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.

10.3390/ijms19061798 http://scihub22266oqcxt.onion/10.3390/ijms19061798 C6032267!6032267 !29912162     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29912162 &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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 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\29912162 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Int+J+Mol+Sci 2018 ; 19 (6 ): ä Nephropedia Template TP {{tp|p=29912162 |t=2018. Regulation and Function of TMEM16F in Renal Podocytes |pdf=|usr=}}{{29912162 }} gab.com Text Regulation and Function of TMEM16F in Renal Podocytes JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=29912162 #FOAvip The Ca(2+)-activated phospholipid scramblase and ion channel TMEM16F is expressed in podocytes of renal glomeruli. Podocytes are specialized cells that form interdigitating foot processes as an essential component of the glomerular filter. These cells, which participate in generation of the primary urine, are often affected during primary glomerular diseases, such as glomerulonephritis and secondary hypertensive or diabetic nephropathy, which always leads to proteinuria. Because the function of podocytes is known to be controlled by intracellular Ca(2+) signaling, it is important to know about the role of Ca(2+)-activated TMEM16F in these cells. To that end, we generated an inducible TMEM16F knockdown in the podocyte cell line AB8, and produced a conditional mouse model with knockout of TMEM16F in podocytes and renal epithelial cells of the nephron. We found that knockdown of TMEM16F did not produce proteinuria or any obvious phenotypic changes. Knockdown of TMEM16F affected cell death of tubular epithelial cells but not of glomerular podocytes when analyzed in TUNEL assays. Surprisingly, and in contrast to other cell types, TMEM16F did not control intracellular Ca(2+) signaling and was not responsible for Ca(2+)-activated whole cell currents in podocytes. TMEM16F levels in podocytes were enhanced after inhibition of the endolysosomal pathway and after treatment with angiotensin II. Renal knockout of TMEM16F did not compromise renal morphology and serum electrolytes. Taken together, in contrast to other cell types, such as platelets, bone cells, and immune cells, TMEM16F shows little effect on basal properties of podocytes and does not appear to be essential for renal function. Twit Text FOAVip Regulation and Function of TMEM16F in Renal Podocytes ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=29912162 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29912162 #FOAvip English Wikipedia <ref>{{Cite pmid|29912162 }}</ref> Regulation and Function of TMEM16F in Renal Podocytes #MMPMID29912162 Schenk LK ; Ousingsawat J ; Skryabin BV ; Schreiber R ; Pavenstädt H ; Kunzelmann K Int J Mol Sci 2018[Jun]; 19 (6 ): ä PMID29912162 show ga The Ca(2+)-activated phospholipid scramblase and ion channel TMEM16F is expressed in podocytes of renal glomeruli. Podocytes are specialized cells that form interdigitating foot processes as an essential component of the glomerular filter. These cells, which participate in generation of the primary urine, are often affected during primary glomerular diseases, such as glomerulonephritis and secondary hypertensive or diabetic nephropathy, which always leads to proteinuria. Because the function of podocytes is known to be controlled by intracellular Ca(2+) signaling, it is important to know about the role of Ca(2+)-activated TMEM16F in these cells. To that end, we generated an inducible TMEM16F knockdown in the podocyte cell line AB8, and produced a conditional mouse model with knockout of TMEM16F in podocytes and renal epithelial cells of the nephron. We found that knockdown of TMEM16F did not produce proteinuria or any obvious phenotypic changes. Knockdown of TMEM16F affected cell death of tubular epithelial cells but not of glomerular podocytes when analyzed in TUNEL assays. Surprisingly, and in contrast to other cell types, TMEM16F did not control intracellular Ca(2+) signaling and was not responsible for Ca(2+)-activated whole cell currents in podocytes. TMEM16F levels in podocytes were enhanced after inhibition of the endolysosomal pathway and after treatment with angiotensin II. Renal knockout of TMEM16F did not compromise renal morphology and serum electrolytes. Taken together, in contrast to other cell types, such as platelets, bone cells, and immune cells, TMEM16F shows little effect on basal properties of podocytes and does not appear to be essential for renal function. |Action Potentials [MESH] |Animals [MESH] |Anoctamins/*genetics/metabolism [MESH] |Apoptosis [MESH] |Calcium Signaling [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Mice [MESH] |Phenotype [MESH] |Phospholipid Transfer Proteins/*genetics/metabolism [MESH]Regulation and Function of TMEM16F in Renal Podocytes (epmc).pdf DeepDyve Pubget Overpricing