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10.1016/j.celrep.2015.09.048 http://scihub22266oqcxt.onion/10.1016/j.celrep.2015.09.048 C4916766!4916766!26565900     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2015 ; 13 (5): 874-83 Nephropedia Template TP {{tp|p=26565900|t=2015. A Role for IFITM Proteins in Restriction of Mycobacterium tuberculosis Infection |pdf=|usr=}}{{26565900}} gab.com Text A Role for IFITM Proteins in Restriction of Mycobacterium tuberculosis Infection JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26565900 #FOAvip The interferon (IFN)-induced transmembrane (IFITM) proteins are critical mediators of the host antiviral response. Here, we expand the role of IFITM proteins to host defense against intracellular bacterial infection by demonstrating that they restrict Mycobacterium tuberculosis (MTb) intracellular growth. Simultaneous knockdown of IFITM1, IFITM2, and IFITM3 by RNAi significantly enhances MTb growth in human monocytic and alveolar/epithelial cells, whereas individual overexpression of each IFITM impairs MTb growth in these cell types. Furthermore, MTb infection, Toll-like receptor 2 and 4 ligands, and several proinflammatory cytokines induce IFITM1?3 gene expression in human myeloid cells. We find that IFITM3 co-localizes with early and, in particular, late MTb phagosomes, and overexpression of IFITM3 enhances endosomal acidification in MTb-infected monocytic cells. These findings provide evidence that the antiviral IFITMs participate in the restriction of mycobacterial growth, and they implicate IFITM-mediated endosomal maturation in its antimycobacterial activity. Twit Text FOAVip A Role for IFITM Proteins in Restriction of Mycobacterium tuberculosis Infection ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26565900 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26565900 #FOAvip English Wikipedia <ref>{{Cite pmid|26565900}}</ref> A Role for IFITM Proteins in Restriction of Mycobacterium tuberculosis Infection #MMPMID26565900 Ranjbar S; Haridas V; Jasenosky LD; Falvo JV; Goldfeld AE Cell Rep 2015[Nov]; 13 (5): 874-83 PMID26565900show ga The interferon (IFN)-induced transmembrane (IFITM) proteins are critical mediators of the host antiviral response. Here, we expand the role of IFITM proteins to host defense against intracellular bacterial infection by demonstrating that they restrict Mycobacterium tuberculosis (MTb) intracellular growth. Simultaneous knockdown of IFITM1, IFITM2, and IFITM3 by RNAi significantly enhances MTb growth in human monocytic and alveolar/epithelial cells, whereas individual overexpression of each IFITM impairs MTb growth in these cell types. Furthermore, MTb infection, Toll-like receptor 2 and 4 ligands, and several proinflammatory cytokines induce IFITM1?3 gene expression in human myeloid cells. We find that IFITM3 co-localizes with early and, in particular, late MTb phagosomes, and overexpression of IFITM3 enhances endosomal acidification in MTb-infected monocytic cells. These findings provide evidence that the antiviral IFITMs participate in the restriction of mycobacterial growth, and they implicate IFITM-mediated endosomal maturation in its antimycobacterial activity. äA Role for IFITM Proteins in Restriction of Mycobacterium tuberculosis(epmc).pdf DeepDyve Pubget Overpricing