Related Experiment Video

Updated: Aug 8, 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

Gene-specific mechanisms of p53 transcriptional control and prospects for cancer therapy

Lois Resnick-Silverman1, James J Manfredi

  • 1Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA.

Journal of Cellular Biochemistry
|May 6, 2006
PubMed

Insights

The tumor suppressor p53 protein regulates gene activation crucial for preventing cancer. Understanding how cancer disables p53 function can lead to new therapies restoring its tumor-suppressing activity.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Genetics

Background:

  • The tumor suppressor protein p53 is a transcription factor that responds to DNA damage and genotoxic stress.
  • p53 activation leads to downstream targets involved in cell cycle arrest, apoptosis, DNA repair, and senescence.
  • p53's function is influenced by DNA binding, conformation, modifications, cofactor interactions, stability, and localization.

Purpose of the Study:

  • To define key features regulating p53's gene-specific activation.
  • To identify how these features are compromised in cancer cells.
  • To explore therapeutic strategies for restoring wild-type p53 function in cancer.

Main Methods:

  • This review synthesizes existing literature on p53 regulation and function.
  • It analyzes factors influencing p53's sequence-specific DNA binding and transcriptional activity.
  • The review examines alterations in these factors within the context of cancer.

Main Results:

  • p53's gene-specific activation relies on precise DNA binding, conformation, post-translational modifications, cofactor interactions, stability, and subcellular localization.
  • These regulatory features are frequently impaired in cancer cells, leading to loss of tumor suppressor function.
  • Dysregulation of p53 pathways is a common hallmark of many human cancers.

Conclusions:

  • Restoring wild-type p53 function by targeting its regulatory mechanisms offers a promising therapeutic avenue for cancer treatment.
  • Understanding the molecular basis of p53 inactivation in cancer is essential for developing effective p53-based therapies.
  • Targeted strategies to reactivate p53 could provide novel treatments for a wide range of malignancies.

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.
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...