ArticleProceedings of the National Academy of Sciences of the United States of America1997
Selective induction of p53 and chemosensitivity in RB-deficient cells by E1A mutants unable to bind the RB-related proteins.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 103 citations in OpenAlex.
- The E1a Adenoviral Gene Upregulates the Yamanaka Factors to Induce Partial Cellular Reprogramming.Cells · 2023Article
- Developmental Acquisition ofGenes · 2021Review
- p53-intact cancers escape tumor suppression through loss of long noncoding RNA Dino.Cell reports · 2021Article
- Sensitisation to mitoxantrone-induced apoptosis by the oncolytic adenovirus Ad∆∆ through Bcl-2-dependent attenuation of autophagy.Oncogenesis · 2018Article
- KAP1 Is a Host Restriction Factor That Promotes Human Adenovirus E1B-55K SUMO Modification.Journal of virology · 2016Article
- PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the tumor-suppressor p53.Oncogene · 2016Article
- MKP1 mediates chemosensitizer effects of E1a in response to cisplatin in non-small cell lung carcinoma cells.Oncotarget · 2015Article
- Defects in DNA Repair Genes Predict Response to Neoadjuvant Cisplatin-based Chemotherapy in Muscle-invasive Bladder Cancer.European urology · 2015Article
- E1a promotes c-Myc-dependent replicative stress: implications in glioblastoma radiosensitization.Cell cycle (Georgetown, Tex.) · 2014Article
- Activation of p53 following ionizing radiation, but not other stressors, is dependent on the proline-rich domain (PRD).Oncogene · 2013Article
- Article
- The E4orf6/E1B55K E3 ubiquitin ligase complexes of human adenoviruses exhibit heterogeneity in composition and substrate specificity.Journal of virology · 2011Article
- Transcriptional tools: Small molecules for modulating CBP KIX-dependent transcriptional activators.Biopolymers · 2011Article
- Adenovirus 5 E1A enhances histone deacetylase inhibitors-induced apoptosis through Egr-1-mediated Bim upregulation.Oncogene · 2010Article
- Oncogene-induced sensitization to chemotherapy-induced death requires induction as well as deregulation of E2F1.Cancer research · 2010Article
- Enforced expression of PPP1R13L increases tumorigenesis and invasion through p53-dependent and p53-independent mechanisms.Molecular carcinogenesis · 2009Article
- Heat shock factor 1 deficiency via its downstream target gene alphaB-crystallin (Hspb5) impairs p53 degradation.Journal of cellular biochemistry · 2009Article
- E2F-1 transcriptional activity is a critical determinant of Mdm2 antagonist-induced apoptosis in human tumor cell lines.Oncogene · 2008Article
- pRB-E2F1 complexes are resistant to adenovirus E1A-mediated disruption.Journal of virology · 2008Article
- Adenovirus E1A targets p400 to induce the cellular oncoprotein Myc.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The adenovirus E1A oncoprotein renders primary cells sensitive to the induction of apoptosis by diverse stimuli, including many anticancer agents. E1A-expressing cells accumulate p53 protein, and p53 potentiates drug-induced apoptosis. To determine how E1A promotes chemosensitivity, a series of E1A mutants were introduced into primary human and mouse fibroblasts using high-titer recombinant retroviruses, allowing analysis of E1A in genetically normal cells outside the context of adenovirus infection. Mutations that disrupted apoptosis and chemosensitivity separated into two complementation groups, which correlated precisely with the ability of E1A to associate with either the p300/CBP or retinoblastoma protein families. Furthermore, E1A mutants incapable of binding RB, p107, and p130 conferred chemosensitivity to fibroblasts derived from RB-deficient mice, but not fibroblasts from mice lacking p107 or p130. Hence, inactivation of RB, but not p107 or p130, is required for chemosensitivity induced by E1A. Finally, the same E1A functions that promote drug-induced apoptosis also induce p53. Together, these data demonstrate that p53 accumulation and chemosensitivity are linked to E1A's oncogenic potential, and identify a strategy to selectively induce apoptosis in RB-deficient tumor cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.