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Role of NF-κB in p53-mediated programmed cell death
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Cites
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Ashkenazi, A., & Dixit, V. M. (1998) · Science · doi:10.1126/science.281.5381.1305 · Cited by 5,866
Transcriptional Cross Talk between NF-κB and p53
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Cited by
Integrating cell-signalling pathways with NF-κB and IKK function
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DRAM, a p53-Induced Modulator of Autophagy, Is Critical for Apoptosis
Crighton, D., Wilkinson, S., O'Prey, J., Syed, N., Smith, P., Harrison, P. R., Gasco, M., Garrone, O., Crook, T., & Ryan, K. M. (2006) · Cell · doi:10.1016/j.cell.2006.05.034 · Cited by 1,380
Self-citationInflammation and cancer: how hot is the link?
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Non-Cell-Autonomous Tumor Suppression by p53
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“As has been observed in other contexts (Ryan et al., 2000), p53 triggered NF-kB activation as assessed by the nuclear accumulation of the NF-kB subunit p65 (Figures 6B and S6A).”
BackgroundInhibiting NF-κB activation by small molecules as a therapeutic strategy
Gupta, S. C., Sundaram, C., Reuter, S., & Aggarwal, B. B. (2010) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2010.05.004 · Cited by 762
Regulation and function of the p53 tumor suppressor protein
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Good cop, bad cop: the different faces of NF-κB
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Cross talk between stimulated NF-κB and the tumor suppressor p53
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The DNA Damage Response in Neurons: Die by Apoptosis or Survive in a Senescence-Like State?
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An Alternative Splice Form of Mdm2 Induces p53-independent Cell Growth and Tumorigenesis
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NFκB/p53 crosstalk—a promising new therapeutic target
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p53 directly regulates the glycosidase FUCA1 to promote chemotherapy-induced cell death
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Metadata
- Authors
- Ryan, K. M., Ernst, M. K., Rice, N. R., & Vousden, K. H.
- Venue
- Nature
- Published
- 2000-04
- Volume
- 404
- Issue
- 6780
- Pages
- 892-897
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1526999767
- Cited by
- 740
- References
- 2
- FWCI
- 22.54
- Type
- journal article
- Language
- en
- Open access
- closed
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Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
