Resistance of mRNA translation to acute endoplasmic reticulum stress-inducing agents in herpes simplex virus type 1-infected cells requires multiple virus-encoded functions. (Q35023672)

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English	Resistance of mRNA translation to acute endoplasmic reticulum stress-inducing agents in herpes simplex virus type 1-infected cells requires multiple virus-encoded functions.	scientific article

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27 December 2019

Resistance of mRNA translation to acute endoplasmic reticulum stress-inducing agents in herpes simplex virus type 1-infected cells requires multiple virus-encoded functions (English)

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27 December 2019

endoplasmic reticulum

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2

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Matthew Mulvey

1

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Ian Mohr

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1 August 2006

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27 December 2019

Journal of Virology

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27 December 2019

7354-7363

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27 December 2019

Reovirus induces and benefits from an integrated cellular stress response

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Phosphorylation and dephosphorylation events that regulate viral mRNA translation

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mRNA decay during herpes simplex virus (HSV) infections: protein-protein interactions involving the HSV virion host shutoff protein and translation factors eIF4H and eIF4A.

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Herpes simplex virus 1 infection activates the endoplasmic reticulum resident kinase PERK and mediates eIF-2alpha dephosphorylation by the gamma(1)34.5 protein

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Herpes simplex virus virion host shutoff protein is stimulated by translation initiation factors eIF4B and eIF4H

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Regulation of eIF2alpha phosphorylation by different functions that act during discrete phases in the herpes simplex virus type 1 life cycle

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Protein synthesis and endoplasmic reticulum stress can be modulated by the hepatitis C virus envelope protein E2 through the eukaryotic initiation factor 2alpha kinase PERK

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Control of PERK eIF2alpha kinase activity by the endoplasmic reticulum stress-induced molecular chaperone P58IPK.

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Replication of a cytopathic strain of bovine viral diarrhea virus activates PERK and induces endoplasmic reticulum stress-mediated apoptosis of MDBK cells

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Herpes simplex virus type 1 evades the effects of antibody and complement in vivo

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mRNA degradation by the virion host shutoff (Vhs) protein of herpes simplex virus: genetic and biochemical evidence that Vhs is a nuclease

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Transcriptional and translational control in the Mammalian unfolded protein response

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Hepatitis C virus subgenomic replicons induce endoplasmic reticulum stress activating an intracellular signaling pathway

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Japanese encephalitis virus infection initiates endoplasmic reticulum stress and an unfolded protein response

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mRNA decay during herpesvirus infections: interaction between a putative viral nuclease and a cellular translation factor

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Feedback inhibition of the unfolded protein response by GADD34-mediated dephosphorylation of eIF2alpha

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Pancreatic eukaryotic initiation factor-2alpha kinase (PEK) homologues in humans, Drosophila melanogaster and Caenorhabditis elegans that mediate translational control in response to endoplasmic reticulum stress

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1 reference

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1 reference

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The molecular chaperone hsp40 regulates the activity of P58IPK, the cellular inhibitor of PKR.

1 reference

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Calnexin associates with the precursors of glycoproteins B, C, and D of herpes simplex virus type 1.

1 reference

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A herpesvirus genetic element which affects translation in the absence of the viral GADD34 function

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1 reference

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1 reference

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Identifiers

10.1128/JVI.00479-06

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27 December 2019

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27 December 2019

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27 December 2019

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