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10.1073/pnas.1707364114 http://scihub22266oqcxt.onion/10.1073/pnas.1707364114 C5642699!5642699 !28973891     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 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 Deprecated: Implicit conversion from float 245.2 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 Deprecated: Implicit conversion from float 245.2 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 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28973891 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (41 ): 10948-10953 Nephropedia Template TP {{tp|p=28973891 |t=2017. Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4 |pdf=|usr=}}{{28973891 }} gab.com Text Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4 JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28973891 #FOAvip C4a is a small protein released from complement component C4 upon activation of the complement system's classical and lectin pathways, which are important constituents of innate immune surveillance. Despite the structural similarity between C4a and well-described anaphylatoxins C3a and C5a, the binding partner and biological function of C4a have remained elusive. Using a cell-based reporter assay, we screened C4a against a panel of both known and orphan G protein-coupled receptors and now provide evidence that C4a is a ligand for protease-activated receptor (PAR)1 and PAR4. Whereas C4a showed no activity toward known anaphylatoxin receptors, it acted as an agonist for both PAR1 and PAR4 with nanomolar activity. In human endothelial cells, ERK activation by C4a was mediated through both PAR1 and PAR4 in a G?(i)-independent signaling pathway. Like other PAR1 activators, C4a induced calcium mobilization through the PAR1/G?(q)/PLC? signaling axis. Moreover, C4a increased stress fiber formation and enhanced endothelial permeability, both of which were reduced by PAR1 antagonists. In sum, our study identifies C4a as an untethered agonist for PAR1 and PAR4 with effects on cellular activation and endothelial permeability, thereby revealing another instance of cross-talk between the complement system and other host defense pathways. Twit Text FOAVip Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4 ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28973891 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28973891 #FOAvip English Wikipedia <ref>{{Cite pmid|28973891 }}</ref> Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4 #MMPMID28973891 Wang H ; Ricklin D ; Lambris JD Proc Natl Acad Sci U S A 2017[Oct]; 114 (41 ): 10948-10953 PMID28973891 show ga C4a is a small protein released from complement component C4 upon activation of the complement system's classical and lectin pathways, which are important constituents of innate immune surveillance. Despite the structural similarity between C4a and well-described anaphylatoxins C3a and C5a, the binding partner and biological function of C4a have remained elusive. Using a cell-based reporter assay, we screened C4a against a panel of both known and orphan G protein-coupled receptors and now provide evidence that C4a is a ligand for protease-activated receptor (PAR)1 and PAR4. Whereas C4a showed no activity toward known anaphylatoxin receptors, it acted as an agonist for both PAR1 and PAR4 with nanomolar activity. In human endothelial cells, ERK activation by C4a was mediated through both PAR1 and PAR4 in a G?(i)-independent signaling pathway. Like other PAR1 activators, C4a induced calcium mobilization through the PAR1/G?(q)/PLC? signaling axis. Moreover, C4a increased stress fiber formation and enhanced endothelial permeability, both of which were reduced by PAR1 antagonists. In sum, our study identifies C4a as an untethered agonist for PAR1 and PAR4 with effects on cellular activation and endothelial permeability, thereby revealing another instance of cross-talk between the complement system and other host defense pathways. |*Complement Activation [MESH] |Calcium/*metabolism [MESH] |Cells, Cultured [MESH] |Complement C4a/genetics/*metabolism [MESH] |Endothelium, Vascular/cytology/*metabolism [MESH] |Humans [MESH] |Mitogen-Activated Protein Kinase 1/metabolism [MESH] |Mitogen-Activated Protein Kinase 3/metabolism [MESH] |Receptor, PAR-1/*agonists/metabolism [MESH] |Receptors, G-Protein-Coupled/metabolism [MESH] |Receptors, Thrombin/*agonists/metabolism [MESH]Complement-activation fragment C4a mediates effector functions by bind(epmc).pdf DeepDyve Pubget Overpricing