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c-Abl regulates early growth response protein (EGR1) in response to oxidative stress

Jeremy R Stuart1, Hidehiko Kawai, Kelvin K C Tsai

  • 1Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.

Oncogene
|August 11, 2005
PubMed

Insights

The c-Abl tyrosine kinase regulates cell growth and apoptosis. It induces Early Growth Response-1 (EGR1) gene expression via the MEK/ERK pathway, impacting the apoptotic response to oxidative stress.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • c-Abl is a tyrosine kinase involved in regulating cell growth and apoptosis.
  • Oxidative stress can trigger cellular responses mediated by kinases.

Purpose of the Study:

  • To identify genes regulated by c-Abl kinase activity.
  • To elucidate the signaling pathway involved in c-Abl-mediated gene regulation and apoptosis.

Main Methods:

  • Inducible c-Abl expression cell lines
  • Microarray analysis
  • Promoter mapping
  • Western blotting
  • MEK/ERK pathway inhibition (PD 95089, dominant-negative mutant)
  • c-Abl knockout murine embryonic fibroblasts (MEFs)

Main Results:

  • c-Abl kinase activity induces Early Growth Response-1 (EGR1) gene expression.
  • c-Abl transactivates EGR1 through distal serum response elements (SREs) via the MEK/ERK pathway.
  • Hydrogen peroxide-induced EGR1 expression is dependent on c-Abl.
  • EGR1 activity partially mitigates c-Abl-induced apoptosis.

Conclusions:

  • c-Abl promotes EGR1 induction via the MEK/ERK pathway.
  • This pathway is critical for regulating the apoptotic response to oxidative stress.

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