The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
E1A signaling to p53 involves the p19ARFtumor suppressor
Open accessAbstract
The adenovirus E1A oncogene activates p53 through a signaling pathway involving the retinoblastoma protein and the tumor suppressor p19 ARF. The ability of E1A to induce p53 and its transcriptional targets is severely compromised in ARF-null cells, which remain resistant to apoptosis following serum depletion or adriamycin treatment. Reintroduction of p19 ARF restores p53 accumulation and resensitizes ARF-null cells to apoptotic signals. Therefore, p19 ARF functions as part of a p53-dependent failsafe mechanism to counter uncontrolled proliferation. Synergistic effects between the p19 ARF and DNA damage pathways in inducing p53 may contribute to E1A’s ability to enhance radio- and chemosensitivity.
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Citations
Cites
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Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19
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Cited by
The regulation of E2F by pRB-family proteins.
Dyson, N. (1998) · Genes & Development · doi:10.1101/gad.12.15.2245 · Cited by 2,317
The p53 pathway: positive and negative feedback loops
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Self-citation
Metadata
- Authors
- de Stanchina, E., McCurrach, M. E., Zindy, F., Shieh, S.-Y., Ferbeyre, G., Samuelson, A. V., Prives, C., Roussel, M. F., Sherr, C. J., & Lowe, S. W.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1998-08-01
- Volume
- 12
- Issue
- 15
- Pages
- 2434-2442
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2100876151
- Cited by
- 609
- References
- 17
- Type
- posted content
- Language
- en
- Open access
- diamond
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- de Stanchina, E., McCurrach, M. E., Zindy, F., Shieh, S.-Y., Ferbeyre, G., Samuelson, A. V., Prives, C., Roussel, M. F., Sherr, C. J., & Lowe, S. W. (1998). E1A signaling to p53 involves the p19ARFtumor suppressor. Genes & Development. https://doi.org/10.1101/gad.12.15.2434
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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