Herpes simplex virus infection selectively stimulates accumulation of beta interferon reporter gene mRNA by a posttranscriptional mechanism.
about
UL54-null pseudorabies virus is attenuated in mice but productively infects cells in cultureMapping of functional regions in the amino-terminal portion of the herpes simplex virus ICP27 regulatory protein: importance of the leucine-rich nuclear export signal and RGG Box RNA-binding domain.Evaluation of colocalization interactions between the IE110, IE175, and IE63 transactivator proteins of herpes simplex virus within subcellular punctate structuresAn activity specified by the osteosarcoma line U2OS can substitute functionally for ICP0, a major regulatory protein of herpes simplex virus type 1Herpes simplex virus trans-regulatory protein ICP27 stabilizes and binds to 3' ends of labile mRNA.The herpes simplex virus type 1 regulatory protein ICP27 coimmunoprecipitates with anti-Sm antiserum, and the C terminus appears to be required for this interactionCooperation between herpes simplex virus type 1-encoded ICP0 and Tat to support transcription of human immunodeficiency virus type 1 long terminal repeat in vivo can occur in the absence of the TAR binding site.Post-transcriptional control of the interferon system.Primary activation of interferon A and interferon B gene transcription by interferon regulatory factor 3The herpes simplex virus regulatory protein ICP27 contributes to the decrease in cellular mRNA levels during infection.Varicella-zoster virus open reading frame 4 encodes a transcriptional activator that is functionally distinct from that of herpes simplex virus homology ICP27.Physical interaction between the herpes simplex virus type 1 immediate-early regulatory proteins ICP0 and ICP4.Identification of a large bent DNA domain and binding sites for serum response factor adjacent to the NFI repeat cluster and enhancer region in the major IE94 promoter from simian cytomegalovirus.A major transactivator of varicella-zoster virus, the immediate-early protein IE62, contains a potent N-terminal activation domain.The role of herpes simplex virus ICP27 in the regulation of UL24 gene expression by differential polyadenylationTransactivation of a viral target gene by herpes simplex virus ICP27 is posttranscriptional and does not require the endogenous promoter or polyadenylation site.Mutually exclusive binding of two cellular factors within a critical promoter region of the gene for the IE110k protein of herpes simplex virus.Herpes simplex virus-1 infection causes the secretion of a type I interferon-antagonizing protein and inhibits signaling at or before Jak-1 activation.
P2860
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P2860
Herpes simplex virus infection selectively stimulates accumulation of beta interferon reporter gene mRNA by a posttranscriptional mechanism.
description
1992 nî lūn-bûn
@nan
1992年の論文
@ja
1992年論文
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1992年論文
@zh-hant
1992年論文
@zh-hk
1992年論文
@zh-mo
1992年論文
@zh-tw
1992年论文
@wuu
1992年论文
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1992年论文
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name
Herpes simplex virus infection ...... posttranscriptional mechanism.
@ast
Herpes simplex virus infection ...... posttranscriptional mechanism.
@en
type
label
Herpes simplex virus infection ...... posttranscriptional mechanism.
@ast
Herpes simplex virus infection ...... posttranscriptional mechanism.
@en
prefLabel
Herpes simplex virus infection ...... posttranscriptional mechanism.
@ast
Herpes simplex virus infection ...... posttranscriptional mechanism.
@en
P2093
P2860
P1433
P1476
Herpes simplex virus infection ...... posttranscriptional mechanism.
@en
P2093
P2860
P304
P407
P577
1992-06-01T00:00:00Z