Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis.
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Imaging poliovirus entry in live cellsAssociation of the human papillomavirus type 16 E7 oncoprotein with the 600-kDa retinoblastoma protein-associated factor, p600p600, a unique protein required for membrane morphogenesis and cell survival.A dual role of cyclin E in cell proliferation and apoptosis may provide a target for cancer therapyHuman scribble (Vartul) is targeted for ubiquitin-mediated degradation by the high-risk papillomavirus E6 proteins and the E6AP ubiquitin-protein ligaseViruses associated with human cancerMechanisms of virus immune evasion lead to development from chronic inflammation to cancer formation associated with human papillomavirus infectionAPC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathwayFunctional Roles of E6 and E7 Oncoproteins in HPV-Induced Malignancies at Diverse Anatomical SitesPapillomavirus E6 oncoproteins.Papillomavirus E6 PDZ interactions can be replaced by repression of p53 to promote episomal human papillomavirus genome maintenanceHuman papillomavirus 16 E5 induces bi-nucleated cell formation by cell-cell fusion.Physical labeling of papillomavirus-infected, immortal, and cancerous cervical epithelial cells reveal surface changes at immortal stageHuman papillomavirus type 16 E7 binds to E2F1 and activates E2F1-driven transcription in a retinoblastoma protein-independent manner.Evidence that proteasome-dependent degradation of the retinoblastoma protein in cells lacking A-type lamins occurs independently of gankyrin and MDM2.The E7 oncoprotein of human papillomavirus type 16 stabilizes p53 through a mechanism independent of p19(ARF).Clink, a nanovirus-encoded protein, binds both pRB and SKP1.Human papillomavirus type 16 E6 induces self-ubiquitination of the E6AP ubiquitin-protein ligaseRole of Rb-dependent and Rb-independent functions of papillomavirus E7 oncogene in head and neck cancer.The human papillomavirus E6 oncogene dysregulates the cell cycle and contributes to cervical carcinogenesis through two independent activities.The human papillomavirus type 16 E6 gene alone is sufficient to induce carcinomas in transgenic animals.p21cip1 Degradation in differentiated keratinocytes is abrogated by costabilization with cyclin E induced by human papillomavirus E7.Destabilization of the retinoblastoma tumor suppressor by human papillomavirus type 16 E7 is not sufficient to overcome cell cycle arrest in human keratinocytes.Disruption of retinoblastoma protein family function by human papillomavirus type 16 E7 oncoprotein inhibits lens development in part through E2F-1.Systematic identification of interactions between host cell proteins and E7 oncoproteins from diverse human papillomaviruses.Three regions of the pRB pocket domain affect its inactivation by human papillomavirus E7 proteins.Inactivation of both the retinoblastoma tumor suppressor and p21 by the human papillomavirus type 16 E7 oncoprotein is necessary to inhibit cell cycle arrest in human epithelial cells.Genetic analysis of high-risk e6 in episomal maintenance of human papillomavirus genomes in primary human keratinocytes.Apoptotic caspases regulate induction of iPSCs from human fibroblasts.A humanized mouse model of HPV-associated pathology driven by E7 expressionBiological activities and molecular targets of the human papillomavirus E7 oncoprotein.Expression of human papillomavirus type 16 E7 is sufficient to significantly increase expression of angiogenic factors but is not sufficient to induce endothelial cell migration.The high-risk HPV16 E7 oncoprotein mediates interaction between the transcriptional coactivator CBP and the retinoblastoma protein pRb.Warts, cancer and ubiquitylation: lessons from the papillomaviruses.A synthetic E7 gene of human papillomavirus type 16 that yields enhanced expression of the protein in mammalian cells and is useful for DNA immunization studies.Stabilization of the retinoblastoma protein by A-type nuclear lamins is required for INK4A-mediated cell cycle arrestIdentification of biomarkers that distinguish human papillomavirus (HPV)-positive versus HPV-negative head and neck cancers in a mouse model.The E7 open reading frame acts in cis and in trans to mediate differentiation-dependent activities in the human papillomavirus type 16 life cycle.Pathway profiling and rational trial design for studies in advanced stage cervical carcinoma: a review and a perspective.Human papillomavirus type 16 E6 and E 7 proteins alter NF-kB in cultured cervical epithelial cells and inhibition of NF-kB promotes cell growth and immortalization
P2860
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P2860
Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis.
description
1997 nî lūn-bûn
@nan
1997年の論文
@ja
1997年学术文章
@wuu
1997年学术文章
@zh-cn
1997年学术文章
@zh-hans
1997年学术文章
@zh-my
1997年学术文章
@zh-sg
1997年學術文章
@yue
1997年學術文章
@zh
1997年學術文章
@zh-hant
name
Destabilization of the RB tumo ...... type 16 E7-induced apoptosis.
@en
type
label
Destabilization of the RB tumo ...... type 16 E7-induced apoptosis.
@en
prefLabel
Destabilization of the RB tumo ...... type 16 E7-induced apoptosis.
@en
P356
P1433
P1476
Destabilization of the RB tumo ...... type 16 E7-induced apoptosis.
@en
P2093
P304
P356
10.1006/VIRO.1997.8851
P407
P50
P577
1997-12-01T00:00:00Z