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Related Experiment Video

Updated: Jun 26, 2026

Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay
09:07

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Estrogen directly activates AID transcription and function.

Siim Pauklin1, Isora V Sernández, Gudrun Bachmann

  • 1DNA Editing Laboratory, Cancer Research UK, Clare Hall Laboratories, South Mimms, EN6 3LD, England, UK.

The Journal of Experimental Medicine
|January 14, 2009
PubMed
Summary
This summary is machine-generated.

Estrogen enhances the expression of activation-induced deaminase (AID), a DNA-altering enzyme. This estrogen-induced AID can increase DNA instability, potentially driving autoimmunity and cancer.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Estrogen influences immunity, autoimmunity, and cancer, with its molecular targets being well-documented.
  • Activation-induced deaminase (AID) is crucial for immunoglobulin gene diversification but its dysregulation can lead to immune alterations and oncogenesis.
  • Estrogen's role in immune responses and cancer suggests potential molecular links.

Purpose of the Study:

  • To investigate the direct molecular mechanism by which estrogen affects AID expression and function.
  • To determine if estrogen-induced AID impacts DNA stability beyond immunoglobulin loci.
  • To explore the therapeutic potential of estrogen antagonists in mitigating estrogen-driven DNA instability.

Main Methods:

  • Analysis of estrogen-estrogen receptor complex binding to the AID promoter.
  • Measurement of AID messenger RNA and protein levels following estrogen treatment.
  • Assessment of somatic hypermutation (SHM) and class switch recombination (CSR) at immunoglobulin loci.
  • Evaluation of c-myc oncogene translocations as a marker of genotoxicity.
  • Investigation of estrogen's effect on related DNA deaminase family members (APOBEC3B, -3F, -3G).
  • Testing the inhibitory effect of tamoxifen on estrogen-induced AID expression.

Main Results:

  • Estrogen-estrogen receptor complex directly binds to the AID promoter, increasing AID messenger RNA and protein levels.
  • Estrogen enhances SHM and CSR at the immunoglobulin locus.
  • Estrogen induces significant translocations of the c-myc oncogene, indicating genotoxicity beyond the Ig locus.
  • Estrogen induces AID expression by over 20-fold in non-immune tissues like breast and ovaries.
  • The estrogenic effect on AID expression is partially conserved in APOBEC3B, -3F, and -3G.
  • Tamoxifen, an estrogen antagonist, inhibits estrogen-induced AID expression.

Conclusions:

  • Estrogen directly enhances AID expression and activity through binding to the AID promoter.
  • Estrogen-induced AID leads to DNA instability not only at immunoglobulin loci but also at other genomic sites, such as the c-myc oncogene.
  • Estrogen's ability to induce AID expression and DNA instability may underlie its role in driving autoimmunity and oncogenesis.
  • Targeting estrogen signaling with antagonists like tamoxifen may offer a strategy to inhibit AID-dependent DNA damage and associated diseases.