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Related Experiment Videos

Regulation of CYP1A1 expression.

Y Fujii-Kuriyama1, H Imataka, K Sogawa

  • 1Department of Chemistry, Faculty of Science, Tohoku University, Sendai, Japan.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|January 6, 1992
PubMed
Summary

The study identifies two key DNA sequences regulating CYP1A1 gene expression: an inducible xenobiotic responsive element (XRE) and a constitutive element near the TATA sequence. These elements and their binding factors are crucial for high-level inducible expression of CYP1A1.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Cytochrome P450 1A1 (CYP1A1) is a key enzyme in the oxidative metabolism of xenobiotics and drugs.
  • Its synthesis is inducible in various tissues, including liver and lung, upon exposure to specific chemicals.

Purpose of the Study:

  • To investigate the regulatory mechanisms governing the induction of CYP1A1 gene expression.
  • To identify and characterize the DNA sequences and protein factors involved in CYP1A1 gene regulation.

Main Methods:

  • Utilized DNA transfer assays with isolated genomic DNA to study gene regulation.
  • Analyzed nuclear extracts from Hepa-1 and rat liver cells to identify DNA-binding factors.

Main Results:

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  • Identified at least two distinct cis-acting regulatory DNA sequences upstream of the CYP1A1 gene.
  • Discovered a xenobiotic responsive element (XRE) acting as an inducible enhancer, distributed multiple times between -0.5 and -3.5 kb.
  • Located a constitutive regulatory element upstream of the TATA sequence, essential for basal expression.

    • Conclusions:

    • Both the XRE and the constitutive element are necessary for high-level inducible expression of CYP1A1.
    • Cognate DNA-binding factors for these elements were identified in nuclear extracts of cells exhibiting inducible CYP1A1 expression.
    • The findings provide insights into the molecular mechanisms controlling CYP1A1 gene expression in response to xenobiotics.