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10.1038/cddis.2014.233 http://scihub22266oqcxt.onion/10.1038/cddis.2014.233 C4047869!4047869 !24874739     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24874739 &cmd=llinks): Failed to open stream: HTTP request failed! 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Macropinocytosis and TAK1 mediate anti-inflammatory to pro-inflammatory macrophage differentiation by HIV-1 Nef |pdf=|usr=}}{{24874739 }} gab.com Text Macropinocytosis and TAK1 mediate anti-inflammatory to pro-inflammatory macrophage differentiation by HIV-1 Nef JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24874739 #FOAvip Macrophages (M?) are functionally classified into two types, anti-inflammatory M2 and pro-inflammatory M1. Importantly, we recently revealed that soluble HIV-1 proteins, particularly the pathogenetic protein Nef, preferentially activate M2-M? and drive them towards an M1-like M?, which might explain the sustained immune activation seen in HIV-1-infected patients. Here, we show that the preferential effect of Nef on M2-M? is mediated by TAK1 (TGF-?-activated kinase 1) and macropinocytosis. As with MAP kinases and NF-?B pathway, Nef markedly activated TAK1 in M-CSF-derived M2-M? but not in GM-CSF-derived M1-M?. Two Nef mutants, which were unable to activate MAP kinases and NF-?B pathway, failed to activate TAK1. Indeed, the TAK1 inhibitor 5Z-7-oxozeaenol as well as the ectopic expression of a dominant-negative mutant of TAK1 or TRAF2, an upstream molecule of TAK1, inhibited Nef-induced signaling activation and M1-like phenotypic differentiation of M2-M?. Meanwhile, the preferential effect of Nef on M2-M? correlated with the fact the Nef entered M2-M? more efficiently than M1-M?. Importantly, the macropinosome formation inhibitor EIPA completely blocked the internalization of Nef into M2-M?. Because the macropinocytosis activity of M2-M? was higher than that of M1-M?, our findings indicate that Nef enters M2-M? efficiently by exploiting their higher macropinocytosis activity and drives them towards M1-like M? by activating TAK1. Twit Text FOAVip Macropinocytosis and TAK1 mediate anti-inflammatory to pro-inflammatory macrophage differentiation by HIV-1 Nef ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24874739 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24874739 #FOAvip English Wikipedia <ref>{{Cite pmid|24874739 }}</ref> Macropinocytosis and TAK1 mediate anti-inflammatory to pro-inflammatory macrophage differentiation by HIV-1 Nef #MMPMID24874739 Hashimoto M ; Nasser H ; Chihara T ; Suzu S Cell Death Dis 2014[May]; 5 (5 ): e1267 PMID24874739 show ga Macrophages (M?) are functionally classified into two types, anti-inflammatory M2 and pro-inflammatory M1. Importantly, we recently revealed that soluble HIV-1 proteins, particularly the pathogenetic protein Nef, preferentially activate M2-M? and drive them towards an M1-like M?, which might explain the sustained immune activation seen in HIV-1-infected patients. Here, we show that the preferential effect of Nef on M2-M? is mediated by TAK1 (TGF-?-activated kinase 1) and macropinocytosis. As with MAP kinases and NF-?B pathway, Nef markedly activated TAK1 in M-CSF-derived M2-M? but not in GM-CSF-derived M1-M?. Two Nef mutants, which were unable to activate MAP kinases and NF-?B pathway, failed to activate TAK1. Indeed, the TAK1 inhibitor 5Z-7-oxozeaenol as well as the ectopic expression of a dominant-negative mutant of TAK1 or TRAF2, an upstream molecule of TAK1, inhibited Nef-induced signaling activation and M1-like phenotypic differentiation of M2-M?. Meanwhile, the preferential effect of Nef on M2-M? correlated with the fact the Nef entered M2-M? more efficiently than M1-M?. Importantly, the macropinosome formation inhibitor EIPA completely blocked the internalization of Nef into M2-M?. Because the macropinocytosis activity of M2-M? was higher than that of M1-M?, our findings indicate that Nef enters M2-M? efficiently by exploiting their higher macropinocytosis activity and drives them towards M1-like M? by activating TAK1. |*Cell Differentiation [MESH] |*Pinocytosis [MESH] |Animals [MESH] |Cell Line [MESH] |HIV-1/genetics/*metabolism [MESH] |Humans [MESH] |Inflammation/genetics/metabolism/pathology [MESH] |MAP Kinase Kinase Kinases/antagonists & inhibitors/genetics/*metabolism [MESH] |MAP Kinase Signaling System/drug effects/genetics [MESH] |Macrophages/*metabolism [MESH] |Mice [MESH] |Zearalenone/analogs & derivatives/pharmacology [MESH]Macropinocytosis and TAK1 mediate anti-inflammatory to pro-inflammator(epmc).pdf DeepDyve Pubget Overpricing