Disease relevance of Rgs2

• In contrast, progesterone treatment prolonged pregnancy beyond day 25 and attenuated the decline in RGS2 messenger RNA levels [1].
• Current activation was prevented by pertussis toxin (PTX) or after coexpression of the betagamma-scavenger transducin-Galpha.I(GIRK) inhibition by all three nucleotide receptors was insensitive to PTX and was significantly reduced after coexpression of RGS2 protein, known to inhibit G(q)alpha signaling [2].

High impact information on Rgs2

• Here we report that RGS2 reduces cAMP production by odorant-stimulated olfactory epithelium membranes, in which the alpha(s) family member alpha(olf) links odorant receptors to adenylyl cyclase activation [3].
• RGS2 regulates signal transduction in olfactory neurons by attenuating activation of adenylyl cyclase III [3].
• These data may reveal a functional role for the upregulation of RGS2 expression in in vivo systems [4].
• Expression of RGS2 alters the coupling of metabotropic glutamate receptor 1a to M-type K+ and N-type Ca2+ channels [4].
• Here, we demonstrate that mRNA encoding a member of the regulator of G-protein signaling (RGS) family, RGS2, is rapidly induced in neurons of the hippocampus, cortex, and striatum in response to stimuli that evoke plasticity [5].

Biological context of Rgs2

• Tyrosine kinase inhibition and calcium deprivation did not affect the up-regulation of RGS2 mRNA after Ang II stimulation [6].
• In drug-naive animals, acute amphetamine induced the expression of RGS2, 3, and 5 and the immediate early genes c-fos and zif/268 [7].
• The D1 antagonist SCH23390 and D2 agonist quinpirole caused a down-regulation of RGS2 (- 25.0% and - 35.0%) and an up-regulation of RGS4 (+ 57.2% and + 52.5%) [8].
• Depending on the drug used, the degree of receptor occupancy did (D1 agonist and RGS2) or did not (D2 antagonist and RGS2) run parallel to RGS gene expression changes, indicating that certain drug effects are direct and others indirect [9].
• OBJECTIVE: The purpose of this study was to determine the potential physiologic roles of myometrial regulator of G protein signaling-2 (RGS2), a G protein-associated GTPase, by the analysis of the changes in RGS2 messenger RNA expression during pregnancy and parturition and to examine factors that regulate these changes [1].

Anatomical context of Rgs2

• Specific regulation of RGS2 messenger RNA by angiotensin II in cultured vascular smooth muscle cells [6].
• In hippocampus, RGS2 mRNA levels were markedly increased 2 h following acute ECS [10].
• In prefrontal cortex, RGS2 mRNA levels were increased several-fold 2 h following an acute ECS [10].
• In addition, to delineate the implication of RGS2 in pre- and/or postsynaptic functions in the basal ganglia, we performed lesions of the nigrostriatal pathway by 6-hydroxydopamine (6-OHDA) and striatal quinolinic acid lesions [11].
• In the neocortex, RGS2 mRNA was enriched in the superficial cortical plate at P2, in contrast to RGS4, which was enriched in more mature neurons of the deeper layer V and VI [12].

Associations of Rgs2 with chemical compounds

• The stability of RGS2 mRNA did not appear to be affected by Ang II [6].
• The D1 dopamine receptor-selective antagonist SCH-23390 had no effect by itself but strongly attenuated RGS2 mRNA induction by amphetamine [7].
• The D1 agonist SKF82958 and D2 antagonist haloperidol caused an up-regulation of RGS2 (+ 38.0% and + 41.6%, respectively) [8].
• These effects were due to modulation of the RGS-2 gene transcription rate, which increased by 35% with 1,25-(OH)(2)D(3) and decreased by 63% with dexamethasone pretreatment [13].
• Single injections of cocaine, amphetamine, or methamphetamine increased RGS2 mRNA levels in rat striatum by two- to fourfold [7].

Regulatory relationships of Rgs2

• RGS4 was up-regulated only when RGS2 was down-regulated [8].

Other interactions of Rgs2

• In sharp contrast, prior exposure to amphetamine did not reduce the induction of RGS2 and RGS3 mRNAs to a challenge dose of amphetamine, indicating that control of these genes is resistant to amphetamine-induced tolerance [7].
• Regulation of RGS-2 may constitute a novel mechanism by which steroids modulate signaling via the PTH/PTHrP receptor and other G protein-coupled receptors in bone [13].

Analytical, diagnostic and therapeutic context of Rgs2

• The distribution of RGS2 mRNA and protein has been studied in parallel by performing in situ hybridization and immunoautoradiography on adjacent rat brain sections [11].
• The results clearly show a selective increase in the mRNA levels of RGS2, 5 and 8 and a decrease in RGS4 and 9 mRNA levels following nigrostriatal denervation [14].
• Reverse-transcriptase-mediated PCR and Northern blot analysis showed that the expression of GOS8/RGS2 mRNA, which is a member of the regulator of G-protein signalling (RGS) group of proteins, was considerably increased by pretreatment with CTX [15].

References