Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1096/fj.02-0508fje http://scihub22266oqcxt.onion/10.1096/fj.02-0508fje 12594179!ä!12594179 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 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       FASEB+J 2003 ; 17 (6): 758-60 Nephropedia Template TP {{tp|p=12594179|t=2003. Influenza A virus replication is dependent on an antioxidant pathway that involves GSH and Bcl-2 |pdf=|usr=}}{{12594179}} gab.com Text Influenza A virus replication is dependent on an antioxidant pathway that involves GSH and Bcl-2 JO: FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=12594179 #FOAvip Growing evidence indicates that viral replication is regulated by the redox state of the host cell. We demonstrate that cells of different origins display differential permissivity for influenza A virus replication, depending on their intracellular redox power as reflected by Bcl-2 expression and glutathione (GSH) content. Bcl-2 expressing cells were found to have higher intracellular levels of GSH and to produce lower amounts of virus than Bcl-2 negative cells. Two different steps in the virus life-cycle were involved in Bcl-2/GSH mediated viral inhibition: 1) expression of late viral proteins (in particular hemagglutinin and matrix); and 2) nuclear-cytoplasmic translocation of viral ribonucleoproteins (vRNPs). Buthionine-sulfoximine-induced inhibition of GSH synthesis in Bcl-2 expressing cells caused an increase in the expression of late viral proteins but did not restore vRNP export to the cytoplasm. Collectively, our findings show that both Bcl-2 expression and GSH content contribute to the host cell's ability to down-regulate influenza virus replication, although their effects are exerted at different stages of the viral life-cycle. In certain cell populations, this form of down-regulation might conceivably favor the establishment of persistent viral infection. Twit Text FOAVip Influenza A virus replication is dependent on an antioxidant pathway that involves GSH and Bcl-2 ????FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=12594179 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=12594179 #FOAvip English Wikipedia <ref>{{Cite pmid|12594179}}</ref> Influenza A virus replication is dependent on an antioxidant pathway that involves GSH and Bcl-2 #MMPMID12594179 Nencioni L; Iuvara A; Aquilano K; Ciriolo MR; Cozzolino F; Rotilio G; Garaci E; Palamara AT FASEB J 2003[Apr]; 17 (6): 758-60 PMID12594179show ga Growing evidence indicates that viral replication is regulated by the redox state of the host cell. We demonstrate that cells of different origins display differential permissivity for influenza A virus replication, depending on their intracellular redox power as reflected by Bcl-2 expression and glutathione (GSH) content. Bcl-2 expressing cells were found to have higher intracellular levels of GSH and to produce lower amounts of virus than Bcl-2 negative cells. Two different steps in the virus life-cycle were involved in Bcl-2/GSH mediated viral inhibition: 1) expression of late viral proteins (in particular hemagglutinin and matrix); and 2) nuclear-cytoplasmic translocation of viral ribonucleoproteins (vRNPs). Buthionine-sulfoximine-induced inhibition of GSH synthesis in Bcl-2 expressing cells caused an increase in the expression of late viral proteins but did not restore vRNP export to the cytoplasm. Collectively, our findings show that both Bcl-2 expression and GSH content contribute to the host cell's ability to down-regulate influenza virus replication, although their effects are exerted at different stages of the viral life-cycle. In certain cell populations, this form of down-regulation might conceivably favor the establishment of persistent viral infection. |*Virus Replication[MESH] |Animals[MESH] |Antioxidants/*metabolism[MESH] |Blotting, Western[MESH] |Cell Line[MESH] |Glutathione/*metabolism[MESH] |Humans[MESH] |Influenza A virus/*growth & development[MESH] |Proto-Oncogene Proteins c-bcl-2/*biosynthesis[MESH] |Tumor Cells, Cultured[MESH] |U937 Cells[MESH]Influenza A virus replication is dependent on an antioxidant pathway t(epmc).pdf DeepDyve Pubget Overpricing