RGS17/RGSZ2 and the RZ/A family of regulators of G-protein signaling

Nunn, Caroline; Mao, Helen; Chidiac, Peter; Albert, Paul R.

doi:10.1016/j.semcdb.2006.04.001

Cited by 41 publications

(39 citation statements)

References 81 publications

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“…These signaling events are terminated as a consequence of intrinsic GTPase activity of the Gα-subunit, which hydrolyzes bound GTP to GDP, resulting in reassociation of the G-protein heterotrimer (34). The intrinsic GTPase activity of α-subunits is generally insufficient to correlate with the physiological rate of G-protein inactivation, but this activity can be accelerated by the presence of GTPase-activating proteins (GAPs), such as regulator of Gprotein-signaling (RGS) proteins (35).…”

Section: Discussionmentioning

confidence: 99%

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Identification of Hypertension-Susceptibility Genes and Pathways by a Systemic Multiple Candidate Gene Approach: The Millennium Genome Project for Hypertension

et al. 2008

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Section: Discussionmentioning

confidence: 99%

“…The CD/CV hypothesis and common disease rare variant hypothesis have been debated (28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41). In the present study, candidate SNPs were selected on the basis of the common variant hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Identification of Hypertension-Susceptibility Genes and Pathways by a Systemic Multiple Candidate Gene Approach: The Millennium Genome Project for Hypertension

et al. 2008

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“…RGS17 is a member of the RZ (or A) subfamily of small RGS proteins (20e30 kDa), form by other three proteins RGSZ1/RGS20 and Ga-interacting protein (GAIP)/RGS19 and RGSZ1 variant Ret-RGS (Nunn et al, 2006;Zhang et al, 2012a). This subfamily is characterized by a cysteine-rich motif that may serve as a palmitoylation site for membrane association (Mao et al, 2004) and by a very short (10e11 aa) carboxyl terminus (De Vries et al, 1995;Mao et al, 2004).…”

Section: Rgs17 (Rgsz2)mentioning

confidence: 99%

Regulators of G-Protein-Signaling Proteins: Negative Modulators of G-Protein-Coupled Receptor Signaling

Woodard

Jardín

Berna‐Erro

et al. 2015

International Review of Cell and Molecular Biology

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“…G z -GAP (also called RGSZ1) plays a role in attenuating mu opioid receptor inhibition of cAMP (58). RGS-17 has been shown to regulate G i/o , G z , and G q signaling (59,60). Rap1GapII also interacts with Gα i2 , and this interaction leads to a decrease in Rap1 activity (61).…”

Section: G I/o Signalingmentioning

confidence: 99%

Regulation of neurite outgrowth by Gi/o signaling pathways

Kenneth¹

2008

Front Biosci

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Neurogenesis is a long and winding journey. A neural progenitor cell migrates long distances, differentiates by forming a single axon and multiple dendrites, undergoes maturation, and ultimately survives. The initial formation of neurites during neuronal differentiation, commonly referred to as "neurite outgrowth," can be induced by a large repertoire of signals that stimulate an array of receptors and downstream signaling pathways. The G i/o family of heterotrimeric Gproteins are abundantly expressed in the brain and enriched at neuronal growth cones. Recent evidence has uncovered several G i/o -coupled receptors that induce neurite outgrowth and has begun to elucidate the underlying molecular mechanisms. Emerging data suggests that signals from several G i/o -coupled receptors converge at the transcription factor STAT3 to regulate neurite outgrowth and at Rac1 and Cdc42 to regulate cytoskeletal reorganization. Physiologically, signaling through G i/o -coupled cannabinoid receptors is critical for proper central nervous system development. As the mechanisms by which G i/o -coupled receptors regulate neurite outgrowth are clarified, it is becoming evident that modulating signals from G i/o and their receptors has great potential for the treatment of neurodegenerative diseases. KeywordsG-protein; Neurite Outgrowth; Cell Signaling; Cannabinoid Receptor; Neurodegeneration; Review INTRODUCTIONNeuronal differentiation is a complex process that integrates many signals to drive electrophysiological, morphological, and transcriptional changes (1,2,3,4). This process is characterized by the initial formation of immature neurites, commonly referred to as "neurite outgrowth." The neurites then further develop into a single axon and multiple dendrites, followed by maturation of the neuron and the formation of dendritic spines (1). Many signals at the cell surface are integrated to shape axonal and dendritic outgrowths as well as their directionality and maturation (5,6,7,8). Not surprisingly, neurite outgrowth is precisely regulated due to its importance in the proper development of the organism. During neurite outgrowth, signals at the membrane are transduced to a large repertoire of enzymes to ultimately trigger changes in gene transcription in the nucleus. In addition, the signals produce vast changes in the actin and microtubule cytoskeletal networks in order to generate and stabilize the growing neurites (1,8 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptA diverse array of ligands including neurotrophins, cytokines, hormones, and neurotransmitters can stimulate neurite outgrowth upon binding to their cognate receptors (5,7,9,10,11,12,13,14). Heterotrimeric guanine nucleotide-binding proteins (G-proteins) are one of the most widely used signal transduction systems in mammals, and signaling through the G i/o family of G-proteins regulates neurite outgrowth. In cortical neurons, dopaminemediated stimulation of the D2 dopamine receptor can induce axonal neurite elongation (10). Similarl...

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RGS17/RGSZ2 and the RZ/A family of regulators of G-protein signaling

Cited by 41 publications

References 81 publications

Identification of Hypertension-Susceptibility Genes and Pathways by a Systemic Multiple Candidate Gene Approach: The Millennium Genome Project for Hypertension

Identification of Hypertension-Susceptibility Genes and Pathways by a Systemic Multiple Candidate Gene Approach: The Millennium Genome Project for Hypertension

Regulators of G-Protein-Signaling Proteins: Negative Modulators of G-Protein-Coupled Receptor Signaling

Regulation of neurite outgrowth by Gi/o signaling pathways

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