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Related Concept Videos

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...
Mismatch Repair01:36

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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).

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Related Experiment Video

Updated: May 16, 2026

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
06:24

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Published on: February 13, 2019

Cancer mutations in RAD51 and its paralogues.

Anna L Valentine1, Isabella L Huth2, Nika M Duff1

  • 1Biology Program, The Ohio State University, Marion, Ohio, United States of America.

Plos One
|May 14, 2026
PubMed
Summary
This summary is machine-generated.

Cancer cells exhibit chromosomal instability despite normal RAD51 function, a paradox explained by increased mutations in RAD51 paralogues like RAD51B, RAD51C, and RAD51D, some of which are hereditary.

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Last Updated: May 16, 2026

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
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Published on: February 13, 2019

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Detection of Homologous Recombination Intermediates via Proximity Ligation and Quantitative PCR in Saccharomyces cerevisiae
07:55

Detection of Homologous Recombination Intermediates via Proximity Ligation and Quantitative PCR in Saccharomyces cerevisiae

Published on: September 11, 2022

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • RAD51 recombinase is crucial for DNA repair, protecting against chromosomal instability.
  • Human RAD51 function is partly handled by paralogues that evolved via gene duplication.
  • Cancers often display increased chromosomal instability, yet RAD51 mutations are surprisingly rare, creating the 'RAD51 paradox'.

Purpose of the Study:

  • To investigate the "RAD51 paradox" by analyzing mutations in RAD51 and its paralogues in cancer genomes.
  • To determine if mutations in RAD51 paralogues contribute to genomic instability in cancer.
  • To assess the functional impact and hereditary nature of identified mutations.

Main Methods:

  • Queried COSMIC database for RAD51 and paralogue mutations in cancer genomes.
  • Utilized algorithms to predict mutation pathogenicity and in silico 3D structure analysis for functional impact.
  • Performed gene expression and evolutionary analyses.
  • Compared COSMIC mutation data with ClinVar for hereditary mutations.

Main Results:

  • Increased mutations observed in RAD51B, RAD51C, and RAD51D paralogues in human cancers.
  • Many paralogue mutations were predicted to be pathogenic or destabilize enzyme function.
  • No significant changes in paralogue expression levels or selective evolutionary pressure were found.
  • A subset of RAD51C and RAD51D mutations are hereditary.

Conclusions:

  • The "RAD51 paradox" is explained by increased mutations in RAD51 paralogues compensating for the lack of RAD51 mutations.
  • RAD51 paralogue mutations contribute to genomic instability in cancer.
  • Hereditary mutations in RAD51C and RAD51D are implicated in cancer development.