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Related Experiment Videos

The human androgen receptor: structure/function relationship in normal and pathological situations.

A O Brinkmann1, G Jenster, G G Kuiper

  • 1Department of Endocrinology and Reproduction, Erasmus University, Rotterdam, The Netherlands.

The Journal of Steroid Biochemistry and Molecular Biology
|March 1, 1992
PubMed
Summary

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Variable loss of functional activities of androgen receptor mutants in patients with androgen insensitivity syndrome.

Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation·2013

The human androgen receptor (hAR) has distinct functional regions. Mutations in the hAR gene cause androgen insensitivity syndrome (AIS) in 46, XY individuals, leading to inactive receptors and significant health impacts.

Area of Science:

  • Molecular Endocrinology
  • Genetics
  • Cell Biology

Background:

  • The human androgen receptor (hAR) plays a crucial role in male sexual development and function.
  • Understanding the structure-function relationship of hAR is vital for diagnosing and treating androgen-related disorders.
  • hAR exhibits heterogeneity in prostate cancer cells and is implicated in androgen insensitivity syndrome (AIS).

Purpose of the Study:

  • To delineate the functional domains of the human androgen receptor (hAR).
  • To investigate the structural basis of hAR dysfunction in prostate cancer cells and AIS.
  • To identify specific mutations in the hAR gene associated with impaired receptor activity.

Main Methods:

  • Expression of hAR deletion mutants in COS and HeLa cells.

Related Experiment Videos

  • Metabolic labeling with radioactive orthophosphate to study hAR phosphorylation.
  • Structural analysis of the AR gene in LNCaP cells and individuals with AIS.

    • Main Results:

    • Distinct domains of hAR were identified for hormone binding, DNA binding, transactivation, and nuclear translocation.
    • hAR in LNCaP cells is a heterogeneous phosphoprotein, existing as 110 kDa and 112 kDa forms.
    • Mutations in LNCaP cells and individuals with AIS lead to altered binding specificity, transactivation, and functionally inactive AR proteins.

    Conclusions:

    • The hAR is a heterogeneous phosphoprotein with distinct functional domains.
    • Point mutations in the hAR gene can cause functionally inactive receptors, leading to AIS in 46, XY individuals.
    • hAR dysfunction significantly impacts phenotype and fertility in affected individuals.