ArticleEndocrinology2011
Transgenic overexpression of the extra-large Gsα variant XLαs enhances Gsα-mediated responses in the mouse renal proximal tubule in vivo.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- A biallelically active embryonic enhancer dictates GNAS imprinting through allele-specific conformations.Nature communications · 2025Article
- Gsα Regulates Macrophage Foam Cell Formation During Atherosclerosis.Circulation research · 2024Article
- A G protein-coupled, IP3/protein kinase C pathway controlling the synthesis of phosphaturic hormone FGF23.JCI insight · 2019Article
- GNAS mutations and heterotopic ossification.Bone · 2018Review
- Large G protein α-subunit XLαs limits clathrin-mediated endocytosis and regulates tissue iron levels in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Heterotrimeric G proteins in the control of parathyroid hormone actions.Journal of molecular endocrinology · 2017Review
- Article
- The G protein α subunit variant XLαs promotes inositol 1,4,5-trisphosphate signaling and mediates the renal actions of parathyroid hormone in vivo.Science signaling · 2015Article
- Postnatal establishment of allelic Gαs silencing as a plausible explanation for delayed onset of parathyroid hormone resistance owing to heterozygous Gαs disruption.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Article
- The N termini of a-subunit isoforms are involved in signaling between vacuolar H+-ATPase (V-ATPase) and cytohesin-2.The Journal of biological chemistry · 2013Article
- The GNAS complex locus and human diseases associated with loss-of-function mutations or epimutations within this imprinted gene.Hormone research in paediatrics · 2013Review
- An update on the clinical and molecular characteristics of pseudohypoparathyroidism.Current opinion in endocrinology, diabetes, and obesity · 2012Review
- Loss of XLαs (extra-large αs) imprinting results in early postnatal hypoglycemia and lethality in a mouse model of pseudohypoparathyroidism Ib.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Postnatal changes in the expression pattern of the imprinted signalling protein XLαs underlie the changing phenotype of deficient mice.PloS one · 2012Article
- Extra-long Gαs variant XLαs protein escapes activation-induced subcellular redistribution and is able to provide sustained signaling.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
Abstract
XLαs, a variant of the stimulatory G protein α-subunit (Gsα), can mediate receptor-activated cAMP generation and, thus, mimic the actions of Gsα in transfected cells. However, it remains unknown whether XLαs can act in a similar manner in vivo. We have now generated mice with ectopic transgenic expression of rat XLαs in the renal proximal tubule (rptXLαs mice), where Gsα mediates most actions of PTH. Western blots and quantitative RT-PCR showed that, while Gsα and type-1 PTH receptor levels were unaltered, protein kinase A activity and 25-hydroxyvitamin D 1-α-hydroxylase (Cyp27b1) mRNA levels were significantly higher in renal proximal tubules of rptXLαs mice than wild-type littermates. Immunohistochemical analysis of kidney sections showed that the sodium-phosphate cotransporter type 2a was modestly reduced in brush border membranes of male rptXLαs mice compared to gender-matched controls. Serum calcium, phosphorus, and 1,25 dihydroxyvitamin D were within the normal range, but serum PTH was ∼30% lower in rptXLαs mice than in controls (152 ± 16 vs. 222 ± 41 pg/ml; P < 0.05). After crossing the rptXLαs mice to mice with ablation of maternal Gnas exon 1 (E1(m-/+)), male offspring carrying both the XLαs transgene and maternal Gnas exon 1 ablation (rptXLαs/E1(m-/+)) were significantly less hypocalcemic than gender-matched E1(m-/+) littermates. Both E1(m-/+) and rptXLαs/E1(m-/+) offspring had higher serum PTH than wild-type littermates, but the degree of secondary hyperparathyroidism tended to be lower in rptXLαs/E1(m-/+) mice. Hence, transgenic XLαs expression in the proximal tubule enhanced Gsα-mediated responses, indicating that XLαs can mimic Gsα in vivo.
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