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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...
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...
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
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.

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Related Experiment Video

Updated: Jun 30, 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

Recent advances in p53 research: an interdisciplinary perspective.

M Olivier1, A Petitjean, V Marcel

  • 11Group of Molecular Carcinogenesis and Biomarkers, International Agency for Research on Cancer, World Health Organization, Lyon, France. molivier@iarc.fr

Cancer Gene Therapy
|September 20, 2008
PubMed
Summary
This summary is machine-generated.

Mutant p53 proteins, altered TP53 gene products, gain new cancer-promoting functions. Research reveals their impact on gene expression and potential as therapeutic targets for cancer detection and treatment.

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

Published on: December 30, 2025

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: Jun 30, 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

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:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The TP53 gene is crucial in human cancer research.
  • Mutant p53 proteins, resulting from TP53 gene mutations, accumulate in cancer cells and exhibit gain-of-function effects.
  • These mutations can alter the expression of multiple genes, influencing cancer development.

Purpose of the Study:

  • To review advances in understanding normal and mutant p53 proteins.
  • To explore the abnormal regulation and distribution of p53 in human cancers.
  • To describe new therapeutic strategies targeting p53 alterations.

Main Methods:

  • Review of experimental evidence on mutant p53 gain-of-function effects.
  • Analysis of clinical studies correlating TP53 mutations with gene expression patterns.
  • Examination of structural, biochemical, and functional properties of p53 proteins.

Main Results:

  • Mutant p53 proteins demonstrate specific gain-of-function effects by perturbing gene expression.
  • Targeted expression of mutant p53 enhances cancer formation in mouse models.
  • Clinical data show correlations between TP53 mutations and cancer-related gene expression patterns.

Conclusions:

  • Alterations in p53 function are critical in shaping cancer gene expression.
  • Understanding mutant p53 offers new opportunities for cancer detection, prognosis, prevention, and therapy.
  • Translational research integrating p53 knowledge can improve cancer patient outcomes.