Rapid induction of senescence in human cervical carcinoma cells.
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Degradation of tyrosine phosphatase PTPN3 (PTPH1) by association with oncogenic human papillomavirus E6 proteins.The haplotype-resolved genome and epigenome of the aneuploid HeLa cancer cell lineHPV in oropharyngeal cancer: the basics to know in clinical practiceStructure based identification and characterization of flavonoids that disrupt human papillomavirus-16 E6 functionDirect binding of retromer to human papillomavirus type 16 minor capsid protein L2 mediates endosome exit during viral infectionDysregulation of Autophagy Contributes to Anal CarcinogenesisDepletion of the cdk inhibitor p16INK4a differentially affects proliferation of established cervical carcinoma cells.The mRNA decay factor tristetraprolin (TTP) induces senescence in human papillomavirus-transformed cervical cancer cells by targeting E6-AP ubiquitin ligase.Human papillomavirus type 16 E1 E4-induced G2 arrest is associated with cytoplasmic retention of active Cdk1/cyclin B1 complexes.Epstein-Barr virus provides a survival factor to Burkitt's lymphomas.HUMAN PAPILLOMAVIRUS ASSOCIATION WITH HEAD AND NECK CANCERS: UNDERSTANDING VIRUS BIOLOGY AND USING IT IN THE DEVELOPMENT OF CANCER DIAGNOSTICSIn vitro progression of human papillomavirus 16 episome-associated cervical neoplasia displays fundamental similarities to integrant-associated carcinogenesis.Molecular determinants of terminal growth arrest induced in tumor cells by a chemotherapeutic agentDistinct mechanisms of cell cycle arrest control the decision between differentiation and senescence in human neuroblastoma cells.The human DEK proto-oncogene is a senescence inhibitor and an upregulated target of high-risk human papillomavirus E7HPV16 oncoproteins induce MMPs/RECK-TIMP-2 imbalance in primary keratinocytes: possible implications in cervical carcinogenesis.Inactivation of the human papillomavirus E6 or E7 gene in cervical carcinoma cells by using a bacterial CRISPR/Cas RNA-guided endonuclease.Pathogenesis of human papillomaviruses in differentiating epithelia.Persistence of high-grade cervical dysplasia and cervical cancer requires the continuous expression of the human papillomavirus type 16 E7 oncogene.Endogenous human papillomavirus E6 and E7 proteins differentially regulate proliferation, senescence, and apoptosis in HeLa cervical carcinoma cellsmiR-29 and miR-30 regulate B-Myb expression during cellular senescence.Vaccination of rabbits with an adenovirus vector expressing the papillomavirus E2 protein leads to clearance of papillomas and infection.RNA interference of human papillomavirus type 18 E6 and E7 induces senescence in HeLa cells.Re-expression of HPV16 E2 in SiHa (human cervical cancer) cells potentiates NF-κB activation induced by TNF-α concurrently increasing senescence and survivalDependence of intracellular and exosomal microRNAs on viral E6/E7 oncogene expression in HPV-positive tumor cells.Recent Insights into the Control of Human Papillomavirus (HPV) Genome Stability, Loss, and Degradation.How will HPV vaccines affect cervical cancer?Targeting the human papillomavirus E6 and E7 oncogenes through expression of the bovine papillomavirus type 1 E2 protein stimulates cellular motility.Systematic analysis of the amino acid residues of human papillomavirus type 16 E7 conserved region 3 involved in dimerization and transformation.Modulation of apoptosis by human papillomavirus (HPV) oncoproteins.Primary human cervical carcinoma cells require human papillomavirus E6 and E7 expression for ongoing proliferation.Short-term induction and long-term suppression of HPV16 oncogene silencing by RNA interference in cervical cancer cellsHuman papillomavirus E7 repression in cervical carcinoma cells initiates a transcriptional cascade driven by the retinoblastoma family, resulting in senescence.Specific down-modulation of Notch1 signaling in cervical cancer cells is required for sustained HPV-E6/E7 expression and late steps of malignant transformation.The DNA binding domain of a papillomavirus E2 protein programs a chimeric nuclease to cleave integrated human papillomavirus DNA in HeLa cervical carcinoma cells.A new E6/P63 pathway, together with a strong E7/E2F mitotic pathway, modulates the transcriptome in cervical cancer cellsKnock down of p53 or its ubiquitin ligase E6AP does not affect the sensitivity of human papillomavirus-positive cervical cancer cells to cisplatin.Future directions in research, treatment and prevention of HPV-related squamous cell carcinoma of the head and neck.Cervical cancers require the continuous expression of the human papillomavirus type 16 E7 oncoprotein even in the presence of the viral E6 oncoproteinThe role of integration in oncogenic progression of HPV-associated cancers
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Rapid induction of senescence in human cervical carcinoma cells.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on September 2000
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Rapid induction of senescence in human cervical carcinoma cells.
@en
Rapid induction of senescence in human cervical carcinoma cells.
@nl
type
label
Rapid induction of senescence in human cervical carcinoma cells.
@en
Rapid induction of senescence in human cervical carcinoma cells.
@nl
prefLabel
Rapid induction of senescence in human cervical carcinoma cells.
@en
Rapid induction of senescence in human cervical carcinoma cells.
@nl
P2093
P2860
P356
P1476
Rapid induction of senescence in human cervical carcinoma cells.
@en
P2093
P2860
P304
10978-10983
P356
10.1073/PNAS.97.20.10978
P407
P577
2000-09-01T00:00:00Z