Related Experiment Video

Updated: Aug 11, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

The p53 gene family

W G Kaelin1

  • 1Howard Hughes Medical Institute and Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, MA 02115, USA. william_kaelin@dfci.harvard.edu

Oncogene
|January 5, 2000
PubMed

Insights

p73 and p63 proteins are p53 homologs that rarely mutate in cancer. Evidence does not firmly support p73 and p63 as tumor suppressors, despite earlier hypotheses.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • p73 and p63 are homologous to p53, capable of binding p53 DNA sites and inducing apoptosis.
  • Unlike p53, p73 and p63 genes exhibit complex alternative splicing, producing diverse protein isoforms.
  • p73 and p63 are infrequently mutated in human cancers, unlike p53.

Purpose of the Study:

  • To evaluate the role of p73 and p63 in cancer, specifically addressing their tumor suppressor potential.
  • To critically assess the hypothesis that p73 monoallelic expression contributes to carcinogenesis.

Main Methods:

  • Comparative analysis of p53, p73, and p63 protein functions.
  • Review of mutation data in human cancers for p53, p73, and p63.
  • Examination of p73 expression levels and allelic variation in tumor samples.

Main Results:

  • p73 and p63 can activate p53-responsive genes and induce apoptosis when overproduced.
  • p63 alternative splicing generates proteins with distinct biological activities.
  • p73 and p63 are rarely mutated in cancer, and p73 inactivation is not essential for viral transformation.
  • p73 mRNA levels are often elevated in tumors, not decreased.
  • Inter- and intra-individual variations exist in p73 monoallelic expression.

Conclusions:

  • Current evidence does not establish p73 and p63 as tumor suppressors.
  • The proposed link between p73 monoallelic expression and carcinogenesis requires cautious interpretation due to expression variability and increased mRNA levels in tumors.

More Related Videos

Purification of Ubiquitinated p53 Proteins from Mammalian Cells10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Gene Families01:57

Gene Families

Gene families consist of groups of genes proposed to have originated from a common ancestor. Typically these arise through events in which a gene or genes are mistakenly duplicated during cell division. Unlike their parent genes (which are subject to selection pressure to maintain function), these gene copies do not need to preserve their sequences and may evolve at a relatively faster rate.
Occasionally these regions can be adapted to take on new roles within the organism, becoming novel genes...
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...