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Ryuichi Sugiyama - One of the best experts on this subject based on the ideXlab platform.
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induction of heAt shock protein 70 by ProstAglAndin A1 inhibits hiv 1 vif mediAted degrAdAtion of Apobec3g
Antiviral Research, 2013Co-Authors: Ryuichi Sugiyama, Makoto Abe, Hironori Nishitsuji, Yuko Murakami, Hiroaki Takeuchi, Hiroshi TakakuAbstract:AbstrAct Previous studies hAve demonstrAted thAt cyclopentenone ProstAglAndins (cyPGs) inhibit humAn immunodeficiency virus type 1 (HIV-1) replicAtion in vArious cell types. This AntivirAl Activity hAs been AssociAted with the induction of heAt-shock protein 70 (HSP70) in infected cells. We investigAted A new role of ProstAglAndin A 1 (PGA 1 ) in the replicAtion of HIV-1 in non-permissive cells. BecAuse overexpression of HSP70 blocks the virAl infectivity fActor (Vif)-mediAted degrAdAtion of APOBEC3G (A3G) viA the ubiquitin–proteAsome pAthwAy, we exAmined the effects of PGA 1 on A3G And HIV-1 replicAtion. The induction of HSP70 synthesis by PGA 1 blocked Vif-mediAted A3G degrAdAtion And enhAnced the incorporAtion of A3G into both wild-type And Vif-deficient viruses. Furthermore, we determined the virAl titer of HIV-1 pArticles produced from PGA 1 -treAted 293T cells. The induction of HSP70 synthesis by PGA 1 significAntly reduced the virAl titer in the presence of A3G. AdditionAlly, the p24 GAg Antigen levels were drAmAticAlly reduced in non-permissive cells treAted once or repeAtedly with PGA 1 . Thus, we showed thAt PGA 1 inhibits HIV-1 replicAtion, At leAst in pArt, by blocking Vif-mediAted A3G degrAdAtion.
Hiroshi Takaku - One of the best experts on this subject based on the ideXlab platform.
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induction of heAt shock protein 70 by ProstAglAndin A1 inhibits hiv 1 vif mediAted degrAdAtion of Apobec3g
Antiviral Research, 2013Co-Authors: Ryuichi Sugiyama, Makoto Abe, Hironori Nishitsuji, Yuko Murakami, Hiroaki Takeuchi, Hiroshi TakakuAbstract:AbstrAct Previous studies hAve demonstrAted thAt cyclopentenone ProstAglAndins (cyPGs) inhibit humAn immunodeficiency virus type 1 (HIV-1) replicAtion in vArious cell types. This AntivirAl Activity hAs been AssociAted with the induction of heAt-shock protein 70 (HSP70) in infected cells. We investigAted A new role of ProstAglAndin A 1 (PGA 1 ) in the replicAtion of HIV-1 in non-permissive cells. BecAuse overexpression of HSP70 blocks the virAl infectivity fActor (Vif)-mediAted degrAdAtion of APOBEC3G (A3G) viA the ubiquitin–proteAsome pAthwAy, we exAmined the effects of PGA 1 on A3G And HIV-1 replicAtion. The induction of HSP70 synthesis by PGA 1 blocked Vif-mediAted A3G degrAdAtion And enhAnced the incorporAtion of A3G into both wild-type And Vif-deficient viruses. Furthermore, we determined the virAl titer of HIV-1 pArticles produced from PGA 1 -treAted 293T cells. The induction of HSP70 synthesis by PGA 1 significAntly reduced the virAl titer in the presence of A3G. AdditionAlly, the p24 GAg Antigen levels were drAmAticAlly reduced in non-permissive cells treAted once or repeAtedly with PGA 1 . Thus, we showed thAt PGA 1 inhibits HIV-1 replicAtion, At leAst in pArt, by blocking Vif-mediAted A3G degrAdAtion.
Undurti N Das - One of the best experts on this subject based on the ideXlab platform.
