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

4.6K
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...
4.6K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.3K
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...
9.3K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

6.4K
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...
6.4K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.8K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.8K
Negative Regulator Molecules01:23

Negative Regulator Molecules

35.8K
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.
35.8K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.9K
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...
7.9K

You might also read

Related Articles

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

Sort by
Same author

Integrative Transcriptomic and Proteomic Profiling Identifies S100P as a Potential Functional Biomarker for Sessile Serrated Lesions.

Digestive diseases and sciences·2026
Same author

Efficacy of NEPA for prevention of chemotherapy induced nausea and vomiting in head and neck cancer patients receiving cisplatin-based chemotherapy.

European journal of clinical pharmacology·2026
Same author

Regulation of autophagy by the p53 family and the implications for cancer therapies.

Discover oncology·2026
Same author

Assessing gallium arsenide health risk: critical insights for protecting workers and the environment.

Environment international·2026
Same author

Causal cross-trait mapping at single-cell resolution identifies shared immunogenetic drivers of migraine and Meniere's disease.

The journal of headache and pain·2026
Same author

CXCL8 Drives MMP1 Upregulation and Promotes Metastatic Progression in Oral Cancer Through CXCR1/2-Mediated JAK1/STAT3 Activation.

International journal of biological sciences·2026

Related Experiment Video

Updated: Sep 3, 2025

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

9.6K

P63 and P73 Activation in Cancers with p53 Mutation.

Bi-He Cai1, Yun-Chien Hsu1, Fang-Yu Yeh1

  • 1School of Medicine, I-Shou University, No. 8, Yida Rd., Jiaosu Village Yanchao District, Kaohsiung 82445, Taiwan.

Biomedicines
|July 27, 2022
PubMed
Summary

This review explores drug therapies for p53 mutations, a key tumor suppressor. It discusses targeting p53, p63, and p73 for cancer treatment, focusing on missense and nonsense mutations.

Keywords:
aggregationanti-cancer drugsgain of functionmutationp53p63p73

More Related Videos

Establishment of a Clinic-based Biorepository
07:50

Establishment of a Clinic-based Biorepository

Published on: May 29, 2017

6.6K
Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method
09:32

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

11.1K

Related Experiment Videos

Last Updated: Sep 3, 2025

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

9.6K
Establishment of a Clinic-based Biorepository
07:50

Establishment of a Clinic-based Biorepository

Published on: May 29, 2017

6.6K
Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method
09:32

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

11.1K

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The p53 family (p53, p63, p73) has tumor suppressor roles.
  • p53 exhibits high mutation rates in cancers, losing its suppressor function.
  • Missense and nonsense mutations are the most common p53 alterations.

Purpose of the Study:

  • To review potential drug therapies for p53 missense and nonsense mutations.
  • To explore the therapeutic potential of p63 and p73 activators as anti-cancer agents.
  • To summarize p63 and p73 activators and strategies to enhance their efficacy, especially for p53 gain-of-function mutants.

Main Methods:

  • Literature review of existing research on p53 family mutations.
  • Analysis of drug therapies targeting specific p53 mutations (missense, nonsense).
  • Summary of p63 and p73 activators and their mechanisms.

Main Results:

  • p53 mutations impair tumor suppression, necessitating therapeutic interventions.
  • p63 and p73 activators show promise as alternative anti-cancer strategies.
  • Strategies for improving activator responses against p53 gain-of-function mutants are discussed.

Conclusions:

  • Targeting p53 mutations and utilizing p63/p73 activators represent viable therapeutic avenues in oncology.
  • Further research into enhancing p63/p73 activator efficacy is crucial for effective cancer treatment.
  • Understanding p53 family dynamics is key to developing novel anti-cancer drugs.