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How Many Transcription Factors Does it Take to Turn on the Heme Oxygenase-1 (2007)
| Venue: | Gene? Am J Respir Cell Mol Biol |
| Citations: | 41 - 0 self |
BibTeX
@ARTICLE{Alam07howmany,
author = {Jawed Alam and Julia L. Cook},
title = {How Many Transcription Factors Does it Take to Turn on the Heme Oxygenase-1},
journal = {Gene? Am J Respir Cell Mol Biol},
year = {2007}
}
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Abstract
The ability to communicate with the environment and respond to changes—particularly those of an adverse 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 (i.e., the oxidative cleavage of b-type heme molecules to yield equimolar quantities of biliverdin IX�, 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 use 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–�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. In this article we provide a review and analysis of the data supporting this proposition.
Keyphrases
heme oxygenase-1 many transcription factor cellular stress response nuclear factor reaction product cellular stress condition gene expression program stress condition functional overlap heat-shock factor individual family important regulator key component potent antioxidant b-type heme molecule oxidative cleavage overall cellular stress response molecular constituent activator protein-1 family different aspect transcription factor different set cell function rate-limiting reaction adverse nature specific circumstance carbon monoxide biliverdin ix heme catabolism cell use multiple cytoprotective activity equimolar quantity stress-responsive transcription factor target gene ho-1 gene
