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Published ahead of print on September 21, 2006, doi:10.1165/rcmb.2006-0340TR

Am. J. Respir. Cell Mol. Biol., Volume 36, Number 2, February 2007, 166-174

A more recent version of this article appeared on February 1, 2007
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Submitted on September 8, 2006
Revised on September 21, 2006

How Many Transcription Factors Does it Take to Turn on the Heme Oxygenase-1 Gene?

Jawed Alam1* and Julia L Cook1

1 Department of Molecular Genetics, Ochsner Medical Center, New Orleans, LA, USA

* To whom correspondence should be addressed. E-mail: jalam{at}ochsner.org.

The ability to communicate with the environment and respond to changes - particularly those of an adversarial nature - within that environment is critical for cell function and survival. A key component of the overall cellular stress response includes adjustments in the gene expression program in favor of proteins that manifest activities capable of frustrating and eventually eliminating the molecular constituents of the stress condition. One protein providing such cytoprotective activity is heme oxygenase-1 (HO-1), an enzyme that catalyzes the rate-limiting reaction in heme catabolism - the oxidative cleavage of b-type heme molecules to yield equimolar quantities of biliverdin IX{alpha}, carbon monoxide and iron. Because of the potent antioxidant, anti-inflammatory and signaling properties of the reaction products, the HO-1 gene (hmox1) is frequently activated under a variety of cellular stress conditions. Cells employ multiple signaling pathways and transcription factors to fine-tune their response to a specific circumstance. Among these factors, members of the heat-shock factor, nuclear factor-{kappa}B, nuclear factor-erythroid 2 and activator protein-1 families are arguably the most important regulators of the cellular stress response in vertebrates. Although there is functional overlap between individual families, each broadly regulates different aspects of the cellular stress response and thus, with some exceptions, modulates the expression of different sets of targets genes. To the best of our knowledge, hmox1 is unique in that it is proposed to be directly regulated by all four of these stress-responsive transcription factors. Here we provide a review and analysis of the data supporting this proposition.




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