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

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...
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.
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...
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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

You might also read

Related Articles

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

Sort by
Same author

[Translated article] Patient With Neuropathic Ulcers and Morphea Treated With Apremilast.

Actas dermo-sifiliograficas·2025
Same author

Patient with Neuropathic Ulcers and Morphea Treated with Apremilast.

Actas dermo-sifiliograficas·2025
Same author

A randomised study comparing performance and safety of Eyestil Plus<sup>®</sup> vs Vismed Multi<sup>®</sup> in moderate-to-severe dry eye syndrome patients.

European journal of ophthalmology·2024
Same author

CDK9 inhibition as an effective therapy for small cell lung cancer.

Cell death & disease·2024
Same author

Clozapine but not lithium reverses aberrant tyrosine uptake in patients with bipolar disorder.

Psychopharmacology·2023
Same author

The myokinetic stimulation interface: activation of proprioceptive neural responses with remotely actuated magnets implanted in rodent forelimb muscle.

Journal of neural engineering·2022

Related Experiment Video

Updated: May 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

p53 regulates a non-apoptotic death induced by ROS.

J Montero1, C Dutta, D van Bodegom

  • 1Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02115, USA.

Cell Death and Differentiation
|May 25, 2013
PubMed
Summary

The tumor suppressor p53 regulates necrotic cell death by modulating poly (ADP-ribose) polymerase (PARP) activity. Loss of p53 function confers resistance to PARP-mediated necrosis, impacting cancer therapy outcomes.

More Related Videos

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

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

Published on: December 30, 2025

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

Related Experiment Videos

Last Updated: May 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

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

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

Published on: December 30, 2025

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

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • DNA damage activates p53 and poly (ADP-ribose) polymerase (PARP).
  • p53 is known to regulate apoptosis.
  • PARP-1 activation promotes necrotic cell death and energetic collapse.

Purpose of the Study:

  • To identify a novel role for p53 in regulating PARP enzymatic activity.
  • To investigate p53's role in necrotic cell death.
  • To understand how p53 loss affects cancer cell resistance to chemotherapy.

Main Methods:

  • Experiments were conducted in mouse embryonic fibroblasts.
  • Human colorectal and breast cancer cell lines were utilized.
  • Assessed the impact of p53 loss of function on PARP-mediated cell death.

Main Results:

  • p53 loss of function promotes resistance to necrotic, PARP-mediated cell death.
  • p53 modulates PARP enzymatic activity to regulate necrosis.
  • p53 regulates both apoptotic and necrotic cell death pathways.

Conclusions:

  • p53 plays a critical role in regulating necrotic cell death.
  • Cancer cells may lose p53 to resist both apoptosis and necrosis.
  • p53 status influences resistance to chemotherapy and radiation via non-apoptotic mechanisms.