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ArAchidonic Acid And other unsAturAted fAtty Acids And some of their metAbolites function As endogenous AntimicrobiAl molecules A review
Journal of Advanced Research, 2018Co-Authors: Undurti N DasAbstract:Our body is endowed with severAl endogenous Anti-microbiAl compounds such As interferon, cytokines, free rAdicAls, etc. However, little Attention hAs been pAid to the possibility thAt lipids could function As AntimicrobiAl compounds. In this short review, the AntimicrobiAl Actions of vArious polyunsAturAted fAtty Acids (PUFAs, mAinly free Acids) And their putAtive mechAnisms of Action Are described. In generAl, PUFAs kill microbes by their direct Action on microbiAl cell membrAnes, enhAncing generAtion of free rAdicAls, Augmenting the formAtion of lipid peroxides thAt Are cytotoxic, And by increAsing the formAtion of their bioActive metAbolites, such As ProstAglAndins, lipoxins, resolvins, protectins And mAresins thAt enhAnce the phAgocytic Action of leukocytes And mAcrophAges. Higher intAkes of α-linolenic And cis-linoleic Acids (ALA And LA respectively) And fish (A rich source of eicosApentAenoic Acid And docosAhexAenoic Acid) might reduce the risk pneumoniA. Previously, it wAs suggested thAt polyunsAturAted fAtty Acids (PUFAs): linoleic, α-linolenic, γ-linolenic (GLA), dihomo-GLA (DGLA), ArAchidonic (AA), eicosApentAenoic (EPA), And docosAhexAenoic Acids (DHA) function As endogenous Anti-bActeriAl, Anti-fungAl, Anti-virAl, Anti-pArAsitic, And immunomodulAting Agents. A vAriety of bActeriA Are sensitive to the growth inhibitory Actions of LA And ALA in vitro. Hydrolyzed linseed oil cAn kill methicillin-resistAnt StAphylococcus Aureus. Both LA And AA hAve the Ability to inActivAte herpes, influenzA, SendAi, And Sindbis virus within minutes of contAct. AA, EPA, And DHA induce deAth of PlAsmodium fAlcipArum both in vitro And in vivo. ProstAglAndin E1 (PGE1) And ProstAglAndin A (PGA), derived from DGLA, AA, And EPA inhibit virAl replicAtion And show Anti-virAl Activity. OrAl mucosA, epidermAl cells, lymphocytes And mAcrophAges contAin And releAse significAnt Amounts of PUFAs on stimulAtion. PUFAs stimulAte NADPH-dependent superoxide production by mAcrophAges, neutrophils And lymphocytes to kill the invAding microorgAnisms. Cytokines induce the releAse of PUFAs from cell membrAne lipid pool, A potentiAl mechAnism for their AntimicrobiAl Action. AA, EPA, And DHA give rise to lipoxins (LXs), resolvins, protectins, And mAresins thAt limit And resolve inflAmmAtion And hAve AntimicrobiAl Actions. Thus, PUFAs And their metAbolites hAve broAd AntimicrobiAl Actions.
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ArAchidonic Acid And other unsAturAted fAtty Acids And some of their metAbolites function As endogenous AntimicrobiAl molecules: A review
Elsevier, 2018Co-Authors: Undurti N DasAbstract:Our body is endowed with severAl endogenous Anti-microbiAl compounds such As interferon, cytokines, free rAdicAls, etc. However, little Attention hAs been pAid to the possibility thAt lipids could function As AntimicrobiAl compounds. In this short review, the AntimicrobiAl Actions of vArious polyunsAturAted fAtty Acids (PUFAs, mAinly free Acids) And their putAtive mechAnisms of Action Are described. In generAl, PUFAs kill microbes by their direct Action on microbiAl cell membrAnes, enhAncing generAtion of free rAdicAls, Augmenting the formAtion of lipid peroxides thAt Are cytotoxic, And by increAsing the formAtion of their bioActive metAbolites, such As ProstAglAndins, lipoxins, resolvins, protectins And mAresins thAt enhAnce the phAgocytic Action of leukocytes And mAcrophAges. Higher intAkes of α-linolenic And cis-linoleic Acids (ALA And LA respectively) And fish (A rich source of eicosApentAenoic Acid And docosAhexAenoic Acid) might reduce the risk pneumoniA. Previously, it wAs suggested thAt polyunsAturAted fAtty Acids (PUFAs): linoleic, α-linolenic, γ-linolenic (GLA), dihomo-GLA (DGLA), ArAchidonic (AA), eicosApentAenoic (EPA), And docosAhexAenoic Acids (DHA) function As endogenous Anti-bActeriAl, Anti-fungAl, Anti-virAl, Anti-pArAsitic, And immunomodulAting Agents. A vAriety of bActeriA Are sensitive to the growth inhibitory Actions of LA And ALA in vitro. Hydrolyzed linseed oil cAn kill methicillin-resistAnt StAphylococcus Aureus. Both LA And AA hAve the Ability to inActivAte herpes, influenzA, SendAi, And Sindbis virus within minutes of contAct. AA, EPA, And DHA induce deAth of PlAsmodium fAlcipArum both in vitro And in vivo. ProstAglAndin E1 (PGE1) And ProstAglAndin A (PGA), derived from DGLA, AA, And EPA inhibit virAl replicAtion And show Anti-virAl Activity. OrAl mucosA, epidermAl cells, lymphocytes And mAcrophAges contAin And releAse significAnt Amounts of PUFAs on stimulAtion. PUFAs stimulAte NADPH-dependent superoxide production by mAcrophAges, neutrophils And lymphocytes to kill the invAding microorgAnisms. Cytokines induce the releAse of PUFAs from cell membrAne lipid pool, A potentiAl mechAnism for their AntimicrobiAl Action. AA, EPA, And DHA give rise to lipoxins (LXs), resolvins, protectins, And mAresins thAt limit And resolve inflAmmAtion And hAve AntimicrobiAl Actions. Thus, PUFAs And their metAbolites hAve broAd AntimicrobiAl Actions. Keywords: UnsAturAted fAtty Acids, MicrobicidAl, Free rAdicAls, ProstAglAndins, Lipoxin A4, Cytokine
Makoto Abe - One of the best experts on this subject based on the ideXlab platform.
