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10.4049/jimmunol.1500532 http://scihub22266oqcxt.onion/10.4049/jimmunol.1500532 C4868657!4868657 !26976957     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26976957 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2016 ; 196 (9 ): 3828-33 Nephropedia Template TP {{tp|p=26976957 |t=2016. G?i2 and G?i3 Differentially Regulate Arrest from Flow and Chemotaxis in Mouse Neutrophils |pdf=|usr=}}{{26976957 }} gab.com Text G i2 and G i3 Differentially Regulate Arrest from Flow and Chemotaxis in Mouse Neutrophils JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26976957 #FOAvip Leukocyte recruitment to inflammation sites progresses in a multistep cascade. Chemokines regulate multiple steps of the cascade, including arrest, transmigration, and chemotaxis. The most important chemokine receptor in mouse neutrophils is CXCR2, which couples through G?i2- and G?i3-containing heterotrimeric G proteins. Neutrophils arrest in response to CXCR2 stimulation. This is defective in G?i2-deficient neutrophils. In this study, we show that G?i3-deficient neutrophils showed reduced transmigration but normal arrest in mice. We also tested G?i2- or G?i3-deficient neutrophils in a CXCL1 gradient generated by a microfluidic device. G?i3-, but not G?i2-, deficient neutrophils showed significantly reduced migration and directionality. This was confirmed in a model of sterile inflammation in vivo. G?i2-, but not G?i3-, deficient neutrophils showed decreased Ca(2+) flux in response to CXCR2 stimulation. Conversely, G?i3-, but not G?i2-, deficient neutrophils exhibited reduced AKT phosphorylation upon CXCR2 stimulation. We conclude that G?i2 controls arrest and G?i3 controls transmigration and chemotaxis in response to chemokine stimulation of neutrophils. Twit Text FOAVip G i2 and G i3 Differentially Regulate Arrest from Flow and Chemotaxis in Mouse Neutrophils ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26976957 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26976957 #FOAvip English Wikipedia <ref>{{Cite pmid|26976957 }}</ref> G?i2 and G?i3 Differentially Regulate Arrest from Flow and Chemotaxis in Mouse Neutrophils #MMPMID26976957 Kuwano Y ; Adler M ; Zhang H ; Groisman A ; Ley K J Immunol 2016[May]; 196 (9 ): 3828-33 PMID26976957 show ga Leukocyte recruitment to inflammation sites progresses in a multistep cascade. Chemokines regulate multiple steps of the cascade, including arrest, transmigration, and chemotaxis. The most important chemokine receptor in mouse neutrophils is CXCR2, which couples through G?i2- and G?i3-containing heterotrimeric G proteins. Neutrophils arrest in response to CXCR2 stimulation. This is defective in G?i2-deficient neutrophils. In this study, we show that G?i3-deficient neutrophils showed reduced transmigration but normal arrest in mice. We also tested G?i2- or G?i3-deficient neutrophils in a CXCL1 gradient generated by a microfluidic device. G?i3-, but not G?i2-, deficient neutrophils showed significantly reduced migration and directionality. This was confirmed in a model of sterile inflammation in vivo. G?i2-, but not G?i3-, deficient neutrophils showed decreased Ca(2+) flux in response to CXCR2 stimulation. Conversely, G?i3-, but not G?i2-, deficient neutrophils exhibited reduced AKT phosphorylation upon CXCR2 stimulation. We conclude that G?i2 controls arrest and G?i3 controls transmigration and chemotaxis in response to chemokine stimulation of neutrophils. |Animals [MESH] |Calcium Signaling/genetics [MESH] |Cell Movement/genetics [MESH] |Cells, Cultured [MESH] |Chemokine CXCL1/metabolism [MESH] |Chemotaxis/genetics [MESH] |GTP-Binding Protein alpha Subunit, Gi2/genetics/*metabolism [MESH] |GTP-Binding Protein alpha Subunits, Gi-Go/genetics/*metabolism [MESH] |Mice [MESH] |Mice, 129 Strain [MESH] |Mice, Knockout [MESH] |Neutrophils/*immunology [MESH] |Protein Binding [MESH] |Receptors, Interleukin-8B/metabolism [MESH]G?i2 and G?i3 Differentially Regulate Arrest from Flow and Chemotaxis (epmc).pdf DeepDyve Pubget Overpricing