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10.1016/j.kint.2020.10.024 http://scihub22266oqcxt.onion/10.1016/j.kint.2020.10.024 33159963!7914218!33159963     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33159963&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Kidney+Int 2021 ; 99 (3): 598-608 Nephropedia Template TP {{tp|p=33159963|t=2021. Targeting fibroblast growth factor 23-responsive pathways uncovers controlling genes in kidney mineral metabolism |pdf=|usr=}}{{33159963}} gab.com Text Targeting fibroblast growth factor 23-responsive pathways uncovers controlling genes in kidney mineral metabolism JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=33159963 #FOAvip Fibroblast Growth Factor 23 (FGF23) is a bone-derived hormone that reduces kidney phosphate reabsorption and 1,25(OH)2 vitamin D synthesis via its required co-receptor alpha-Klotho. To identify novel genes that could serve as targets to control FGF23-mediated mineral metabolism, gene array and single-cell RNA sequencing were performed in wild type mouse kidneys. Gene array demonstrated that heparin-binding EGF-like growth factor (HBEGF) was significantly up-regulated following one-hour FGF23 treatment of wild type mice. Mice injected with HBEGF had phenotypes consistent with partial FGF23-mimetic activity including robust induction of Egr1, and increased Cyp24a1 mRNAs. Single cell RNA sequencing showed overlapping HBEGF and EGF-receptor expression mostly in the proximal tubule, and alpha-Klotho expression in proximal and distal tubule segments. In alpha-Klotho-null mice devoid of canonical FGF23 signaling, HBEGF injections significantly increased Egr1 and Cyp24a1 with correction of basally elevated Cyp27b1. Additionally, mice placed on a phosphate deficient diet to suppress FGF23 had endogenously increased Cyp27b1 mRNA, which was rescued in mice receiving HBEGF. In HEK293 cells with stable alpha-Klotho expression, FGF23 and HBEGF increased CYP24A1 mRNA expression. HBEGF, but not FGF23 bioactivity was blocked with EGF-receptor inhibition. Thus, our findings support that the paracrine/autocrine factor HBEGF could play novel roles in controlling genes downstream of FGF23 via targeting common signaling pathways. Twit Text FOAVip Targeting fibroblast growth factor 23-responsive pathways uncovers controlling genes in kidney mineral metabolism ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=33159963 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33159963 #FOAvip English Wikipedia <ref>{{Cite pmid|33159963}}</ref> Targeting fibroblast growth factor 23-responsive pathways uncovers controlling genes in kidney mineral metabolism #MMPMID33159963 Ni P; Clinkenbeard EL; Noonan ML; Richardville JM; McClintick J; Hato T; Janosevic D; Cheng YH; El-Achkar TM; Eadon MT; Dagher PC; White KE Kidney Int 2021[Mar]; 99 (3): 598-608 PMID33159963show ga Fibroblast Growth Factor 23 (FGF23) is a bone-derived hormone that reduces kidney phosphate reabsorption and 1,25(OH)2 vitamin D synthesis via its required co-receptor alpha-Klotho. To identify novel genes that could serve as targets to control FGF23-mediated mineral metabolism, gene array and single-cell RNA sequencing were performed in wild type mouse kidneys. Gene array demonstrated that heparin-binding EGF-like growth factor (HBEGF) was significantly up-regulated following one-hour FGF23 treatment of wild type mice. Mice injected with HBEGF had phenotypes consistent with partial FGF23-mimetic activity including robust induction of Egr1, and increased Cyp24a1 mRNAs. Single cell RNA sequencing showed overlapping HBEGF and EGF-receptor expression mostly in the proximal tubule, and alpha-Klotho expression in proximal and distal tubule segments. In alpha-Klotho-null mice devoid of canonical FGF23 signaling, HBEGF injections significantly increased Egr1 and Cyp24a1 with correction of basally elevated Cyp27b1. Additionally, mice placed on a phosphate deficient diet to suppress FGF23 had endogenously increased Cyp27b1 mRNA, which was rescued in mice receiving HBEGF. In HEK293 cells with stable alpha-Klotho expression, FGF23 and HBEGF increased CYP24A1 mRNA expression. HBEGF, but not FGF23 bioactivity was blocked with EGF-receptor inhibition. Thus, our findings support that the paracrine/autocrine factor HBEGF could play novel roles in controlling genes downstream of FGF23 via targeting common signaling pathways. |*Fibroblast Growth Factors/genetics[MESH] |*Vitamin D[MESH] |Animals[MESH] |Fibroblast Growth Factor-23[MESH] |Glucuronidase/genetics[MESH] |HEK293 Cells[MESH] |Humans[MESH] |Kidney[MESH] |Mice[MESH] |Minerals[MESH]Targeting fibroblast growth factor 23-responsive pathways uncovers con(epmc).pdf DeepDyve Pubget Overpricing