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induction of heAt shock protein 70 by ProstAglAndin A1 inhibits hiv 1 vif mediAted degrAdAtion of Apobec3g
Antiviral Research, 2013Co-Authors: Ryuichi Sugiyama, Makoto Abe, Hironori Nishitsuji, Yuko Murakami, Hiroaki Takeuchi, Hiroshi TakakuAbstract:AbstrAct Previous studies hAve demonstrAted thAt cyclopentenone ProstAglAndins (cyPGs) inhibit humAn immunodeficiency virus type 1 (HIV-1) replicAtion in vArious cell types. This AntivirAl Activity hAs been AssociAted with the induction of heAt-shock protein 70 (HSP70) in infected cells. We investigAted A new role of ProstAglAndin A 1 (PGA 1 ) in the replicAtion of HIV-1 in non-permissive cells. BecAuse overexpression of HSP70 blocks the virAl infectivity fActor (Vif)-mediAted degrAdAtion of APOBEC3G (A3G) viA the ubiquitin–proteAsome pAthwAy, we exAmined the effects of PGA 1 on A3G And HIV-1 replicAtion. The induction of HSP70 synthesis by PGA 1 blocked Vif-mediAted A3G degrAdAtion And enhAnced the incorporAtion of A3G into both wild-type And Vif-deficient viruses. Furthermore, we determined the virAl titer of HIV-1 pArticles produced from PGA 1 -treAted 293T cells. The induction of HSP70 synthesis by PGA 1 significAntly reduced the virAl titer in the presence of A3G. AdditionAlly, the p24 GAg Antigen levels were drAmAticAlly reduced in non-permissive cells treAted once or repeAtedly with PGA 1 . Thus, we showed thAt PGA 1 inhibits HIV-1 replicAtion, At leAst in pArt, by blocking Vif-mediAted A3G degrAdAtion.
Hironori Nishitsuji - One of the best experts on this subject based on the ideXlab platform.
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induction of heAt shock protein 70 by ProstAglAndin A1 inhibits hiv 1 vif mediAted degrAdAtion of Apobec3g
Antiviral Research, 2013Co-Authors: Ryuichi Sugiyama, Makoto Abe, Hironori Nishitsuji, Yuko Murakami, Hiroaki Takeuchi, Hiroshi TakakuAbstract:AbstrAct Previous studies hAve demonstrAted thAt cyclopentenone ProstAglAndins (cyPGs) inhibit humAn immunodeficiency virus type 1 (HIV-1) replicAtion in vArious cell types. This AntivirAl Activity hAs been AssociAted with the induction of heAt-shock protein 70 (HSP70) in infected cells. We investigAted A new role of ProstAglAndin A 1 (PGA 1 ) in the replicAtion of HIV-1 in non-permissive cells. BecAuse overexpression of HSP70 blocks the virAl infectivity fActor (Vif)-mediAted degrAdAtion of APOBEC3G (A3G) viA the ubiquitin–proteAsome pAthwAy, we exAmined the effects of PGA 1 on A3G And HIV-1 replicAtion. The induction of HSP70 synthesis by PGA 1 blocked Vif-mediAted A3G degrAdAtion And enhAnced the incorporAtion of A3G into both wild-type And Vif-deficient viruses. Furthermore, we determined the virAl titer of HIV-1 pArticles produced from PGA 1 -treAted 293T cells. The induction of HSP70 synthesis by PGA 1 significAntly reduced the virAl titer in the presence of A3G. AdditionAlly, the p24 GAg Antigen levels were drAmAticAlly reduced in non-permissive cells treAted once or repeAtedly with PGA 1 . Thus, we showed thAt PGA 1 inhibits HIV-1 replicAtion, At leAst in pArt, by blocking Vif-mediAted A3G degrAdAtion.
