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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

Mismatch Repair

Overview
Mismatch Repair01:36

Mismatch Repair

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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: Jun 12, 2026

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
09:35

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches

Published on: April 20, 2021

AID and somatic hypermutation.

Robert W Maul1, Patricia J Gearhart

  • 1Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA.

Advances in Immunology
|June 1, 2010
PubMed
Summary
This summary is machine-generated.

Activation-induced deaminase (AID) precisely regulates DNA mutation in B cells for antibody diversity. This process balances immunoglobulin gene alteration with genome integrity, preventing disease and cancer.

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Characterizing Mutational Load and Clonal Composition of Human Blood

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Related Experiment Videos

Last Updated: Jun 12, 2026

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
09:35

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches

Published on: April 20, 2021

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
08:12

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes

Published on: November 1, 2011

Characterizing Mutational Load and Clonal Composition of Human Blood
07:58

Characterizing Mutational Load and Clonal Composition of Human Blood

Published on: July 11, 2019

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Peripheral B cells modify antibody affinity and isotype through somatic DNA mutation.
  • DNA modification is a tightly regulated process due to risks of disease and cancer.

Purpose of the Study:

  • To summarize the current understanding of how activation-induced deaminase (AID) functions.
  • To explain the mechanism of somatic hypermutation in B cells.

Main Methods:

  • Review of existing literature on B cell DNA mutation and repair pathways.
  • Analysis of the role of activation-induced deaminase (AID) in immunoglobulin gene diversification.

Main Results:

  • Activation-induced deaminase (AID) converts cytosine to uracil in immunoglobulin loci.
  • Deoxyuracil residues are mutagenic, mimicking thymidine during DNA replication.
  • B cells manipulate DNA repair pathways to control deoxyuracil repair.

Conclusions:

  • A complex regulatory balance exists to promote immunoglobulin gene mutation while maintaining overall genome integrity.
  • Activation-induced deaminase (AID) is central to generating antibody diversity through controlled somatic hypermutation.