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10.1172/JCI30087 http://scihub22266oqcxt.onion/10.1172/JCI30087 17380208!1821066!17380208     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2007 ; 117 (4): 1078-87 Nephropedia Template TP {{tp|p=17380208|t=2007. Intersectin links WNK kinases to endocytosis of ROMK1 |pdf=|usr=}}{{17380208}} gab.com Text Intersectin links WNK kinases to endocytosis of ROMK1 JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=17380208 #FOAvip With-no-lysine (WNK) kinases are a novel family of protein kinases characterized by an atypical placement of the catalytic lysine. Mutations of 2 family members, WNK1 and WNK4, cause pseudohypoaldosteronism type 2 (PHA2), an autosomal-dominant disease characterized by hypertension and hyperkalemia. WNK1 and WNK4 stimulate clathrin-dependent endocytosis of renal outer medullar potassium 1 (ROMK1), and PHA2-causing mutations of WNK4 increase the endocytosis. How WNKs stimulate endocytosis of ROMK1 and how mutations of WNK4 increase the endocytosis are unknown. Intersectin (ITSN) is a multimodular endocytic scaffold protein. Here we show that WNK1 and WNK4 interacted with ITSN and that the interactions were crucial for stimulation of endocytosis of ROMK1 by WNKs. The stimulation of endocytosis of ROMK1 by WNK1 and WNK4 required specific proline-rich motifs of WNKs, but did not require their kinase activity. WNK4 interacted with ROMK1 as well as with ITSN. Disease-causing WNK4 mutations enhanced interactions of WNK4 with ITSN and ROMK1, leading to increased endocytosis of ROMK1. These results provide a molecular mechanism for stimulation of endocytosis of ROMK1 by WNK kinases. Twit Text FOAVip Intersectin links WNK kinases to endocytosis of ROMK1 ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=17380208 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17380208 #FOAvip English Wikipedia <ref>{{Cite pmid|17380208}}</ref> Intersectin links WNK kinases to endocytosis of ROMK1 #MMPMID17380208 He G; Wang HR; Huang SK; Huang CL J Clin Invest 2007[Apr]; 117 (4): 1078-87 PMID17380208show ga With-no-lysine (WNK) kinases are a novel family of protein kinases characterized by an atypical placement of the catalytic lysine. Mutations of 2 family members, WNK1 and WNK4, cause pseudohypoaldosteronism type 2 (PHA2), an autosomal-dominant disease characterized by hypertension and hyperkalemia. WNK1 and WNK4 stimulate clathrin-dependent endocytosis of renal outer medullar potassium 1 (ROMK1), and PHA2-causing mutations of WNK4 increase the endocytosis. How WNKs stimulate endocytosis of ROMK1 and how mutations of WNK4 increase the endocytosis are unknown. Intersectin (ITSN) is a multimodular endocytic scaffold protein. Here we show that WNK1 and WNK4 interacted with ITSN and that the interactions were crucial for stimulation of endocytosis of ROMK1 by WNKs. The stimulation of endocytosis of ROMK1 by WNK1 and WNK4 required specific proline-rich motifs of WNKs, but did not require their kinase activity. WNK4 interacted with ROMK1 as well as with ITSN. Disease-causing WNK4 mutations enhanced interactions of WNK4 with ITSN and ROMK1, leading to increased endocytosis of ROMK1. These results provide a molecular mechanism for stimulation of endocytosis of ROMK1 by WNK kinases. |*Endocytosis[MESH] |Adaptor Proteins, Vesicular Transport/*metabolism[MESH] |Cell Line[MESH] |Clathrin/metabolism[MESH] |Gene Expression Regulation[MESH] |Humans[MESH] |Intracellular Signaling Peptides and Proteins[MESH] |Kidney[MESH] |Minor Histocompatibility Antigens[MESH] |Potassium Channels, Inwardly Rectifying/genetics/*metabolism[MESH] |Proline[MESH] |Protein Serine-Threonine Kinases/chemistry/genetics/*metabolism[MESH] |WNK Lysine-Deficient Protein Kinase 1[MESH]Intersectin links WNK kinases to endocytosis of ROMK1 (epmc).pdf DeepDyve Pubget Overpricing