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Related Concept Videos

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...
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.
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...
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...

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Related Experiment Video

Updated: Jun 12, 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

Decision Making by p53: Life versus Death.

Lingyan Jiang1, M Saeed Sheikh, Ying Huang

  • 1Department of Pharmacology, State University of New York, Upstate Medical University, Syracuse, New York.

Molecular and Cellular Pharmacology
|June 2, 2010
PubMed
Summary
This summary is machine-generated.

The tumor suppressor p53 protein acts as a central regulator in the cellular DNA damage response. It integrates signals to decide cell fate, promoting survival or apoptosis.

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Last Updated: Jun 12, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
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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
  • Genetics

Background:

  • The tumor suppressor protein p53 is a critical component of the cellular signaling network that responds to DNA damage.
  • p53 functions as a transcription factor and also in a transcription-independent manner, playing a key role in cellular processes.
  • Its activation is rapid following DNA damage, with phosphorylation being an initial signaling event.

Purpose of the Study:

  • To review the current understanding of p53's role in cellular decision-making following DNA damage.
  • To elucidate how p53 integrates diverse cellular signals to determine cell fate.
  • To highlight the transcriptional and transcription-independent functions of p53 in DNA damage response.

Main Methods:

  • Literature review of studies on p53 function in DNA damage response.
  • Analysis of signaling pathways involving p53 activation and regulation.
  • Examination of p53's role in cell cycle arrest, apoptosis, and cell survival.

Main Results:

  • p53 acts as a molecular node, integrating signals from DNA damage.
  • Cellular context and damage type/severity dictate p53 activation and function.
  • p53's activities are regulated by protein degradation, post-translational modifications, and cofactor interactions.
  • p53's transcriptional role in activating target genes for cell cycle arrest or apoptosis is critical.
  • Transcription-independent functions further fine-tune p53's role in cell fate determination.

Conclusions:

  • p53 plays a pivotal role in determining the fate of cells experiencing DNA damage.
  • Its ability to assess and integrate signals allows it to direct cells towards survival or death.
  • Understanding p53 regulation is crucial for comprehending cellular responses to genotoxic stress.