Interferon-beta treatment of cervical keratinocytes naturally infected with human papillomavirus 16 episomes promotes rapid reduction in episome numbers and emergence of latent integrants.
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Inactivation of p53 rescues the maintenance of high risk HPV DNA genomes deficient in expression of E6Human papillomavirus type 16 E5 protein induces expression of beta interferon through interferon regulatory factor 1 in human keratinocytesInterferon-inducible protein, P56, inhibits HPV DNA replication by binding to the viral protein E1Evasion of host immune defenses by human papillomavirusHigh-risk human papillomavirus targets crossroads in immune signalingHigh-resolution genomic profiling of human papillomavirus-associated vulval neoplasia.In vitro progression of human papillomavirus 16 episome-associated cervical neoplasia displays fundamental similarities to integrant-associated carcinogenesis.Human papillomaviruses and the interferon responseImmune therapy for human papillomaviruses-related cancers.Viral carcinogenesis: factors inducing DNA damage and virus integrationVirus transcript levels and cell growth rates after naturally occurring HPV16 integration events in basal cervical keratinocytes.Oncogenic potential of Human Papillomavirus (HPV) and its relation with cervical cancer.Suppression of STAT-1 expression by human papillomaviruses is necessary for differentiation-dependent genome amplification and plasmid maintenance.Recent Insights into the Control of Human Papillomavirus (HPV) Genome Stability, Loss, and Degradation.Epithelial cell responses to infection with human papillomavirus.Interferon Kappa Inhibits Human Papillomavirus 31 Transcription by Inducing Sp100 ProteinsLack of correlation between predicted and actual off-target effects of short-interfering RNAs targeting the human papillomavirus type 16 E7 oncogene.Intrabody strategies for the treatment of human papillomavirus-associated disease.LIN28 Expression in malignant germ cell tumors downregulates let-7 and increases oncogene levelsHPV16 oncogene expression levels during early cervical carcinogenesis are determined by the balance of epigenetic chromatin modifications at the integrated virus genomeAPOBEC3 deaminases induce hypermutation in human papillomavirus 16 DNA upon beta interferon stimulation.Viral load, gene expression and mapping of viral integration sites in HPV16-associated HNSCC cell lines.Next-generation treatment strategies for human papillomavirus-related head and neck squamous cell carcinoma: where do we go?Overexpression of the oncostatin M receptor in cervical squamous cell carcinoma cells is associated with a pro-angiogenic phenotype and increased cell motility and invasiveness.Interferon Gamma Prevents Infectious Entry of Human Papillomavirus 16 via an L2-Dependent Mechanism.High-risk human papillomaviruses repress constitutive kappa interferon transcription via E6 to prevent pathogen recognition receptor and antiviral-gene expression.HPV Integration in Head and Neck Squamous Cell Carcinomas: Cause and Consequence.The human papillomavirus E7 oncoprotein as a regulator of transcription.Host cell restriction factors that limit transcription and replication of human papillomavirus.Depletion of HPV16 early genes induces autophagy and senescence in a cervical carcinogenesis model, regardless of viral physical state.Functional evidence that Drosha overexpression in cervical squamous cell carcinoma affects cell phenotype and microRNA profiles.Development of a cellular assay system to study the genome replication of high- and low-risk mucosal and cutaneous human papillomavirusesHuman papillomavirus episome stability is reduced by aphidicolin and controlled by DNA damage response pathways.Roles of APOBEC3A and APOBEC3B in Human Papillomavirus Infection and Disease Progression.Integration of Human Papillomavirus Genomes in Head and Neck Cancer: Is It Time to Consider a Paradigm Shift?The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Interferon treatment of human keratinocytes harboring extrachromosomal, persistent HPV-16 plasmid genomes induces de novo viral integration.Human papillomavirus E6 proteins mediate resistance to interferon-induced growth arrest through inhibition of p53 acetylation.The PxDLLCxE sequence in conserved region 2 of human papilloma virus 18 protein E7 is required for E7 binding to centromere protein C.Innate Antiviral Immunity in the Skin.
P2860
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P2860
Interferon-beta treatment of cervical keratinocytes naturally infected with human papillomavirus 16 episomes promotes rapid reduction in episome numbers and emergence of latent integrants.
description
2006 nî lūn-bûn
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2006年の論文
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2006年学术文章
@wuu
2006年学术文章
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2006年学术文章
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@zh-hans
2006年学术文章
@zh-my
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name
Interferon-beta treatment of c ...... mergence of latent integrants.
@en
Interferon-beta treatment of c ...... mergence of latent integrants.
@nl
type
label
Interferon-beta treatment of c ...... mergence of latent integrants.
@en
Interferon-beta treatment of c ...... mergence of latent integrants.
@nl
prefLabel
Interferon-beta treatment of c ...... mergence of latent integrants.
@en
Interferon-beta treatment of c ...... mergence of latent integrants.
@nl
P2093
P356
P1433
P1476
Interferon-beta treatment of c ...... mergence of latent integrants.
@en
P2093
Andrew E Teschendorff
Ian Roberts
M Trent Herdman
Margaret A Stanley
Mark R Pett
Nicholas Coleman
William O F Alazawi
Xiao-Yin Zhang
P304
P356
10.1093/CARCIN/BGL172
P407
P577
2006-09-14T00:00:00Z