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10.1002/eji.201444994 http://scihub22266oqcxt.onion/10.1002/eji.201444994 C4432939!4432939!25616060     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 267.2 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\25616060.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Eur+J+Immunol 2015 ; 45 (4): 1059-68 Nephropedia Template TP {{tp|p=25616060|t=2015. The NF-?B regulator Bcl-3 modulates inflammation in contact hypersensitivity reactions in radioresistant cells |pdf=|usr=}}{{25616060}} gab.com Text The NF- B regulator Bcl-3 modulates inflammation in contact hypersensitivity reactions in radioresistant cells JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25616060 #FOAvip Bcl-3 is an atypical member of the I?B family. Bcl-3 functions as a cofactor of p50/NF-?B1 or p52/NF-?B2 homodimers in nuclei, where it modulates NF-?B-regulated transcription in a context-dependent way. Bcl-3 has tumorigenic potential, is critical in host defense of pathogens, and has been reported to ameliorate or exacerbate inflammation, depending on disease model. However, cell-specific functions of Bcl-3 remain largely unknown. Here, we explored the role of Bcl-3 in a contact hypersensitivity (CHS) mouse model, which depends on the interplay between keratinocytes and immune cells. Bcl-3-deficient mice exhibited an exacerbated and prolonged CHS response to oxazolone. Increased inflammation correlated with higher production of chemokines CXCL2, CXCL9 and CXCL10, and consequently increased recruitment of neutrophils and CD8+ T cells. Bone marrow chimera experiments indicated that the ability of Bcl-3 to reduce the CHS response depended on Bcl-3 activity in radioresistant cells. Specific ablation of Bcl-3 in keratinocytes resulted in increased production of CXCL9 and CXCL10 and sustained recruitment of specifically CD8+ T cells. These findings identify Bcl-3 as a critical player during the later stage of the CHS reaction to limit inflammation via actions in radioresistant cells, including keratinocytes. Twit Text FOAVip The NF- B regulator Bcl-3 modulates inflammation in contact hypersensitivity reactions in radioresistant cells ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25616060 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25616060 #FOAvip English Wikipedia <ref>{{Cite pmid|25616060}}</ref> The NF-?B regulator Bcl-3 modulates inflammation in contact hypersensitivity reactions in radioresistant cells #MMPMID25616060 Tassi I; Rikhi N; Claudio E; Wang H; Tang W; Ha Hl; Saret S; Kaplan DH; Siebenlist U Eur J Immunol 2015[Apr]; 45 (4): 1059-68 PMID25616060show ga Bcl-3 is an atypical member of the I?B family. Bcl-3 functions as a cofactor of p50/NF-?B1 or p52/NF-?B2 homodimers in nuclei, where it modulates NF-?B-regulated transcription in a context-dependent way. Bcl-3 has tumorigenic potential, is critical in host defense of pathogens, and has been reported to ameliorate or exacerbate inflammation, depending on disease model. However, cell-specific functions of Bcl-3 remain largely unknown. Here, we explored the role of Bcl-3 in a contact hypersensitivity (CHS) mouse model, which depends on the interplay between keratinocytes and immune cells. Bcl-3-deficient mice exhibited an exacerbated and prolonged CHS response to oxazolone. Increased inflammation correlated with higher production of chemokines CXCL2, CXCL9 and CXCL10, and consequently increased recruitment of neutrophils and CD8+ T cells. Bone marrow chimera experiments indicated that the ability of Bcl-3 to reduce the CHS response depended on Bcl-3 activity in radioresistant cells. Specific ablation of Bcl-3 in keratinocytes resulted in increased production of CXCL9 and CXCL10 and sustained recruitment of specifically CD8+ T cells. These findings identify Bcl-3 as a critical player during the later stage of the CHS reaction to limit inflammation via actions in radioresistant cells, including keratinocytes. äThe NF-?B regulator Bcl-3 modulates inflammation in contact hypersensi(epmc).pdf DeepDyve Pubget Overpricing