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10.1007/s00424-020-02491-1 http://scihub22266oqcxt.onion/10.1007/s00424-020-02491-1 33200256!7782375!33200256     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 245.2 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 Deprecated: Implicit conversion from float 245.2 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 Deprecated: Implicit conversion from float 245.2 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 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 278.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33200256.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Pflugers+Arch 2021 ; 473 (1): 79-93 Nephropedia Template TP {{tp|p=33200256|t=2021. Deletion of the transcription factor Prox-1 specifically in the renal distal convoluted tubule causes hypomagnesemia via reduced expression of TRPM6 and NCC |pdf=|usr=}}{{33200256}} gab.com Text Deletion of the transcription factor Prox-1 specifically in the renal distal convoluted tubule causes hypomagnesemia via reduced expression of TRPM6 and NCC JO: Pflugers Arch http://www.kidney.de/pget.php?&tw=1&pmid=33200256 #FOAvip The renal distal convoluted tubule (DCT) is critical for the fine-tuning of urinary ion excretion and the control of blood pressure. Ion transport along the DCT is tightly controlled by posttranscriptional mechanisms including a complex interplay of kinases, phosphatases, and ubiquitin ligases. Previous work identified the transcription factor Prox-1 as a gene significantly enriched in the DCT of adult mice. To test if Prox-1 contributes to the transcriptional regulation of DCT function and structure, we developed a novel mouse model (NCC(cre):Prox-1(flox/flox)) for an inducible deletion of Prox-1 specifically in the DCT. The deletion of Prox-1 had no obvious impact on DCT structure and growth independent whether the deletion was achieved in newborn or adult mice. Furthermore, DCT-specific Prox-1 deficiency did not alter DCT-proliferation in response to loop diuretic treatment. Likewise, the DCT-specific deletion of Prox-1 did not cause other gross phenotypic abnormalities. Body weight, urinary volume, Na(+) and K(+) excretion as well as plasma Na(+), K(+), and aldosterone levels were similar in Prox-1(DCT)(KO) and Prox-1(DCT)(Ctrl) mice. However, Prox-1(DCT)(KO) mice exhibited a significant hypomagnesemia with a profound downregulation of the DCT-specific apical Mg(2+) channel TRPM6 and the NaCl cotransporter (NCC) at both mRNA and protein levels. The expression of other proteins involved in distal tubule Mg(2+) and Na(+) handling was not affected. Thus, Prox-1 is a DCT-enriched transcription factor that does not control DCT growth but contributes to the molecular control of DCT-dependent Mg(2+) homeostasis in the adult kidney. Twit Text FOAVip Deletion of the transcription factor Prox-1 specifically in the renal distal convoluted tubule causes hypomagnesemia via reduced expression of TRPM6 and NCC ????Pflugers Arch http://www.kidney.de/pget.php?&tw=1&pmid=33200256 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33200256 #FOAvip English Wikipedia <ref>{{Cite pmid|33200256}}</ref> Deletion of the transcription factor Prox-1 specifically in the renal distal convoluted tubule causes hypomagnesemia via reduced expression of TRPM6 and NCC #MMPMID33200256 Schnoz C; Moser S; Kratschmar DV; Odermatt A; Loffing-Cueni D; Loffing J Pflugers Arch 2021[Jan]; 473 (1): 79-93 PMID33200256show ga The renal distal convoluted tubule (DCT) is critical for the fine-tuning of urinary ion excretion and the control of blood pressure. Ion transport along the DCT is tightly controlled by posttranscriptional mechanisms including a complex interplay of kinases, phosphatases, and ubiquitin ligases. Previous work identified the transcription factor Prox-1 as a gene significantly enriched in the DCT of adult mice. To test if Prox-1 contributes to the transcriptional regulation of DCT function and structure, we developed a novel mouse model (NCC(cre):Prox-1(flox/flox)) for an inducible deletion of Prox-1 specifically in the DCT. The deletion of Prox-1 had no obvious impact on DCT structure and growth independent whether the deletion was achieved in newborn or adult mice. Furthermore, DCT-specific Prox-1 deficiency did not alter DCT-proliferation in response to loop diuretic treatment. Likewise, the DCT-specific deletion of Prox-1 did not cause other gross phenotypic abnormalities. Body weight, urinary volume, Na(+) and K(+) excretion as well as plasma Na(+), K(+), and aldosterone levels were similar in Prox-1(DCT)(KO) and Prox-1(DCT)(Ctrl) mice. However, Prox-1(DCT)(KO) mice exhibited a significant hypomagnesemia with a profound downregulation of the DCT-specific apical Mg(2+) channel TRPM6 and the NaCl cotransporter (NCC) at both mRNA and protein levels. The expression of other proteins involved in distal tubule Mg(2+) and Na(+) handling was not affected. Thus, Prox-1 is a DCT-enriched transcription factor that does not control DCT growth but contributes to the molecular control of DCT-dependent Mg(2+) homeostasis in the adult kidney. |Animals[MESH] |Aquaporin 2/genetics/metabolism[MESH] |Gene Deletion[MESH] |Gene Expression Regulation/*physiology[MESH] |Homeodomain Proteins/genetics/*metabolism[MESH] |Kidney Tubules, Distal/cytology/*drug effects[MESH] |Magnesium/metabolism[MESH] |Mice[MESH] |Potassium/metabolism[MESH] |Prospero-Related Homeobox 1 Protein[MESH] |Sodium/metabolism[MESH] |Solute Carrier Family 12, Member 1/genetics/*metabolism[MESH] |Solute Carrier Family 12, Member 3/genetics/metabolism[MESH] |TRPM Cation Channels/genetics/*metabolism[MESH]Deletion of the transcription factor Prox-1 specifically in the renal (epmc).pdf DeepDyve Pubget Overpricing