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.

10.1152/ajprenal.00298.2010 http://scihub22266oqcxt.onion/10.1152/ajprenal.00298.2010 20685822!2957253!20685822     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 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2010 ; 299 (4): F689-701 Nephropedia Template TP {{tp|p=20685822|t=2010. TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology |pdf=|usr=}}{{20685822}} gab.com Text TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=20685822 #FOAvip Loss or dysfunction of podocytes is a major cause of glomerular kidney disease. Several genetic forms of glomerular disease are caused by mutations in genes that encode structural elements of the slit diaphragm or the underlying cytoskeleton of podocyte foot processes. The recent discovery that gain-of-function mutations in Ca(2+)-permeable canonical transient receptor potential-6 channels (TRPC6) underlie a subset of familial forms of focal segmental glomerulosclerosis (FSGS) has focused attention on the basic cellular physiology of podocytes. Several recent studies have examined the role of Ca(2+) dynamics in normal podocyte function and their possible contributions to glomerular disease. This review summarizes the properties of TRPC6 and related channels, focusing on their permeation and gating properties, the nature of mutations associated with familial FSGS, and the role of TRPC channels in podocyte cell biology as well as in glomerular pathophysiology. TRPC6 interacts with several proteins in podocytes, including essential slit diaphragm proteins and mechanosensitive large-conductance Ca(2+)-activated K(+) channels. The signaling dynamics controlling ion channel function and localization in podocytes appear to be quite complex. Twit Text FOAVip TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=20685822 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20685822 #FOAvip English Wikipedia <ref>{{Cite pmid|20685822}}</ref> TRPC6 channels and their binding partners in podocytes: role in glomerular filtration and pathophysiology #MMPMID20685822 Dryer SE; Reiser J Am J Physiol Renal Physiol 2010[Oct]; 299 (4): F689-701 PMID20685822show ga Loss or dysfunction of podocytes is a major cause of glomerular kidney disease. Several genetic forms of glomerular disease are caused by mutations in genes that encode structural elements of the slit diaphragm or the underlying cytoskeleton of podocyte foot processes. The recent discovery that gain-of-function mutations in Ca(2+)-permeable canonical transient receptor potential-6 channels (TRPC6) underlie a subset of familial forms of focal segmental glomerulosclerosis (FSGS) has focused attention on the basic cellular physiology of podocytes. Several recent studies have examined the role of Ca(2+) dynamics in normal podocyte function and their possible contributions to glomerular disease. This review summarizes the properties of TRPC6 and related channels, focusing on their permeation and gating properties, the nature of mutations associated with familial FSGS, and the role of TRPC channels in podocyte cell biology as well as in glomerular pathophysiology. TRPC6 interacts with several proteins in podocytes, including essential slit diaphragm proteins and mechanosensitive large-conductance Ca(2+)-activated K(+) channels. The signaling dynamics controlling ion channel function and localization in podocytes appear to be quite complex. |Calcium/physiology[MESH] |Glomerular Filtration Rate/*physiology[MESH] |Glomerulosclerosis, Focal Segmental/genetics/physiopathology[MESH] |Humans[MESH] |Mutation/genetics[MESH] |Podocytes/*physiology[MESH] |Potassium Channels, Calcium-Activated/physiology[MESH] |TRPC Cation Channels/genetics/*physiology[MESH]TRPC6 channels and their binding partners in podocytes: role in glomer(epmc).pdf DeepDyve Pubget Overpricing