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10.3390/ijms22042207 http://scihub22266oqcxt.onion/10.3390/ijms22042207 33672238!7926544!33672238     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 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       Int+J+Mol+Sci 2021 ; 22 (4): ä Nephropedia Template TP {{tp|p=33672238|t=2021. Differential Effects of STCH and Stress-Inducible Hsp70 on the Stability and Maturation of NKCC2 |pdf=|usr=}}{{33672238}} gab.com Text Differential Effects of STCH and Stress-Inducible Hsp70 on the Stability and Maturation of NKCC2 JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33672238 #FOAvip Mutations in the Na-K-2Cl co-transporter NKCC2 lead to type I Bartter syndrome, a life-threatening kidney disease. We previously showed that export from the ER constitutes the limiting step in NKCC2 maturation and cell surface expression. Yet, the molecular mechanisms involved in this process remain obscure. Here, we report the identification of chaperone stress 70 protein (STCH) and the stress-inducible heat shock protein 70 (Hsp70), as two novel binding partners of the ER-resident form of NKCC2. STCH knock-down increased total NKCC2 expression whereas Hsp70 knock-down or its inhibition by YM-01 had the opposite effect. Accordingly, overexpressing of STCH and Hsp70 exerted opposite actions on total protein abundance of NKCC2 and its folding mutants. Cycloheximide chase assay showed that in cells over-expressing STCH, NKCC2 stability and maturation are heavily impaired. In contrast to STCH, Hsp70 co-expression increased NKCC2 maturation. Interestingly, treatment by protein degradation inhibitors revealed that in addition to the proteasome, the ER associated degradation (ERAD) of NKCC2 mediated by STCH, involves also the ER-to-lysosome-associated degradation pathway. In summary, our data are consistent with STCH and Hsp70 having differential and antagonistic effects with regard to NKCC2 biogenesis. These findings may have an impact on our understanding and potential treatment of diseases related to aberrant NKCC2 trafficking and expression. Twit Text FOAVip Differential Effects of STCH and Stress-Inducible Hsp70 on the Stability and Maturation of NKCC2 ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33672238 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33672238 #FOAvip English Wikipedia <ref>{{Cite pmid|33672238}}</ref> Differential Effects of STCH and Stress-Inducible Hsp70 on the Stability and Maturation of NKCC2 #MMPMID33672238 Bakhos-Douaihy D; Seaayfan E; Demaretz S; Komhoff M; Laghmani K Int J Mol Sci 2021[Feb]; 22 (4): ä PMID33672238show ga Mutations in the Na-K-2Cl co-transporter NKCC2 lead to type I Bartter syndrome, a life-threatening kidney disease. We previously showed that export from the ER constitutes the limiting step in NKCC2 maturation and cell surface expression. Yet, the molecular mechanisms involved in this process remain obscure. Here, we report the identification of chaperone stress 70 protein (STCH) and the stress-inducible heat shock protein 70 (Hsp70), as two novel binding partners of the ER-resident form of NKCC2. STCH knock-down increased total NKCC2 expression whereas Hsp70 knock-down or its inhibition by YM-01 had the opposite effect. Accordingly, overexpressing of STCH and Hsp70 exerted opposite actions on total protein abundance of NKCC2 and its folding mutants. Cycloheximide chase assay showed that in cells over-expressing STCH, NKCC2 stability and maturation are heavily impaired. In contrast to STCH, Hsp70 co-expression increased NKCC2 maturation. Interestingly, treatment by protein degradation inhibitors revealed that in addition to the proteasome, the ER associated degradation (ERAD) of NKCC2 mediated by STCH, involves also the ER-to-lysosome-associated degradation pathway. In summary, our data are consistent with STCH and Hsp70 having differential and antagonistic effects with regard to NKCC2 biogenesis. These findings may have an impact on our understanding and potential treatment of diseases related to aberrant NKCC2 trafficking and expression. |Animals[MESH] |Bartter Syndrome/genetics[MESH] |Binding Sites[MESH] |Endoplasmic Reticulum-Associated Degradation[MESH] |Endoplasmic Reticulum/metabolism[MESH] |HEK293 Cells[MESH] |HSP70 Heat-Shock Proteins/genetics/*metabolism[MESH] |Humans[MESH] |Kidney/cytology[MESH] |Mutation[MESH] |Opossums[MESH] |Proteasome Endopeptidase Complex/metabolism[MESH] |Protein Interaction Domains and Motifs[MESH] |Solute Carrier Family 12, Member 1/genetics/*metabolism[MESH]Differential Effects of STCH and Stress-Inducible Hsp70 on the Stabili(epmc).pdf DeepDyve Pubget Overpricing