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.

10.1016/j.jbc.2021.100915 http://scihub22266oqcxt.onion/10.1016/j.jbc.2021.100915 34174287!8318901!34174287     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2021 ; 297 (2): 100915 Nephropedia Template TP {{tp|p=34174287|t=2021. High dietary potassium causes ubiquitin-dependent degradation of the kidney sodium-chloride cotransporter |pdf=|usr=}}{{34174287}} gab.com Text High dietary potassium causes ubiquitin-dependent degradation of the kidney sodium-chloride cotransporter JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=34174287 #FOAvip The thiazide-sensitive sodium-chloride cotransporter (NCC) in the renal distal convoluted tubule (DCT) plays a critical role in regulating blood pressure (BP) and K(+) homeostasis. During hyperkalemia, reduced NCC phosphorylation and total NCC abundance facilitate downstream electrogenic K(+) secretion and BP reduction. However, the mechanism for the K(+)-dependent reduction in total NCC levels is unknown. Here, we show that NCC levels were reduced in ex vivo renal tubules incubated in a high-K(+) medium for 24-48 h. This reduction was independent of NCC transcription, but was prevented using inhibitors of the proteasome (MG132) or lysosome (chloroquine). Ex vivo, high K(+) increased NCC ubiquitylation, but inhibition of the ubiquitin conjugation pathway prevented the high K(+)-mediated reduction in NCC protein. In tubules incubated in high K(+) media ex vivo or in the renal cortex of mice fed a high K(+) diet for 4 days, the abundance and phosphorylation of heat shock protein 70 (Hsp70), a key regulator of ubiquitin-dependent protein degradation and protein folding, were decreased. Conversely, in similar samples the expression of PP1alpha, known to dephosphorylate Hsp70, was also increased. NCC coimmunoprecipitated with Hsp70 and PP1alpha, and inhibiting their actions prevented the high K(+)-mediated reduction in total NCC levels. In conclusion, we show that hyperkalemia drives NCC ubiquitylation and degradation via a PP1alpha-dependent process facilitated by Hsp70. This mechanism facilitates K(+)-dependent reductions in NCC to protect plasma K(+) homeostasis and potentially reduces BP. Twit Text FOAVip High dietary potassium causes ubiquitin-dependent degradation of the kidney sodium-chloride cotransporter ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=34174287 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34174287 #FOAvip English Wikipedia <ref>{{Cite pmid|34174287}}</ref> High dietary potassium causes ubiquitin-dependent degradation of the kidney sodium-chloride cotransporter #MMPMID34174287 Kortenoeven MLA; Esteva-Font C; Dimke H; Poulsen SB; Murali SK; Fenton RA J Biol Chem 2021[Aug]; 297 (2): 100915 PMID34174287show ga The thiazide-sensitive sodium-chloride cotransporter (NCC) in the renal distal convoluted tubule (DCT) plays a critical role in regulating blood pressure (BP) and K(+) homeostasis. During hyperkalemia, reduced NCC phosphorylation and total NCC abundance facilitate downstream electrogenic K(+) secretion and BP reduction. However, the mechanism for the K(+)-dependent reduction in total NCC levels is unknown. Here, we show that NCC levels were reduced in ex vivo renal tubules incubated in a high-K(+) medium for 24-48 h. This reduction was independent of NCC transcription, but was prevented using inhibitors of the proteasome (MG132) or lysosome (chloroquine). Ex vivo, high K(+) increased NCC ubiquitylation, but inhibition of the ubiquitin conjugation pathway prevented the high K(+)-mediated reduction in NCC protein. In tubules incubated in high K(+) media ex vivo or in the renal cortex of mice fed a high K(+) diet for 4 days, the abundance and phosphorylation of heat shock protein 70 (Hsp70), a key regulator of ubiquitin-dependent protein degradation and protein folding, were decreased. Conversely, in similar samples the expression of PP1alpha, known to dephosphorylate Hsp70, was also increased. NCC coimmunoprecipitated with Hsp70 and PP1alpha, and inhibiting their actions prevented the high K(+)-mediated reduction in total NCC levels. In conclusion, we show that hyperkalemia drives NCC ubiquitylation and degradation via a PP1alpha-dependent process facilitated by Hsp70. This mechanism facilitates K(+)-dependent reductions in NCC to protect plasma K(+) homeostasis and potentially reduces BP. |Animals[MESH] |Disease Models, Animal[MESH] |HSP70 Heat-Shock Proteins/*metabolism[MESH] |Hypertension/drug therapy/metabolism/*pathology[MESH] |Kidney Tubules, Distal/*metabolism[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Phosphorylation[MESH] |Potassium, Dietary/*pharmacology[MESH] |Proteolysis[MESH] |Signal Transduction[MESH] |Solute Carrier Family 12, Member 3/genetics/*metabolism[MESH]High dietary potassium causes ubiquitin-dependent degradation of the k(epmc).pdf DeepDyve Pubget Overpricing