ArticleJournal of molecular histology2015
Localization and expression profile of Group I and II Activators of G-protein Signaling in the kidney.
Article in Journal of molecular histology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Intersection of two key signal integrators in the cell: activator of G-protein signaling 3 and dishevelled-2.Journal of cell science · 2020Article
- Deciphering the potential pharmaceutical mechanism of Guzhi Zengsheng Zhitongwan on rat bone and kidney based on the "kidney governing bone" theory.Journal of orthopaedic surgery and research · 2020Article
- Urinary exosomal expression of activator of G protein signaling 3 in polycystic kidney disease.BMC research notes · 2018Article
- Selective Cannabinoid 2 Receptor Stimulation Reduces Tubular Epithelial Cell Damage after Renal Ischemia-Reperfusion Injury.The Journal of pharmacology and experimental therapeutics · 2018Article
- TRIP13-deficient tubular epithelial cells are susceptible to apoptosis following acute kidney injury.Scientific reports · 2017Article
- Heterotrimeric G protein signaling in polycystic kidney disease.Physiological genomics · 2016Review
- Activator of G-protein Signaling 3 Controls Renal Epithelial Cell Survival and ERK5 Activation.Journal of molecular signaling · 2015Article
- Activators of G protein signaling in the kidney.The Journal of pharmacology and experimental therapeutics · 2015Review
- Accessory proteins for heterotrimeric G-proteins in the kidney.Frontiers in physiology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Activators of G-protein Signaling (AGS) are a family of accessory proteins that were discovered as modulators of heterotrimeric G-protein subunits. The primary aim of the present study was to localize Group I and II AGS proteins and determine the renal expression profile using immunohistochemistry and quantitative RT-PCR, respectively, during normal and injured states of the kidney. Group I AGS1 was found to be predominantly localized to the proximal tubule, Group II AGS3 and AGS5 were exclusively localized to the distal tubular segments, and Group II AGS6 was ubiquitously expressed in every nephron segment of the rodent kidney. In rat kidneys following ischemia-reperfusion injury (IRI), Group I AGS1 mRNA was dramatically increased after 24 h by fivefold (P < 0.05), whereas Group II AGS3 and AGS4 mRNA was significantly decreased at the same time point (P < 0.05). No significant change in the transcript levels were detected at other time points for any of the AGS genes between control and IRI groups. In polycystic diseased kidneys, mRNA levels for AGS3, AGS4 and AGS6 was significantly increased (P < 0.05) by 75-80 % in PCK rat kidneys. The identification of Group I and II AGS mRNA and protein in the kidney may provide insight into the potential mechanism of action during normal and varying states of renal disease or injury.
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