The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle.
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Centrosome dysfunction contributes to chromosome instability, chromoanagenesis, and genome reprograming in cancerWhen the genome plays dice: circumvention of the spindle assembly checkpoint and near-random chromosome segregation in multipolar cancer cell mitosesThe forkhead-associated domain protein Cep170 interacts with Polo-like kinase 1 and serves as a marker for mature centriolesHIV-1 Vpr induces defects in mitosis, cytokinesis, nuclear structure, and centrosomesCentrosomal abnormalities, multipolar mitoses, and chromosomal instability in head and neck tumours with dysfunctional telomeresViruses associated with human cancerExcessive centrosome abnormalities without ongoing numerical chromosome instability in a Burkitt's lymphomaHPV Associated Head and Neck CancerThe cytoskeleton in papillomavirus infectionModulation of therapeutic sensitivity by human papillomavirusGenome stability pathways in head and neck cancersThe human papillomavirus E7 proteins associate with p190RhoGAP and alter its function.Centrosome amplification induced by DNA damage occurs during a prolonged G2 phase and involves ATM.Induction of centrosome amplification in p53 siRNA-treated human fibroblast cells by radiation exposure.Human papillomavirus-16 E7 interacts with glutathione S-transferase P1 and enhances its role in cell survivalCentrosomal Nlp is an oncogenic protein that is gene-amplified in human tumors and causes spontaneous tumorigenesis in transgenic mice.Role of human papillomavirus in oropharyngeal squamous cell carcinoma: A review.Papillomavirus type 16 oncogenes downregulate expression of interferon-responsive genes and upregulate proliferation-associated and NF-kappaB-responsive genes in cervical keratinocytesExamination of the pRb-dependent and pRb-independent functions of E7 in vivo.Formation of extra centrosomal structures is dependent on beta-catenin.The human papilloma virus E7 oncoprotein inhibits transforming growth factor-beta signaling by blocking binding of the Smad complex to its target sequence.Chromosome instability in human lung cancers: possible underlying mechanisms and potential consequences in the pathogenesis.Short duration of elevated vIRF-1 expression during lytic replication of human herpesvirus 8 limits its ability to block antiviral responses induced by alpha interferon in BCBL-1 cells.Association between cervical lesion grade and micronucleus frequency in the Papanicolaou testThe DNA damage response in viral-induced cellular transformationA centrosome-autonomous signal that involves centriole disengagement permits centrosome duplication in G2 phase after DNA damage.Pathogenesis of human papillomaviruses in differentiating epithelia.Pin1 regulates centrosome duplication, and its overexpression induces centrosome amplification, chromosome instability, and oncogenesisKrüppel-like factor 4 prevents centrosome amplification following gamma-irradiation-induced DNA damageSubcellular localization of the human papillomavirus 16 E7 oncoprotein in CaSki cells and its detection in cervical adenocarcinoma and adenocarcinoma in situ.Human viruses and cancer.Biological activities and molecular targets of the human papillomavirus E7 oncoprotein.Disruption of oncogene/tumor suppressor networks during human carcinogenesis.The G1 phase Cdks regulate the centrosome cycle and mediate oncogene-dependent centrosome amplification.Adenovirus E1A proteins direct subcellular redistribution of Nek9, a NimA-related kinase.Warts, cancer and ubiquitylation: lessons from the papillomaviruses.Viral carcinogenesis: factors inducing DNA damage and virus integrationCentrosome amplification and the development of cancer.Human papillomaviruses and centrosome duplication errors: modeling the origins of genomic instability.Functional modulation of the metastatic suppressor Nm23-H1 by oncogenic viruses
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P2860
The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on August 2000
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
The human papillomavirus type ...... from the cell division cycle.
@en
The human papillomavirus type ...... from the cell division cycle.
@nl
type
label
The human papillomavirus type ...... from the cell division cycle.
@en
The human papillomavirus type ...... from the cell division cycle.
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prefLabel
The human papillomavirus type ...... from the cell division cycle.
@en
The human papillomavirus type ...... from the cell division cycle.
@nl
P2093
P2860
P356
P1476
The human papillomavirus type ...... from the cell division cycle.
@en
P2093
A Duensing
S Duensing
S Gonzalez
S Piboonniyom
P2860
P304
10002-10007
P356
10.1073/PNAS.170093297
P407
P577
2000-08-01T00:00:00Z