Mis-splicing drives loss of function of p53E224D point mutation
Mouse p53E221D and human p53E224D mutations lead to splice variation and a biologically relevant p53 loss of function in vitro and in vivo.
Authors
- Ian C. Lock (ORCID: https://orcid.org/0000-0001-8247-4514)
- Chang‐Lung Lee (ORCID: https://orcid.org/0000-0002-0673-633X)
- Yan Ma (ORCID: https://orcid.org/0000-0002-1649-8849)
- Nathan H. Leisenring (ORCID: https://orcid.org/0000-0002-3404-4226)
- Warren Floyd (ORCID: https://orcid.org/0000-0003-4371-8453)
- Erin C. Mansell (ORCID: https://orcid.org/0009-0007-9588-8338)
- David G. Kirsch (ORCID: https://orcid.org/0000-0002-2086-205X)
- Lixia Luo (ORCID: https://orcid.org/0000-0002-8413-0501)
- Diana M. Cardona (ORCID: https://orcid.org/0000-0002-6877-2280)
- Eric S. Xu (ORCID: https://orcid.org/0000-0001-9933-9386)
Institutions
- The University of Texas MD Anderson Cancer Center (US)
- Princess Margaret Cancer Centre (CA)
- Duke Medical Center (US)
- Duke University Hospital (US)
Publication Details
- Journal
- PLoS ONE
- Published
- 2025-03-05
- DOI
- https://doi.org/10.1371/journal.pone.0318856
- Primary Topic
- Cancer-related Molecular Pathways
- Type
- article
- Field-Weighted Citation Impact
- 0.00