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Related Concept Videos

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.
Mismatch Repair01:36

Mismatch Repair

Overview
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.
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...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...

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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

Functional characterization of the p53 "mutome".

Eran Kotler1,2, Eran Segal1,2, Moshe Oren1

  • 1Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.

Molecular & Cellular Oncology
|December 8, 2018
PubMed
Summary

This study quantitatively measured thousands of tumor protein p53 (TP53) mutations, expanding beyond common hotspots. The research reveals connections between TP53 mutation structure, function, and clinical impact.

Keywords:
deep mutational scangain of function (GOF)massively-parallel reporter assay (MPRA)mutant p53phenotypic catalogue

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04:56

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

Published on: December 30, 2025

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Phenotypic characterization of tumor protein p53 (TP53) mutations has historically focused on frequent
  • hotspot
  • mutations, representing only about 30% of all cases.
  • A comprehensive understanding of TP53 mutation impact across diverse cancer types remains incomplete.

Purpose of the Study:

  • To quantitatively assess the phenotypic impact of a large number of distinct TP53 mutations.
  • To explore the relationships between TP53 mutation structure, protein function, evolutionary conservation, and clinical outcomes.
  • To broaden the scope of TP53 mutation analysis beyond commonly studied hotspots.

Main Methods:

  • * In vitro assays to measure the functional impact of thousands of unique TP53 mutations.
  • * In vivo studies to evaluate the phenotypic consequences of TP53 mutations in a biological context.
  • * Computational analysis integrating structural, functional, and evolutionary data for TP53 mutations.

Main Results:

  • * Identification of distinct functional classes among thousands of TP53 mutations.
  • * Correlation between specific TP53 mutation characteristics (structure, conservation) and their clinical impact.
  • * Expanded understanding of TP53 mutation landscape beyond known hotspots.

Conclusions:

  • * The study provides a quantitative framework for assessing the impact of a wide spectrum of TP53 mutations.
  • * Findings elucidate the complex interplay between TP53 mutation genotype, protein phenotype, and patient outcomes.
  • * This comprehensive analysis offers valuable insights for cancer diagnostics and therapeutic strategies targeting TP53.