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Interpreting cancer genomes using systematic host network perturbations by tumour virus proteinsViral perturbations of host networks reflect disease etiology.HPV16 E7 oncogene expression in normal human epithelial cells causes molecular changes indicative of an epithelial to mesenchymal transition.Human papillomavirus type 16 E7 oncoprotein associates with the centrosomal component gamma-tubulin.Human papillomavirus type 16 E7 oncoprotein can induce abnormal centrosome duplication through a mechanism independent of inactivation of retinoblastoma protein family members.Perturbation of DROSHA and DICER expression by human papillomavirus 16 oncoproteins.Cyclin-dependent kinase inhibitor indirubin-3'-oxime selectively inhibits human papillomavirus type 16 E7-induced numerical centrosome anomalies.Molecular pathways executing the "trophic sentinel" response in HPV-16 E7-expressing normal human diploid fibroblasts upon growth factor deprivation.Stabilization and functional impairment of the tumor suppressor p53 by the human papillomavirus type 16 E7 oncoprotein.The human papillomavirus E7 protein as a transforming and transactivating factor.Expression of the HPV E7 oncoprotein mimics but does not evoke a p53-dependent cellular DNA damage response pathway.The carboxyl-terminal zinc-binding domain of the human papillomavirus E7 protein can be functionally replaced by the homologous sequences of the E6 protein.Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis.A mutational analysis of the amino terminal domain of the human papillomavirus type 16 E7 oncoprotein.Interactions of the human papillomavirus E7 protein with cell cycle regulators.Human papillomavirus type 16 E7 oncoprotein inhibits the anaphase promoting complex/cyclosome activity by dysregulating EMI1 expression in mitosis.Are selective estrogen receptor modulators (SERMs) a therapeutic option for HPV-associated cervical lesions and cancers?Ki-67, cyclin E, and p16INK4 are complimentary surrogate biomarkers for human papilloma virus-related cervical neoplasia.The human papillomavirus type 16 E7 gene encodes transactivation and transformation functions similar to those of adenovirus E1A.Tripeptidyl Peptidase II Is Required for c-MYC-Induced Centriole Overduplication and a Novel Therapeutic Target in c-MYC-Associated NeoplasmsCullin 1 functions as a centrosomal suppressor of centriole multiplication by regulating polo-like kinase 4 protein levels.Direct association of the HPV16 E7 oncoprotein with cyclin A/CDK2 and cyclin E/CDK2 complexes.The cytokines tumor necrosis factor-alpha (TNF-alpha ) and TNF-related apoptosis-inducing ligand differentially modulate proliferation and apoptotic pathways in human keratinocytes expressing the human papillomavirus-16 E7 oncoprotein.The HPV E7 oncoprotein inhibits tumor necrosis factor alpha-mediated apoptosis in normal human fibroblasts.Dimerization of the human papillomavirus E7 oncoprotein in vivo.Learning old tricks from new viruses.The curious case of APOBEC3 activation by cancer-associated human papillomaviruses.
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description
hulumtues
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հետազոտող
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Karl Münger
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Karl Münger
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Karl Münger
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Karl Münger
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Karl Münger
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Karl Münger
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Karl Münger
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Karl Münger
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Karl Münger
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Karl Münger
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P21
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0000-0003-3288-9935