Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 1996 Jan 23;93(2):728-33.
doi: 10.1073/pnas.93.2.728.

Targeted overexpression of androgen receptor with a liver-specific promoter in transgenic mice

Affiliations
Comparative Study

Targeted overexpression of androgen receptor with a liver-specific promoter in transgenic mice

B Chatterjee et al. Proc Natl Acad Sci U S A. .

Abstract

The rodent liver displays marked age- and sex-dependent changes in androgen sensitivity due to the sexually dimorphic and temporally programmed expression of the androgen receptor (AR) gene. We have altered this normal phenotype by constitutive overexpression of the rat AR transgene in the mouse liver by targeting it via the human phenylalanine hydroxylase (hPAH) gene promoter. These transgenic animals in their heterozygous state produce an approximately 30-fold higher level of the AR in the liver as compared with the nontransgenic control. Androgen inactivation via sulfonation of the hormone by dehydroepiandrosterone sulfotransferase (DST), an androgen-repressible enzyme, also contributes to the age- and sex-dependent regulation of hepatic androgen sensitivity. DST has a broad range of substrate specificity and is responsible for the age- and sex-specific activation of certain polycyclic aromatic hepatocarcinogens as well, by converting them to electrophilic sulfonated derivatives. In the transgenic female, the hepatic expression of DST was approximately 4-fold lower than in normal females, a level comparable to that in normal males. The hPAH-AR mice will serve as a valuable model for studying the sex- and age-invariant expression of liver-specific genes, particularly those involved in the activation of environmental hepatocarcinogens such as the aromatic hydrocarbons.

PubMed Disclaimer

References

    1. Mol Endocrinol. 1988 Dec;2(12):1276-85 - PubMed
    1. J Histochem Cytochem. 1989 Feb;37(2):149-57 - PubMed
    1. EMBO J. 1991 Dec;10(12):3851-9 - PubMed
    1. Endocrinology. 1991 Dec;129(6):3187-99 - PubMed
    1. Science. 1991 Dec 13;254(5038):1636-9 - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources