Related Experiment Video

Updated: Feb 16, 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

10.1K

Control of Nucleotide Metabolism Enables Mutant p53's Oncogenic Gain-of-Function Activity

Valentina Schmidt1, Rachana Nagar2, Luis A Martinez3

  • 1Department of Pathology, Stony Brook University, Stony Brook, NY 11794, USA. valentina.schmidt@stonybrookmedicine.edu.

International Journal of Molecular Sciences
|December 20, 2017
PubMed

Insights

Mutant p53 (mtp53) exhibits gain-of-function (GOF) activities through novel mechanisms. This study reveals that mtp53 GOF involves upregulating nucleotide synthesis and salvage pathways, crucial for cancer research.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The p53 protein is a critical tumor suppressor (wild-type p53 or WTp53) and oncogene (mutant p53 or mtp53).
  • Extensive research has elucidated p53's diverse roles in cellular functions.
  • Emerging evidence highlights novel functions contributing to cancer progression.

Purpose of the Study:

  • To investigate a novel mechanism underlying mutant p53 (mtp53) gain-of-function (GOF) activities.
  • To explore the role of nucleotide metabolism in mtp53-driven oncogenesis.

Main Methods:

  • Analysis of gene expression related to nucleotide synthesis and salvage pathways.
  • Functional assays to assess the impact of mtp53 on these pathways.

Main Results:

  • Mutant p53 (mtp53) upregulates nucleotide de novo synthesis pathways.
  • mtp53 also enhances nucleoside salvage pathways.
  • These metabolic alterations contribute to mtp53's gain-of-function (GOF) activities.

Conclusions:

  • A novel mechanism for mtp53 GOF involves the coordinated upregulation of nucleotide synthesis and salvage.
  • Understanding these metabolic alterations provides new insights into p53's oncogenic functions.
  • Targeting these pathways could offer therapeutic strategies for cancers with mutant p53.
Keywords:
ETS2GOFsnucleotide metabolismp53

More Related Videos

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

237
Purification of Ubiquitinated p53 Proteins from Mammalian Cells10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.8K

Related Concept Videos

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...
5.3K
Biosynthesis of Nucleic Acids01:28

Biosynthesis of Nucleic Acids

Nucleic acid biosynthesis is a fundamental biochemical process that produces the purine and pyrimidine nucleotides essential for DNA and RNA synthesis. This pathway maintains a balanced nucleotide pool, preventing imbalances that could jeopardize genetic integrity and cellular function. Given the crucial role of nucleotides, their synthesis is tightly regulated to ensure proper cellular homeostasis.Purine BiosynthesisThe biosynthesis of purine nucleotides begins with ribose-5-phosphate, a...
1.2K
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...
10.2K
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...
3.2K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
11.5K
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....
9.7K