Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1172/jci.insight.148588 http://scihub22266oqcxt.onion/10.1172/jci.insight.148588 34166227!8410034!34166227     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight 2021 ; 6 (15): ä Nephropedia Template TP {{tp|p=34166227|t=2021. A variant of ASIC2 mediates sodium retention in nephrotic syndrome |pdf=|usr=}}{{34166227}} gab.com Text A variant of ASIC2 mediates sodium retention in nephrotic syndrome JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=34166227 #FOAvip Idiopathic nephrotic syndrome (INS) is characterized by proteinuria and renal sodium retention leading to edema. This sodium retention is usually attributed to epithelial sodium channel (ENaC) activation after plasma aldosterone increase. However, most nephrotic patients show normal aldosterone levels. Using a corticosteroid-clamped (CC) rat model of INS (CC-PAN), we showed that the observed electrogenic and amiloride-sensitive Na retention could not be attributed to ENaC. We then identified a truncated variant of acid-sensing ion channel 2b (ASIC2b) that induced sustained acid-stimulated sodium currents when coexpressed with ASIC2a. Interestingly, CC-PAN nephrotic ASIC2b-null rats did not develop sodium retention. We finally showed that the expression of the truncated ASIC2b in the kidney was dependent on the presence of albumin in the tubule lumen and activation of ERK in renal cells. Finally, the presence of ASIC2 mRNA was also detected in kidney biopsies from patients with INS but not in any of the patients with other renal diseases. We have therefore identified a variant of ASIC2b responsible for the renal Na retention in the pathological context of INS. Twit Text FOAVip A variant of ASIC2 mediates sodium retention in nephrotic syndrome ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=34166227 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34166227 #FOAvip English Wikipedia <ref>{{Cite pmid|34166227}}</ref> A variant of ASIC2 mediates sodium retention in nephrotic syndrome #MMPMID34166227 Fila M; Sassi A; Brideau G; Cheval L; Morla L; Houillier P; Walter C; Gennaoui M; Collignon L; Keck M; Planelles G; Bakouh N; Peuchmaur M; Deschenes G; Anegon I; Remy S; Vogt B; Crambert G; Doucet A JCI Insight 2021[Aug]; 6 (15): ä PMID34166227show ga Idiopathic nephrotic syndrome (INS) is characterized by proteinuria and renal sodium retention leading to edema. This sodium retention is usually attributed to epithelial sodium channel (ENaC) activation after plasma aldosterone increase. However, most nephrotic patients show normal aldosterone levels. Using a corticosteroid-clamped (CC) rat model of INS (CC-PAN), we showed that the observed electrogenic and amiloride-sensitive Na retention could not be attributed to ENaC. We then identified a truncated variant of acid-sensing ion channel 2b (ASIC2b) that induced sustained acid-stimulated sodium currents when coexpressed with ASIC2a. Interestingly, CC-PAN nephrotic ASIC2b-null rats did not develop sodium retention. We finally showed that the expression of the truncated ASIC2b in the kidney was dependent on the presence of albumin in the tubule lumen and activation of ERK in renal cells. Finally, the presence of ASIC2 mRNA was also detected in kidney biopsies from patients with INS but not in any of the patients with other renal diseases. We have therefore identified a variant of ASIC2b responsible for the renal Na retention in the pathological context of INS. |*Kidney/metabolism/pathology[MESH] |*MAP Kinase Signaling System[MESH] |*Nephrotic Syndrome/blood/metabolism[MESH] |*Sodium/blood/metabolism[MESH] |Acid Sensing Ion Channels/*metabolism[MESH] |Albumins/metabolism[MESH] |Animals[MESH] |Disease Models, Animal[MESH] |Gene Expression Profiling[MESH] |Homeostasis[MESH] |Proteinuria/metabolism[MESH] |Rats[MESH]A variant of ASIC2 mediates sodium retention in nephrotic syndrome (epmc).pdf DeepDyve Pubget Overpricing