ArticleMolecular and cellular biology2006
Pleiotropic phenotype of a genomic knock-in of an RGS-insensitive G184S Gnai2 allele.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
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- Role of hippocampal 5-HT1A receptors in the antidepressant-like phenotype of mice expressing RGS-insensitive Gαi2 protein.Neuropharmacology · 2018Article
- Normal Thymocyte Egress, T Cell Trafficking, and CD4Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- The impact of RGS and other G-protein regulatory proteins on Gαi-mediated signaling in immunity.Biochemical pharmacology · 2016Review
- Regulator of G Protein Signaling 7 (RGS7) Can Exist in a Homo-oligomeric Form That Is Regulated by Gαo and R7-binding Protein.The Journal of biological chemistry · 2016Article
- Article
- Platelet Gi protein Gαi2 is an essential mediator of thrombo-inflammatory organ damage in mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- An essential role for RGS protein/Gαi2 interactions in B lymphocyte-directed cell migration and trafficking.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Canonical and noncanonical g-protein signaling helps coordinate actin dynamics to promote macrophage phagocytosis of zymosan.Molecular and cellular biology · 2014Article
- Conditional disruption of interactions between Gαi2 and regulator of G protein signaling (RGS) proteins protects the heart from ischemic injury.BMC pharmacology & toxicology · 2014Article
- Regulator of G-protein signaling 6 (RGS6) promotes anxiety and depression by attenuating serotonin-mediated activation of the 5-HT(1A) receptor-adenylyl cyclase axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Gαi2- and Gαi3-deficient mice display opposite severity of myocardial ischemia reperfusion injury.PloS one · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Signal transduction via guanine nucleotide binding proteins (G proteins) is involved in cardiovascular, neural, endocrine, and immune cell function. Regulators of G protein signaling (RGS proteins) speed the turn-off of G protein signals and inhibit signal transduction, but the in vivo roles of RGS proteins remain poorly defined. To overcome the redundancy of RGS functions and reveal the total contribution of RGS regulation at the Galpha(i2) subunit, we prepared a genomic knock-in of the RGS-insensitive G184S Gnai2 allele. The Galpha(i2)(G184S) knock-in mice show a dramatic and complex phenotype affecting multiple organ systems (heart, myeloid, skeletal, and central nervous system). Both homozygotes and heterozygotes demonstrate reduced viability and decreased body weight. Other phenotypes include shortened long bones, a markedly enlarged spleen, elevated neutrophil counts, an enlarged heart, and behavioral hyperactivity. Heterozygous Galpha(i2)(+/G184S) mice show some but not all of these abnormalities. Thus, loss of RGS actions at Galpha(i2) produces a dramatic and pleiotropic phenotype which is more evident than the phenotype seen for individual RGS protein knockouts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.