Pharmacological cyclin-dependent kinase inhibitors inhibit replication of wild-type and drug-resistant strains of herpes simplex virus and human immunodeficiency virus type 1 by targeting cellular, not viral, proteins
about
Explant-induced reactivation of herpes simplex virus occurs in neurons expressing nuclear cdk2 and cdk4Roscovitine inhibits activation of promoters in herpes simplex virus type 1 genomes independently of promoter-specific factorsTherapeutic targets for HIV-1 infection in the host proteome.Use of a multi-virus array for the study of human viral and retroviral pathogens: gene expression studies and ChIP-chip analysisRoscovitine in cancer and other diseasesCurrent and potential treatments for ubiquitous but neglected herpesvirus infectionsAntiviral activity of CYC202 in HIV-1-infected cellsNovel agents and strategies to treat herpes simplex virus infections.p42/p44 MAPKs are intracellular targets of the CDK inhibitor purvalanol.Site-specific regulation of histone H1 phosphorylation in pluripotent cell differentiationInhibition of human immunodeficiency virus type-1 by cdk inhibitorsTargeted therapy for Kaposi's sarcoma and Kaposi's sarcoma-associated herpesvirus.CDK9 inhibitor FIT-039 prevents replication of multiple DNA viruses.Accumulation of substrates of the anaphase-promoting complex (APC) during human cytomegalovirus infection is associated with the phosphorylation of Cdh1 and the dissociation and relocalization of APC subunits.Human cytomegalovirus infection induces specific hyperphosphorylation of the carboxyl-terminal domain of the large subunit of RNA polymerase II that is associated with changes in the abundance, activity, and localization of cdk9 and cdk7.ViralPhos: incorporating a recursively statistical method to predict phosphorylation sites on virus proteins.Inhibition of S-phase cyclin-dependent kinase activity blocks expression of Epstein-Barr virus immediate-early and early genes, preventing viral lytic replicationInhibition of post-transcriptional RNA processing by CDK inhibitors and its implication in anti-viral therapy.Phosphorylation of the VP16 transcriptional activator protein during herpes simplex virus infection and mutational analysis of putative phosphorylation sites.Development of new antivirals for herpesviruses.Inhibition of HIV-1 replication by P-TEFb inhibitors DRB, seliciclib and flavopiridol correlates with release of free P-TEFb from the large, inactive form of the complexIdentifying protein phosphorylation sites with kinase substrate specificity on human viruses.Cdk inhibitory nucleoside analogs prevent transcription from viral genomes.Inhibition of herpes simplex virus type 1 by the CDK6 inhibitor PD-0332991 (palbociclib) through the control of SAMHD1Geldanamycin, a ligand of heat shock protein 90, inhibits the replication of herpes simplex virus type 1 in vitro.Modulating Innate and Adaptive Immunity by (R)-Roscovitine: Potential Therapeutic Opportunity in Cystic Fibrosis.Five years of progress on cyclin-dependent kinases and other cellular proteins as potential targets for antiviral drugs.The differential requirement for cyclin-dependent kinase activities distinguishes two functions of herpes simplex virus type 1 ICP0.Identification of flavopiridol analogues that selectively inhibit positive transcription elongation factor (P-TEFb) and block HIV-1 replicationNovel HIV-1 therapeutics through targeting altered host cell pathways.Cyclin-dependent kinase activity is required at early times for accurate processing and accumulation of the human cytomegalovirus UL122-123 and UL37 immediate-early transcripts and at later times for virus production.Phosphorylation site mutations affect herpes simplex virus type 1 ICP0 function.Viral serine/threonine protein kinasesPotential of protein kinase inhibitors for treating herpesvirus-associated disease.Design and development of antivirals and intervention strategies against human herpesviruses using high-throughput approach.Herpes simplex virus type 1 induces nuclear accumulation of hyperphosphorylated tau in neuronal cells.Herpes simplex virus-type 2 infectivity and agents that block gap junctional intercellular communication.Varicella-zoster virus infection of human foreskin fibroblast cells results in atypical cyclin expression and cyclin-dependent kinase activity.Varicella-zoster virus IE63 protein phosphorylation by roscovitine-sensitive cyclin-dependent kinases modulates its cellular localization and activity.Roscovitine, a cyclin-dependent kinase inhibitor, prevents replication of varicella-zoster virus.
P2860
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P2860
Pharmacological cyclin-dependent kinase inhibitors inhibit replication of wild-type and drug-resistant strains of herpes simplex virus and human immunodeficiency virus type 1 by targeting cellular, not viral, proteins
description
2002 nî lūn-bûn
@nan
2002 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@ast
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@en
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@nl
type
label
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@ast
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@en
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@nl
prefLabel
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@ast
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@en
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@nl
P2093
P2860
P1433
P1476
Pharmacological cyclin-depende ...... cellular, not viral, proteins
@en
P2093
Andrew Bantly
Farida Shaheen
Laurent Meijer
Luis M Schang
Marie Knockaert
Nathanael S Gray
Priscilla A Schaffer
P2860
P304
P356
10.1128/JVI.76.15.7874-7882.2002
P407
P577
2002-08-01T00:00:00Z