Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

5.1K
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...
5.1K
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

8.6K
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....
8.6K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

7.1K
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...
7.1K
Mismatch Repair01:20

Mismatch Repair

6.2K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
6.2K
Mismatch Repair01:36

Mismatch Repair

43.4K
Overview
43.4K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

5.3K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.3K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Programmable nanobody circuits for cell selection.

bioRxiv : the preprint server for biology·2026
Same author

Multiomic screening platform uncovers the impact of histone mutations on chromatin and cell fate.

bioRxiv : the preprint server for biology·2026
Same author

High-throughput screening identifies NT-1 that synergizes with MRTX1133 against acquired resistant KRAS<sup>G12D</sup> colorectal cancer.

NPJ precision oncology·2026
Same author

Editor's Note: Cell Cycle-Dependent and Schedule-Dependent Antitumor Effects of Sorafenib Combined with Radiation.

Cancer research·2026
Same author

Editor's Note: Tumorigenic Conversion of Primary Human Esophageal Epithelial Cells Using Oncogene Combinations in the Absence of Exogenous Ras.

Cancer research·2026
Same author

A SLiM view of the human proteome.

Nature structural & molecular biology·2026
Same journal

Corrigendum: Inhibition of Myc family proteins eradicates KRas-driven lung cancer in mice.

Genes & development·2026
Same journal

A new perspective on ATR's role in translesion synthesis.

Genes & development·2026
Same journal

Mechanisms coordinating exit from the stem cell state in mammals.

Genes & development·2026
Same journal

Evolutionarily conserved spliceosome-exosome pathway in nuclear mRNA surveillance.

Genes & development·2026
Same journal

CDK1 and CEP97 cooperatively control centriole length to orchestrate ciliogenesis and developmental patterning.

Genes & development·2026
Same journal

Coupling of translesion synthesis with the replisome stabilized at stalled replication forks by ATR.

Genes & development·2026
See all related articles

Related Experiment Video

Updated: Jan 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

10.0K

Mutant p53: evolving perspectives.

Gizem Efe1, Katherine Cunningham1, Anil K Rustgi2

  • 1Vagelos College of Physicians and Surgeons, Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, New York 10032, USA.

Genes & Development
|December 15, 2025
PubMed
Summary
This summary is machine-generated.

Mutant p53 protein, frequently altered in cancers, drives tumor growth through gain-of-function properties. Understanding its complex biology is crucial for developing new cancer therapies.

Keywords:
dominant-negative effectgain of functionloss of functionp53 mutation

More Related Videos

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
12:09

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

Published on: December 30, 2025

18
Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.6K

Related Experiment Videos

Last Updated: Jan 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

10.0K
Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
12:09

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

Published on: December 30, 2025

18
Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.6K

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The p53 tumor suppressor protein is critical for cell cycle regulation.
  • TP53 mutations, primarily missense alterations in the DNA-binding domain (DBD), are prevalent in human cancers.
  • Mutant p53 exhibits gain-of-function (GOF), loss-of-function (LOF), and dominant-negative effects (DNEs), contributing to oncogenesis.

Purpose of the Study:

  • To explore the multifaceted roles of mutant p53 in cancer development.
  • To highlight the importance of understanding p53 mutation consequences in the context of precision medicine.

Main Methods:

  • Utilizing new technologies and advanced model systems.
  • Investigating molecular, cellular, and tissue-level functional consequences of p53 mutations.

Main Results:

  • New technologies reveal detailed functional consequences of p53 mutations.
  • Mutant p53 actively promotes pro-oncogenic activities beyond simple loss of function.

Conclusions:

  • Understanding mutant p53 biology is essential for advancing precision cancer medicine.
  • Targeting genetic mutations, including TP53, holds promise for future cancer therapies.