCR signaling to shape nociceptive circuits and influence pain processing. Despite this, the molecular diversity of RGS proteins that shape KOR signaling and its behavioral consequences remains largely unexplored. Here we report that RGS6, a member of the R7 RGS family, is highly expressed in nociceptive areas and modulates multiple modalities of KOR-dependent anti-nociception and nocifensive behaviors. Using global single and double knockout mouse models we show that this anti-nociceptive phenotype was highly specific to RGS6 within the R7 RGS family. Further we demonstrate that the R7 RGS family displays a lack of functional redundancy in regulation of KOR signaling and behaviors. Using peripherally restricted KOR agonists, we found that KOR-RGS6 anti-nociceptive signaling displays sex differences in a site-specific manner, as females but not males displayed enhanced anti-nociceptive and blunted nocifensive behaviors. Our findings indicate that RGS6 contributes to KOR-dependent anti-nociceptive signaling and influences nociceptive circuits, raising the possibility that it may represent a relevant target for the development of future analgesic strategies. - Source: PubMed
Publication date: 2026/05/08
Blount Alyson PSutton Laurie P - Platelet activation via G protein-coupled receptors (GPCRs) is central to arterial thrombosis. P2Y12 is a canonical Gi-coupled receptor mediating ADP-dependent platelet activation, yet the role of Regulator of G protein Signaling 6 (RGS6), a modulator of Gi signaling, in platelet function and thrombosis remains unclear. - Source: PubMed
Publication date: 2026/04/30
Roytenberg RenatRorabaugh Boyd RYue HongJividen RobbieCameron Scott JLi Wei