RGS7 Antibody - N-terminal region (ARP30216_P050)
- Known as:
- RGS7 Antibody - N-terminal region (ARP30216_P050)
- Catalog number:
- arp30216_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RGS7 Antibody - N-terminal region (ARP30216_P050)
Related genes to: RGS7 Antibody - N-terminal region (ARP30216_P050)
- Gene:
- RGS7 NIH gene
- Name:
- regulator of G protein signaling 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q43
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-19
- Date modifiied:
- 2017-04-13
Related products to: RGS7 Antibody - N-terminal region (ARP30216_P050)
Related articles to: RGS7 Antibody - N-terminal region (ARP30216_P050)
- G protein-coupled receptors (GPCRs) control essential neuronal functions. One GPCR with prominent effects on the nervous system and animal behavior is the mu-opioid receptor (MOR). GPCRs mediate their effects by engaging a gamut of G proteins, which are inhibited by Regulators of G protein Signaling (RGS). At present, how different RGS proteins regulate the magnitude and temporal kinetics of G protein signaling to affect behavior remains unclear. Here, we use an engineered cross-species C. elegans model of MOR signaling (tgMOR) to test how multiple RGS proteins shape MOR signaling and behavioral responses to opioids. Our results indicate opioid-induced effects on locomotor behavior in tgMOR are primarily mediated by Gαo and are modified by opposing Gαq action. We further delineate that EGL-10 (RGS7) is a primary RGS that modulates the magnitude of MOR-meditated responses. In a differential effect, EAT-16 (RGS9) and its regulator RSBP-1 (R7BP) principally influence the timing of behavioral response onset. Thus, a multi-layered RGS network is required to shape the magnitude and kinetics of MOR signaling and ensuing behavioral responses to opioids. The G protein regulatory network revealed here might also have broader implications for other Gαo/i-coupled receptors. - Source: PubMed
Publication date: 2026/04/02
Coleman Deziree LRen Rachel JOpperman Karla JKwan Elizabeth XMartemyanov Kirill AGrill Brock - Child maltreatment is a leading cause of pediatric morbidity and mortality, potentially propagated by DNA methylation (DNAm) changes. We conducted an EWAS meta-analysis (n=175, 554,979 Illumina EPICv1/EPICv2 sites) in buccal swabs from three hospital-based studies of children with traumatic injuries, stratified by study group to include 1) any traumatic injury, 2) fractures, and 3) traumatic brain injuries. Empirical bayes-moderated linear models tested differential DNAm with M-values, followed by near-promoter gene set enrichment analysis. Abuse was associated with methylation at 11 sites (q<0.10), including enhancers of neuroblast differentiation-associated , immunomodulators and , exon 5 of , essential for lysosomal function and cytotoxicity, and , a GTPase essential for synaptic transmission. Enriched biological processes included cranial skeletal system and connective tissue development, neural structure and function, immune regulation, gene expression, and metabolism. Our findings suggest that early abuse may epigenetically affect both proximal injury responses and longer-lived systemic biological dysregulation. - Source: PubMed
Publication date: 2026/03/01
Campbell Kyle ARaut AudreyJulian KelseyKaczor KimMakoroff KathiEverson Todd MPierce Mary Clyde - This study identifies RGS7 as a pivotal therapeutic target for dexmedetomidine (DEX) in Alzheimer's disease (AD). Bioinformatics revealed RGS7 is downregulated in AD, and in vivo, DEX administration in APP/PS1 mice restored its hippocampal expression and reduced Aβ plaque burden. Molecular docking supports a direct DEX-RGS7 interaction. The study links RGS7 to neuroinflammation, showing AD patients have elevated pro-inflammatory M1 macrophages and reduced follicular helper T cells. RGS7 expression negatively correlates with M1 macrophages and positively with follicular helper T cells. Crucially, RGS7 was found in microglia, suggesting DEX acts via RGS7 within these cells to exert its anti-inflammatory effects. With diagnostic potential (AUC = 0.79), the DEX-RGS7 axis is a promising therapeutic pathway for AD. - Source: PubMed
Yang YangliangXu AnjunXie PengchengYang Jingli - Alzheimer's disease (AD) is a common neurodegenerative condition involving a complex blend of disturbances in synaptic development and maintenance, neurovascular cross-talk, ionic and nutrient transport, and mitochondrial metabolism. The precise molecular profile of AD onset with insight for major pathological contributors remains unclear with corresponding impedances in therapeutic development. The current study sought two objectives, as (i) to resolve the molecular pathogenesis from cognitive impairment to the onset of AD-like neuropathology and (ii) whether the novel agent cannabidiol (CBD), noted for its neuroprotective effects, influences the molecular transition associated with AD onset. - Source: PubMed
Publication date: 2025/09/05
Bishara Mary AChum Phoebe PMiot Fritz E LHooda AnkitaHartman Richard EBehringer Erik J - GABA receptors (GABARs) are an important building block in neural activity. Despite their widely hypothesized role in many basic neuronal functions and mental disorder symptomatology, there is a lack of biophysically and biochemically detailed models of these receptors and the way they mediate neuronal inhibition. Here, we developed a computational model for the activation of GABARs and its effects on the activation of G protein-coupled inwardly rectifying potassium (GIRK) channels as well as inhibition of voltage-gated Ca channels. To ensure the generality of our modeling framework, we fit our model to electrophysiological data including patch-clamp and intracellular recordings that described both pre- and postsynaptic effects of the receptor activation. We validated our model using data on postsynaptic effects of GABARs on layer V pyramidal cell firing activity ex vivo and in vivo and confirmed the strong impact of dendritic GIRK channel activation on the neuron output. Finally, we reproduced and dissected the effects of a knockout of RGS7 (a G protein signaling protein) on CA1 pyramidal cell electrophysiological properties, which shows the potential of our model in generating insights on genetic manipulations of the GABAR system and related genetic variants. Our model thus provides a flexible tool for biochemically and biophysically detailed simulations of different aspects of GABAR activation that can reveal both foundational principles of neuronal dynamics and brain disorder-associated traits and treatment options. - Source: PubMed
Publication date: 2025/09/03
Mäki-Marttunen TuomoKismul Jan FredrikPajo KadriSchulz Jan MichaelManninen TiinaEinevoll Gaute TLinne Marja-LeenaAndreassen Ole AKotaleski Jeanette Hellgren