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
. 1996 Jun 25;93(13):6731-6.
doi: 10.1073/pnas.93.13.6731.

Characterization of a murine Ahr null allele: involvement of the Ah receptor in hepatic growth and development

J V Schmidt  1 , G H Su, J K Reddy, M C Simon, C A Bradfield
Affiliations

Characterization of a murine Ahr null allele: involvement of the Ah receptor in hepatic growth and development

J V Schmidt et al. Proc Natl Acad Sci U S A. .

Abstract

The Ah receptor (AHR) is a ligand-activated transcription factor that mediates a pleiotropic response to environmental contaminants such as benzo[a]pyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin. In an effort to gain insight into the physiological role of the AHR and to develop models useful in risk assessment, gene targeting was used to inactivate the murine Ahr gene by homologous recombination. Ahr-/- mice are viable and fertile but show a spectrum of hepatic defects that indicate a role for the AHR in normal liver growth and development. The Ahr-/- phenotype is most severe between 0-3 weeks of age and involves slowed early growth and hepatic defects, including reduced liver weight, transient microvesicular fatty metamorphosis, prolonged extramedullary hematopoiesis, and portal hypercellularity with thickening and fibrosis.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Toxicol Appl Pharmacol. 1992 Sep;116(1):101-9 - PubMed
    1. Mol Pharmacol. 1990 Sep;38(3):306-12 - PubMed
    1. Nature. 1986 Oct 2-8;323(6087):445-8 - PubMed
    1. Life Sci. 1989;45(6):559-65 - PubMed
    1. Nature. 1995 Feb 23;373(6516):702-5 - PubMed

Publication types

Substances