Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway.

Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway. Research Abstract Details 

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Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway. Abstract Text:

Kahori Minami,Yukihiro Tambe,Ryosuke Watanabe,Takahiro Isono,Masataka Haneda,Ken-Ichi Isobe,Toshiyuki Kobayashi,Okio Hino,Hidetoshi Okabe,Tokuhiro Chano,Hirokazu Inoue,Kahori Minami,Yukihiro Tambe,Ryosuke Watanabe,Takahiro Isono,Masataka Haneda,Ken-Ichi Isobe,Toshiyuki Kobayashi,Okio Hino,Hidetoshi Okabe,Tokuhiro Chano,Hirokazu Inoue,

GADD34 is a protein that is induced by a variety of stressors, including DNA damage, heat shock, nutrient deprivation, energy depletion, and endoplasmic reticulum stress. Here, we demonstrated that GADD34 induced by vesicular stomatitis virus (VSV) infection suppressed viral replication in wild-type (WT) mouse embryo fibroblasts (MEFs), whereas replication was enhanced in GADD34-deficient (GADD34-KO) MEFs. Enhanced viral replication in GADD34-KO MEFs was reduced by retroviral gene rescue of GADD34. The level of VSV protein expression in GADD34-KO MEFs was significantly higher than that in WT MEFs. Neither phosphorylation of eIF2alpha nor cellular protein synthesis was correlated with viral replication in GADD34-KO MEFs. On the other hand, phosphorylation of S6 and 4EBP1, proteins downstream of mTOR, was suppressed by VSV infection in WT MEFs but not in GADD34-KO MEFs. GADD34 was able to associate with TSC1/2 and dephosphorylate TSC2 at Thr1462. VSV replication was higher in TSC2-null cells than in TSC2-expressing cells, and constitutively active Akt enhanced VSV replication. On the other hand, rapamycin, an mTOR inhibitor, significantly suppressed VSV replication in GADD34-KO MEFs. These findings demonstrate that GADD34 induced by VSV infection suppresses viral replication via mTOR pathway inhibition, indicating that cross talk between stress-inducible GADD34 and the mTOR signaling pathway plays a critical role in antiviral defense.

Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway. Publishing Authors By Initials

K Minami,Y Tambe,R Watanabe,T Isono,M Haneda,K Isobe,T Kobayashi,O Hino,H Okabe,T Chano,H Inoue,K Minami,Y Tambe,R Watanabe,T Isono,M Haneda,K Isobe,T Kobayashi,O Hino,H Okabe,T Chano,H Inoue,

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Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of virology

VOLUME: 81

Page Numbers: 11106-15

Journal Abbreviation: J. Virol.

ISSN: 0022-538X

DAY: 1

MONTH: 08

YEAR: 2007

Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway. Information

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LANGUAGE: eng

NlmUniqueID: 113724

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Grant and Affiliation Information for Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway.

AFFILIATION: Department of Microbiology, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.

Country: United States

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MEDLINETA: J Virol

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