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...
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...
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.
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...
Molecular Factors Affecting Cell Division01:27

Molecular Factors Affecting Cell Division

Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...

You might also read

Related Articles

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

Sort by
Same author

Quantifying single-cell responses to irradiation in 3D.

Frontiers in bioengineering and biotechnology·2026
Same author

Genetic resonance in the p53 signaling network.

Cell systems·2026
Same author

DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.

Cell reports·2025
Same author

Decoding the Central Dogma: Quantitative Insights into Transcription and Translation Dynamics in the p53-Mediated DNA Damage Response.

Journal of molecular biology·2025
Same author

Comparison of <i>TP53</i> mutations in myelodysplasia and acute leukemia suggests divergent roles in initiation and progression.

Blood neoplasia·2025
Same author

Cell confluency affects p53 dynamics in response to DNA damage.

Molecular biology of the cell·2025
Same journal

Mammalian Respiratory Chain Complex Assemblies and Their Links to Mitochondria Stress-Induced Human Diseases.

Advances in experimental medicine and biology·2026
Same journal

Enzyme Assemblies in Nucleotide Metabolism: Structure, Regulation, and Disease Implications.

Advances in experimental medicine and biology·2026
Same journal

The Pyruvate Dehydrogenase Complex: A 90-Year-Old Enigma Shaping the Future of Structural Enzymology.

Advances in experimental medicine and biology·2026
Same journal

Regulation of the Anti-termination RNA Transcription Complex by Lon-Mediated Lambda N Degradation.

Advances in experimental medicine and biology·2026
Same journal

PCNA Macromolecular Complexes: PCNA Serves as a Molecular Hub Regulating Multiple Cellular Processes Inside and Outside of the Nucleus.

Advances in experimental medicine and biology·2026
Same journal

Dynamic Assemblies in Genome Maintenance.

Advances in experimental medicine and biology·2026
See all related articles

Related Experiment Video

Updated: Jul 1, 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

Oscillations by the p53-Mdm2 feedback loop.

Galit Lahav1

  • 1Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA. galit@hms.harvard.edu

Advances in Experimental Medicine and Biology
|September 12, 2008
PubMed
Summary
This summary is machine-generated.

The p53 protein network, crucial for preventing cancer, exhibits complex oscillatory dynamics in response to cellular stress. Individual cell responses vary, with increased irradiation correlating with more p53 pulses.

More Related Videos

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Related Experiment Videos

Last Updated: Jul 1, 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

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The p53 network is a critical tumor suppressor pathway, activated by cellular stresses like DNA damage and hypoxia.
  • p53 regulates genes involved in cell cycle arrest, senescence, and apoptosis.
  • A negative feedback loop involving Mdm2 regulates p53 degradation, leading to oscillations.

Purpose of the Study:

  • To review models of p53 oscillation dynamics.
  • To explore reasons for cell-to-cell variability in p53 responses.
  • To discuss the functional significance of p53 oscillations in cellular stress responses.

Main Methods:

  • Review of existing quantitative studies on p53 dynamics.
  • Analysis of time-lapse fluorescent microscopy data in individual living cells.
  • Examination of p53 responses to varying levels of irradiation.

Main Results:

  • p53 oscillations are not uniformly damped across cells; individual cells show variable pulse numbers.
  • Increased irradiation correlates with a higher percentage of cells exhibiting multiple p53 pulses.
  • Pulse amplitude and duration remain constant regardless of radiation intensity.

Conclusions:

  • Cellular p53 dynamics exhibit significant heterogeneity, challenging previous models of damped oscillations.
  • The number of p53 pulses may be a key determinant of cellular fate under stress.
  • Further research is needed to elucidate the mechanisms and functional roles of p53 oscillatory dynamics.