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10.1073/pnas.1610963114 http://scihub22266oqcxt.onion/10.1073/pnas.1610963114 C5358369!5358369!28242694     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28242694&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 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (11): 2964-9 Nephropedia Template TP {{tp|p=28242694|t=2017. Receptor-interacting protein kinase 3 promotes platelet activation and thrombosis |pdf=|usr=}}{{28242694}} gab.com Text Receptor-interacting protein kinase 3 promotes platelet activation and thrombosis JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28242694 #FOAvip Receptor-interacting protein kinase 3 (RIP3) is involved in many important biological processes such as necroptosis, apoptosis, and inflammation. Here, using RIP3-knockout mice, we show that RIP3 is essential for in vivo thrombosis and hemostasis. Mice lacking RIP3 exhibited prolonged tail-bleeding times and reduced arterial thrombus formation. We demonstrate that RIP3, expressed in platelets and interacting with G?13, promotes platelet aggregation, secretion, spreading on fibrinogen, and clot retraction. RIP3 inhibitor dose-dependently inhibits platelet aggregation and prevents arterial thrombus formation. Our findings indicate a role for RIP3 in promoting in vivo thrombosis and hemostasis by amplifying platelet activation. RIP3 may represent a novel therapeutic target for thrombotic diseases. Twit Text FOAVip Receptor-interacting protein kinase 3 promotes platelet activation and thrombosis ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28242694 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28242694 #FOAvip English Wikipedia <ref>{{Cite pmid|28242694}}</ref> Receptor-interacting protein kinase 3 promotes platelet activation and thrombosis #MMPMID28242694 Zhang Y; Zhang J; Yan R; Tian J; Zhang Y; Zhang J; Chen M; Cui Q; Zhao L; Hu R; Jiang M; Li Z; Ruan C; He S; Dai K Proc Natl Acad Sci U S A 2017[Mar]; 114 (11): 2964-9 PMID28242694show ga Receptor-interacting protein kinase 3 (RIP3) is involved in many important biological processes such as necroptosis, apoptosis, and inflammation. Here, using RIP3-knockout mice, we show that RIP3 is essential for in vivo thrombosis and hemostasis. Mice lacking RIP3 exhibited prolonged tail-bleeding times and reduced arterial thrombus formation. We demonstrate that RIP3, expressed in platelets and interacting with G?13, promotes platelet aggregation, secretion, spreading on fibrinogen, and clot retraction. RIP3 inhibitor dose-dependently inhibits platelet aggregation and prevents arterial thrombus formation. Our findings indicate a role for RIP3 in promoting in vivo thrombosis and hemostasis by amplifying platelet activation. RIP3 may represent a novel therapeutic target for thrombotic diseases. äReceptor-interacting protein kinase 3 promotes platelet activation and(epmc).pdf DeepDyve Pubget Overpricing