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Related Experiment Video

Updated: Jun 19, 2026

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

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Published on: December 19, 2018

Association between the estrogen receptor TA polymorphism and Harm avoidance.

R Gade-Andavolu1, J Macmurray, D E Comings

  • 1Genetic Research Institute of the Desert, Rancho Mirage, California, United States.

Neuroscience Letters
|October 14, 2009
PubMed
Summary
This summary is machine-generated.

The estrogen receptor alpha (ESR1) gene TA dinucleotide repeat polymorphism is linked to higher Harm Avoidance (HA) temperamental traits in Caucasian university students. This genetic variation may influence personality, particularly in women.

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Area of Science:

  • Behavioral Genetics
  • Neuroendocrinology

Background:

  • Gene variants are increasingly recognized for their role in modulating temperamental traits.
  • The estrogen receptor alpha (ESR1) gene is a candidate for influencing personality, specifically Harm Avoidance (HA).

Purpose of the Study:

  • To investigate the association between the ESR1 TA dinucleotide repeat polymorphism and the HA temperamental trait.
  • To examine this association in a sample of Caucasian university students.

Main Methods:

  • Genotyping of 190 healthy subjects for the ESR1 TA dinucleotide repeat polymorphism.
  • Administration of the Temperament and Character Inventory (TCI) to assess HA.
  • Analysis using ANOVA to compare HA scores based on ESR1 variants (short/long).

Main Results:

  • Harm Avoidance (HA) was significantly associated with age and gender, higher in older and female subjects.
  • Individuals with the S/S variant of the ESR1 TA repeat polymorphism exhibited significantly higher HA scores.
  • Further analysis indicated potential gender-specific differences in HA subscales.

Conclusions:

  • The study suggests a possible role for ESR1 gene variants in modulating Harm Avoidance (HA).
  • Replication and further research into the neurobiological mechanisms underlying ESR1's influence on HA are warranted.