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10.1172/jci.insight.96540 http://scihub22266oqcxt.onion/10.1172/jci.insight.96540 C5846897!5846897!29046478     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight ä ; 2 (20): ä Nephropedia Template TP {{tp|p=29046478|t=ä. Cinacalcet corrects hypercalcemia in mice with an inactivating G?11 mutation |pdf=|usr=}}{{29046478}} gab.com Text Cinacalcet corrects hypercalcemia in mice with an inactivating G 11 mutation JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29046478 #FOAvip Loss-of-function mutations of GNA11, which encodes G-protein subunit ?11 (G?11), a signaling partner for the calcium-sensing receptor (CaSR), result in familial hypocalciuric hypercalcemia type 2 (FHH2). FHH2 is characterized by hypercalcemia, inappropriately normal or raised parathyroid hormone (PTH) concentrations, and normal or low urinary calcium excretion. A mouse model for FHH2 that would facilitate investigations of the in vivo role of G?11 and the evaluation of calcimimetic drugs, which are CaSR allosteric activators, is not available. We therefore screened DNA from > 10,000 mice treated with the chemical mutagen N-ethyl-N-nitrosourea (ENU) for GNA11 mutations and identified a G?11 variant, Asp195Gly (D195G), which downregulated CaSR-mediated intracellular calcium signaling in vitro, consistent with it being a loss-of-function mutation. Treatment with the calcimimetic cinacalcet rectified these signaling responses. In vivo studies showed mutant heterozygous (Gna11+/195G) and homozygous (Gna11195G/195G) mice to be hypercalcemic with normal or increased plasma PTH concentrations and normal urinary calcium excretion. Cinacalcet (30mg/kg orally) significantly reduced plasma albumin?adjusted calcium and PTH concentrations in Gna11+/195G and Gna11195G/195G mice. Thus, our studies have established a mouse model with a germline loss-of-function G?11 mutation that is representative for FHH2 in humans and demonstrated that cinacalcet can correct the associated abnormalities of plasma calcium and PTH. Twit Text FOAVip Cinacalcet corrects hypercalcemia in mice with an inactivating G 11 mutation ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29046478 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29046478 #FOAvip English Wikipedia <ref>{{Cite pmid|29046478}}</ref> Cinacalcet corrects hypercalcemia in mice with an inactivating G?11 mutation #MMPMID29046478 Howles SA; Hannan FM; Gorvin CM; Piret SE; Paudyal A; Stewart M; Hough TA; Nesbit MA; Wells S; Brown SD; Cox RD; Thakker RV JCI Insight ä[]; 2 (20): ä PMID29046478show ga Loss-of-function mutations of GNA11, which encodes G-protein subunit ?11 (G?11), a signaling partner for the calcium-sensing receptor (CaSR), result in familial hypocalciuric hypercalcemia type 2 (FHH2). FHH2 is characterized by hypercalcemia, inappropriately normal or raised parathyroid hormone (PTH) concentrations, and normal or low urinary calcium excretion. A mouse model for FHH2 that would facilitate investigations of the in vivo role of G?11 and the evaluation of calcimimetic drugs, which are CaSR allosteric activators, is not available. We therefore screened DNA from > 10,000 mice treated with the chemical mutagen N-ethyl-N-nitrosourea (ENU) for GNA11 mutations and identified a G?11 variant, Asp195Gly (D195G), which downregulated CaSR-mediated intracellular calcium signaling in vitro, consistent with it being a loss-of-function mutation. Treatment with the calcimimetic cinacalcet rectified these signaling responses. In vivo studies showed mutant heterozygous (Gna11+/195G) and homozygous (Gna11195G/195G) mice to be hypercalcemic with normal or increased plasma PTH concentrations and normal urinary calcium excretion. Cinacalcet (30mg/kg orally) significantly reduced plasma albumin?adjusted calcium and PTH concentrations in Gna11+/195G and Gna11195G/195G mice. Thus, our studies have established a mouse model with a germline loss-of-function G?11 mutation that is representative for FHH2 in humans and demonstrated that cinacalcet can correct the associated abnormalities of plasma calcium and PTH. äCinacalcet corrects hypercalcemia in mice with an inactivating G?11 mu(epmc).pdf DeepDyve Pubget Overpricing