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10.1038/aps.2016.155 http://scihub22266oqcxt.onion/10.1038/aps.2016.155 C5457693!5457693!28260800     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Pharmacol+Sin 2017 ; 38 (5): 651-9 Nephropedia Template TP {{tp|p=28260800|t=2017. A novel STAT3 inhibitor negatively modulates platelet activation and aggregation |pdf=|usr=}}{{28260800}} gab.com Text A novel STAT3 inhibitor negatively modulates platelet activation and aggregation JO: Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=28260800 #FOAvip The signal transducer and activator of transcription 3 (STAT3) plays a critical role in platelet functions. This study sought to understand the effects of the STAT3 inhibitor SC99 on platelet activation and aggregation. Immunoblotting assays were applied to measure the effects of SC99 on the STAT3 signaling pathway. A ChronoLog aggregometer was used to evaluate platelet aggregation. A flow cytometer was used to evaluate P-selectin expression in the presence of SC99. AlamarBlue and Annexin-V staining were used to evaluate platelet viability and apoptosis, respectively. A fluorescence microscope was applied to analyze platelet spreading. SC99 inhibited the phosphorylation of JAK2 and STAT3 in human platelets but had no effects on the phosphorylation of AKT, p65 or Src, all of which are involved in platelet activation. Further studies revealed that SC99 inhibited human platelet aggregation induced by collagen and thrombin in a dose-dependent manner. SC99 inhibited thrombin-induced P-selectin expression and fibrinogen binding to single platelets. Moreover, SC99 inhibited platelet spreading on fibrinogen and clot retraction mediated by outside-in signaling. SC99 inhibited platelet aggregation in mice but it did not significantly prolong the bleeding time. Taken together, the present study revealed that SC99 inhibited platelet activation and aggregation as a STAT3 inhibitor. This agent can be developed as a promising treatment for thrombotic disorders. Twit Text FOAVip A novel STAT3 inhibitor negatively modulates platelet activation and aggregation ????Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=28260800 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28260800 #FOAvip English Wikipedia <ref>{{Cite pmid|28260800}}</ref> A novel STAT3 inhibitor negatively modulates platelet activation and aggregation #MMPMID28260800 Xu Z; Xu Yj; Hao Yn; Ren Lj; Zhang Zb; Xu X; Cao By; Dai Ks; Zhu L; Fang Q; Kong Y; Mao Xl Acta Pharmacol Sin 2017[May]; 38 (5): 651-9 PMID28260800show ga The signal transducer and activator of transcription 3 (STAT3) plays a critical role in platelet functions. This study sought to understand the effects of the STAT3 inhibitor SC99 on platelet activation and aggregation. Immunoblotting assays were applied to measure the effects of SC99 on the STAT3 signaling pathway. A ChronoLog aggregometer was used to evaluate platelet aggregation. A flow cytometer was used to evaluate P-selectin expression in the presence of SC99. AlamarBlue and Annexin-V staining were used to evaluate platelet viability and apoptosis, respectively. A fluorescence microscope was applied to analyze platelet spreading. SC99 inhibited the phosphorylation of JAK2 and STAT3 in human platelets but had no effects on the phosphorylation of AKT, p65 or Src, all of which are involved in platelet activation. Further studies revealed that SC99 inhibited human platelet aggregation induced by collagen and thrombin in a dose-dependent manner. SC99 inhibited thrombin-induced P-selectin expression and fibrinogen binding to single platelets. Moreover, SC99 inhibited platelet spreading on fibrinogen and clot retraction mediated by outside-in signaling. SC99 inhibited platelet aggregation in mice but it did not significantly prolong the bleeding time. Taken together, the present study revealed that SC99 inhibited platelet activation and aggregation as a STAT3 inhibitor. This agent can be developed as a promising treatment for thrombotic disorders. äA novel STAT3 inhibitor negatively modulates platelet activation and a(epmc).pdf DeepDyve Pubget Overpricing