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Updated: Jul 17, 2026
14:57
Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
One, two, three--p53, p63, p73 and chemosensitivity
Martina Müller1, Elisa Schulze Schleithoff, Wolfgang Stremmel
1Department of Internal Medicine IV, Hepatology and Gastroenterology, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany. Martina_Mueller-Schilling@med.uni-heidelberg.de
Summary
The p53 family network, including p53, p63, and p73, is crucial in cancer. Aberrant isoforms (DeltaN) promote tumors and drug resistance, offering therapeutic targets.
Area of Science:
- Molecular biology
- Cancer research
- Genetics
Background:
- The p53 protein network, including p53, p63, and p73, is implicated in apoptosis, tumorigenesis, and drug resistance.
- Understanding the roles of p53 family members is vital for targeted cancer therapies.
Purpose of the Study:
- To review the status and interrelationships of p53 family members in human cancer.
- To explore their critical roles in tumor progression and therapeutic response.
Main Methods:
- Literature review up to December 2006.
- Analysis of p53, p63, and p73 gene structure, including promoters and alternative splicing.
- Examination of isoform functions, particularly transactivation (TA) and dominant-negative (DeltaN) forms.
Main Results:
- p53, p63, and p73 generate multiple isoforms via alternative splicing.
- Full-length TA isoforms induce apoptosis, while DeltaN isoforms act as dominant inhibitors.
- Deregulated DeltaN isoforms of p63 and p73 contribute to oncogenesis and chemoresistance.
Conclusions:
- Modulating TAp63/DeltaNp63 and TAp73/DeltaNp73, along with mutant p53, presents a therapeutic strategy for p53-mutated or DeltaN-isoform-overexpressing tumors.
- Targeting DeltaNp63 and DeltaNp73 can enhance tumor therapy response and reduce metastasis.
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