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10.1161/CIRCULATIONAHA.112.132126 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.112.132126 C4472638!4472638!23266857     free     free     free 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 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 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circulation 2013 ; 127 (4): 476-85 Nephropedia Template TP {{tp|p=23266857|t=2013. STAT3 Regulates Collagen-Induced Platelet Aggregation Independent of its Transcription Factor Activity |pdf=|usr=}}{{23266857}} gab.com Text STAT3 Regulates Collagen-Induced Platelet Aggregation Independent of its Transcription Factor Activity JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=23266857 #FOAvip Background: Platelet hyperactivity induced by inflammation is a known risk factor for atherosclerosis and thrombosis, but its underlying mechanisms remain poorly understood. Methods and Results: The signal transducers and activators of transcription 3 (STAT3) was activated in collagen-stimulated platelets. Activated STAT3 served as a protein scaffold to facilitate the catalytic interaction between the kinase Syk and the substrate PLC?2 to enhance collagen-induced calcium mobilization and platelet activation. The same interaction of STAT3 with Syk and PLC?2 was also detected in HEK293 cells transfected with cDNAs for Syk and PLC?2, and stimulated with interleukin-6 (IL-6). Pharmacological inhibition of STAT3 blocked ~50% of collagen- and a collagen-related peptide-, but not TRAP- or ADP-induced aggregation and ~80% of thrombus formation of human platelets on a collagen matrix. This in vitro phenotype was reproduced in mice infused with STAT3 inhibitors and mice with platelet specific STAT3 deficiency. By forming a complex with its soluble receptor, the proinflammatory cytokine IL-6 enhanced the collagen-induced STAT3 activation in human platelets. Conclusions: These data demonstrate a non-transcriptional activity of STAT3 that facilitates a crosstalk between proinflammatory cytokine and hemostasis/thrombosis signals in platelets. This crosstalk may be responsible for platelet hyperactivity found in conditions of inflammation. Twit Text FOAVip STAT3 Regulates Collagen-Induced Platelet Aggregation Independent of its Transcription Factor Activity ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=23266857 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23266857 #FOAvip English Wikipedia <ref>{{Cite pmid|23266857}}</ref> STAT3 Regulates Collagen-Induced Platelet Aggregation Independent of its Transcription Factor Activity #MMPMID23266857 Zhou Z; Gushiken FC; Bolgiano D; Salsbery BJ; Aghakasiri N; Jing N; Wu X; Vijayan KV; Rumbaut RE; Adachi R; Lopez JA; Dong Jf Circulation 2013[Jan]; 127 (4): 476-85 PMID23266857show ga Background: Platelet hyperactivity induced by inflammation is a known risk factor for atherosclerosis and thrombosis, but its underlying mechanisms remain poorly understood. Methods and Results: The signal transducers and activators of transcription 3 (STAT3) was activated in collagen-stimulated platelets. Activated STAT3 served as a protein scaffold to facilitate the catalytic interaction between the kinase Syk and the substrate PLC?2 to enhance collagen-induced calcium mobilization and platelet activation. The same interaction of STAT3 with Syk and PLC?2 was also detected in HEK293 cells transfected with cDNAs for Syk and PLC?2, and stimulated with interleukin-6 (IL-6). Pharmacological inhibition of STAT3 blocked ~50% of collagen- and a collagen-related peptide-, but not TRAP- or ADP-induced aggregation and ~80% of thrombus formation of human platelets on a collagen matrix. This in vitro phenotype was reproduced in mice infused with STAT3 inhibitors and mice with platelet specific STAT3 deficiency. By forming a complex with its soluble receptor, the proinflammatory cytokine IL-6 enhanced the collagen-induced STAT3 activation in human platelets. Conclusions: These data demonstrate a non-transcriptional activity of STAT3 that facilitates a crosstalk between proinflammatory cytokine and hemostasis/thrombosis signals in platelets. This crosstalk may be responsible for platelet hyperactivity found in conditions of inflammation. äSTAT3 Regulates Collagen-Induced Platelet Aggregation Independent of i(epmc).pdf DeepDyve Pubget Overpricing