The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Degradation of p53 by adenovirus E4orf6 and E1B55K proteins occurs via a novel mechanism involving a Cullin-containing complex
Open accessAbstract
Although MDM2 plays a major role in regulating the stability of the p53 tumor suppressor protein, other poorly understood MDM2-independent pathways also exist. Human adenoviruses have evolved strategies to regulate p53 function and stability to permit efficient viral replication. One mechanism involves adenovirus E1B55K and E4orf6 proteins, which collaborate to target p53 for degradation. To determine the mechanism of this process, a multiprotein E4orf6-associated complex was purified and shown to contain a novel Cullin-containing E3 ubiquitin ligase that is (1) composed of Cullin family member Cul5, Elongins B and C, and the RING-H2 finger protein Rbx1(ROC1); (2) remarkably similar to the von Hippel-Lindau tumor suppressor and SCF (S kp1–C ul1/Cdc53–F-box) E3 ubiquitin ligase complexes; and (3) capable of stimulating ubiquitination of p53 in vitro in the presence of E1/E2 ubiquitin-activating and -conjugating enzymes. Cullins are activated by NEDD8 modification; therefore, to determine whether Cullin complexes are required for adenovirus-induced p53 degradation, studies were conducted in ts41 Chinese hamster ovary cells that are temperature sensitive for the NEDD8 pathway. E4orf6/E1B55K failed to induce the degradation of p53 at the nonpermissive temperature. Thus, our results identify a novel role for the Cullin-based machinery in regulation of p53.
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Cites
Jaakkola, P., Mole, D. R., Tian, Y.-M., Wilson, M. I., Gielbert, J., Gaskell, S. J., Kriegsheim, A. V., Hebestreit, H. F., Mukherji, M., Schofield, C. J., et al. (2001) · Science · doi:10.1126/science.1059796 · Cited by 5,535
The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis
Maxwell, P. H., Wiesener, M. S., Chang, G.-W., Clifford, S. C., Vaux, E. C., Cockman, M. E., Wykoff, C. C., Pugh, C. W., Maher, E. R., & Ratcliffe, P. J. (1999) · Nature · doi:10.1038/20459 · Cited by 5,180
HIFα Targeted for VHL-Mediated Destruction by Proline Hydroxylation: Implications for O 2 Sensing
Ivan, M., Kondo, K., Yang, H., Kim, W., Valiando, J., Ohh, M., Salic, A., Asara, J. M., Lane, W. S., & Kaelin Jr., W. G. (2001) · Science · doi:10.1126/science.1059817 · Cited by 4,735 · cited 1×
“Similarly, recognition of HIF1 by the VHL ubiquitin ligase depends on prior hydroxylation of a proline residue within the HIF1 oxygen-dependent degra- 3112 GENES & DEVELOPMENT dation domain (Ivan et al. 2001; Jaakkola et al. 2001).”
BackgroundTranscriptional Activation by Tetracyclines in Mammalian Cells
Gossen, M., Freundlieb, S., Bender, G., Müller, G., Hillen, W., & Bujard, H. (1995) · Science · doi:10.1126/science.7792603 · Cited by 2,488 · cited 2×
“AdrtTA, which was used as a control vector in some cases, expresses reverse tetracycline transactivator protein (Gossen et al. 1995) and was produced by standard methods (Bett et al.”
MethodOncoprotein MDM2 is a ubiquitin ligase E3 for tumor suppressor p53
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Ohh, M., Park, C. W., Ivan, M., Hoffman, M. A., Kim, T.-Y., Huang, L. E., Pavletich, N., Chau, V., & Kaelin, W. G. (2000) · Nature Cell Biology · doi:10.1038/35017054 · Cited by 1,577
Self-citationKamura, T., Sato, S., Haque, D., Liu, L., Kaelin, W. G., Conaway, R. C., & Conaway, J. W. (1998) · Genes & Development · doi:10.1101/gad.12.24.3872 · Cited by 595
Self-citation
Cited by
Duda, D. M., Borg, L. A., Scott, D. C., Hunt, H. W., Hammel, M., & Schulman, B. A. (2008) · Cell · doi:10.1016/j.cell.2008.07.022 · Cited by 767
Mdm2-Mediated NEDD8 Conjugation of p53 Inhibits Its Transcriptional Activity
Xirodimas, D. P., Saville, M. K., Bourdon, J.-C., Hay, R. T., & Lane, D. P. (2004) · Cell · doi:10.1016/j.cell.2004.06.016 · Cited by 570
Adenovirus oncoproteins inactivate the Mre11–Rad50–NBS1 DNA repair complex
Stracker, T. H., Carson, C. T., & Weitzman, M. D. (2002) · Nature · doi:10.1038/nature00863 · Cited by 522
The Mre11 complex is required for ATM activation and the G2/M checkpoint
Carson, C. T., Schwartz, R. A., Stracker, T. H., Lilley, C. E., Lee, D. V., & Weitzman, M. D. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg630 · Cited by 502
To kill or be killed: viral evasion of apoptosis
Benedict, C. A., Norris, P. S., & Ware, C. F. (2002) · Nature Immunology · doi:10.1038/ni1102-1013 · Cited by 431
Metadata
- Authors
- Querido, E., Blanchette, P., Yan, Q., Kamura, T., Morrison, M., Boivin, D., Kaelin, W. G., Conaway, R. C., Conaway, J. W., & Branton, P. E.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2001-12-01
- Volume
- 15
- Issue
- 23
- Pages
- 3104-3117
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2170543799
- Cited by
- 484
- References
- 7
- Type
- posted content
- Language
- en
- Open access
- diamond
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- CoChat. (2026). Citation check: Degradation of p53 by adenovirus E4orf6 and E1B55K proteins occurs via a novel mechanism involving a Cullin-containing complex. https://app.cochat.ai/papers/10.1101/gad.926401
- The paper
- Querido, E., Blanchette, P., Yan, Q., Kamura, T., Morrison, M., Boivin, D., Kaelin, W. G., Conaway, R. C., Conaway, J. W., & Branton, P. E. (2001). Degradation of p53 by adenovirus E4orf6 and E1B55K proteins occurs via a novel mechanism involving a Cullin-containing complex. Genes & Development. https://doi.org/10.1101/gad.926401
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