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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.
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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

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Related Experiment Video

Updated: Jun 28, 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

The p53 family and programmed cell death.

E C Pietsch1, S M Sykes, S B McMahon

  • 1Division of Medical Sciences, Fox Chase Cancer Center, Philadelphia, PA 19107, USA.

Oncogene
|October 29, 2008
PubMed
Summary

The p53 tumor suppressor, along with its homologs p63 and p73, induces apoptosis to eliminate damaged cells. This review details how these proteins decide between growth arrest and cell death, influenced by modifications and interactions.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cellular Stress Response

Background:

  • p53 is a critical tumor suppressor frequently mutated in human cancers.
  • p53's tumor suppressor function is mediated by inducing apoptosis in stressed cells.
  • p53 has homologs, p63 and p73, that also contribute to apoptosis.

Purpose of the Study:

  • To review the mechanisms by which p53, p63, and p73 induce apoptosis.
  • To focus on factors governing the decision between growth arrest and apoptosis.
  • To examine post-translational modifications and protein-protein interactions influencing this decision.

Main Methods:

  • Literature review of apoptosis induction mechanisms.
  • Analysis of factors mediating cell fate decisions (growth arrest vs. apoptosis).

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Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
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  • Examination of post-translational modifications and protein interactions.

    • Main Results:

    • p53, p63, and p73 are key mediators of apoptosis.
    • The decision between growth arrest and apoptosis is complex.
    • Post-translational modifications and protein interactions critically regulate p53 family function.

    Conclusions:

    • p53, p63, and p73 play vital roles in tumor suppression via apoptosis.
    • Understanding the regulatory mechanisms is crucial for cancer therapy.
    • Further research into protein interactions and modifications can reveal therapeutic targets.