Human cytomegalovirus protein pUL38 induces ATF4 expression, inhibits persistent JNK phosphorylation, and suppresses endoplasmic reticulum stress-induced cell death.
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Adapting the Stress Response: Viral Subversion of the mTOR Signaling PathwayInflammatory and oxidative stress in rotavirus infectionHuman Cytomegalovirus Strategies to Maintain and Promote mRNA TranslationViruses and autophagyModulation of the Translational Landscape During Herpesvirus InfectionHuman cytomegalovirus UL29/28 protein interacts with components of the NuRD complex which promote accumulation of immediate-early RNAA novel immunity system for bacterial nucleic acid degrading toxins and its recruitment in various eukaryotic and DNA viral systems.Human cytomegalovirus protein pUL117 targets the mini-chromosome maintenance complex and suppresses cellular DNA synthesis.Human cytomegalovirus gene UL21a encodes a short-lived cytoplasmic protein and facilitates virus replication in fibroblastsHuman Herpesvirus 6A Exhibits Restrictive Propagation with Limited Activation of the Protein Kinase R-eIF2α Stress Pathway.Human cytomegalovirus inhibits apoptosis by regulating the activating transcription factor 5 signaling pathway in human malignant glioma cells.Severe acute respiratory syndrome coronavirus envelope protein regulates cell stress response and apoptosis.Conserved host response to highly pathogenic avian influenza virus infection in human cell culture, mouse and macaque model systems.Negative regulation of IRF7 activation by activating transcription factor 4 suggests a cross-regulation between the IFN responses and the cellular integrated stress responses.PKR-like endoplasmic reticulum kinase is necessary for lipogenic activation during HCMV infection.Cytomegalovirus downregulates IRE1 to repress the unfolded protein response.Viral effects on metabolism: changes in glucose and glutamine utilization during human cytomegalovirus infection.Human cytomegalovirus exploits interferon-induced transmembrane proteins to facilitate morphogenesis of the virion assembly compartment.The human cytomegalovirus protein pUL38 suppresses endoplasmic reticulum stress-mediated cell death independently of its ability to induce mTORC1 activation.Co-Transcriptomes of Initial Interactions In Vitro between Streptococcus Pneumoniae and Human Pleural Mesothelial Cells.Tuberous Sclerosis Complex Protein 2-Independent Activation of mTORC1 by Human Cytomegalovirus pUL38.Poly(A) binding protein abundance regulates eukaryotic translation initiation factor 4F assembly in human cytomegalovirus-infected cells.Murine cytomegalovirus targets transcription factor ATF4 to exploit the unfolded-protein responseHuman cytomegalovirus pUL29/28 and pUL38 repression of p53-regulated p21CIP1 and caspase 1 promoters during infection.An intein-mediated modulation of protein stability system and its application to study human cytomegalovirus essential gene function.Activation status of integrated stress response pathways in neurones and astrocytes of HIV-associated neurocognitive disorders (HAND) cortex.Murine cytomegalovirus protein pM79 is a key regulator for viral late transcriptionThe endoplasmic reticulum chaperone BiP/GRP78 is important in the structure and function of the human cytomegalovirus assembly compartment.Deletion of the human cytomegalovirus US17 gene increases the ratio of genomes per infectious unit and alters regulation of immune and endoplasmic reticulum stress response genes at early and late times after infection.Identification of cellular proteins that interact with human cytomegalovirus immediate-early protein 1 by protein array assay.Live or let die: manipulation of cellular suicide programs by murine cytomegalovirus.Prevention of cellular suicide by cytomegaloviruses.Functional annotation of human cytomegalovirus gene products: an update.The expanding roles of endoplasmic reticulum stress in virus replication and pathogenesis.Human cytomegalovirus infection maintains mTOR activity and its perinuclear localization during amino acid deprivation.Activating transcription factor 4 underlies the pathogenesis of arsenic trioxide-mediated impairment of macrophage innate immune functions.Human cytomegalovirus induces multiple means to combat reactive oxygen species.Rotavirus infection induces the unfolded protein response of the cell and controls it through the nonstructural protein NSP3ATF4 is directly recruited by TLR4 signaling and positively regulates TLR4-trigged cytokine production in human monocytes.Human leptin protein induces proliferation of A549 cells via inhibition of PKR-like ER kinase and activating transcription factor-6 mediated apoptosis.
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Human cytomegalovirus protein pUL38 induces ATF4 expression, inhibits persistent JNK phosphorylation, and suppresses endoplasmic reticulum stress-induced cell death.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 04 February 2009
@en
vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Human cytomegalovirus protein ...... lum stress-induced cell death.
@en
Human cytomegalovirus protein ...... lum stress-induced cell death.
@nl
type
label
Human cytomegalovirus protein ...... lum stress-induced cell death.
@en
Human cytomegalovirus protein ...... lum stress-induced cell death.
@nl
prefLabel
Human cytomegalovirus protein ...... lum stress-induced cell death.
@en
Human cytomegalovirus protein ...... lum stress-induced cell death.
@nl
P2093
P2860
P921
P356
P1433
P1476
Human cytomegalovirus protein ...... lum stress-induced cell death.
@en
P2093
Baoqin Xuan
Emi Torigoi
Zhikang Qian
P2860
P304
P356
10.1128/JVI.02307-08
P407
P577
2009-02-04T00:00:00Z