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Regulator of G-protein signaling 17
RGS17, RGSZ2, hRGS17
This gene encodes a member of the regulator of G-protein signaling family. This protein contains a conserved, 120 amino acid motif called the RGS domain and a cysteine-rich region. The protein attenuates the signaling activity of G-proteins by binding to activated, GTP-bound G alpha subunits and acting as a GTPase activating protein (GAP), increasing the rate of conversion of the GTP to GDP. This hydrolysis allows the G alpha subunits to bind G beta/gamma subunit heterodimers, forming inactive G-protein heterotrimers, thereby terminating the signal. [provided by RefSeq, Jul 2008] (from
Santella et al., New York City, United States. In Bmc Med Genomics, 2014
Another two genes (RGS17 and NR2E1) at Chr6q showed significantly decreased DNA methylation in tumors with loss of DNA copy number compared to those without, suggesting alternative roles of DNA copy number losses and hypermethylation in the regulation of RGS17 and NR2E1.
Ferraro et al., Philadelphia, United States. In Neuroscience, 2014
Real-time qRT-PCR analysis of Oprm1 and opioid-related genes Rgs17, Ppp1r14c, Vip, and Iyd revealed both between-strain and within-strain expression differences in comparisons of saline- and morphine-treated B6 and D2 mice.
Garzón et al., Madrid, Spain. In Antioxid Redox Signal, 2012
Thus, MOR activation stimulates the complex formed by RGSZ2 (a regulator of G protein signaling) and neural nitric oxide synthase (nNOS) to produce NO, and to recruit PKCγ and Raf-1 in a zinc-dependent manner.
Owens et al., Charlottesville, United States. In Physiol Genomics, 2012
Finally, immunofluorescent staining of mouse atherosclerotic lesions revealed the presence of cells positive for the marker of an IL-1β-stimulated inflammatory SMC, chemokine (C-C motif) ligand 20 (CCL20), but not the PDGF-DD-induced gene, regulator of G protein signaling 17 (RGS17).
Sánchez-Blázquez et al., Madrid, Spain. In Antioxid Redox Signal, 2011
This RGSZ2-dependent regulation of NMDAR activity is relevant to persistent pain disorders associated with heightened NMDAR-mediated glutamate responses and the reduced antinociceptive capacity of opioids.