Enhancer-Mediated Control of Macrophage-Specific Arginase I Expression

  • Pauleau A
  • Rutschman R
  • Lang R
  • et al.
Citations of this article
Mendeley users who have this article in their library.


Arginase I expression in the liver must remain constant throughout life to eliminate excess nitrogen via the urea cycle. In contrast, arginase I expression in macrophages is silent until signals from Th2 cytokines such as IL-4 and IL-13 are received and the mRNA is then induced four to five orders of magnitude. Arginase I is hypothesized to play a regulatory and potentially pathogenic role in diseases such as asthma, parasitic, bacterial, and worm infections by modulating NO levels and promoting fibrosis. We show that Th2-inducible arginase I expression in mouse macrophages is controlled by an enhancer that lies -3 kb from the basal promoter. PU.1, IL-4-induced STAT6, and C/EBPbeta assemble at the enhancer and await the effect of another STAT6-regulated protein(s) that must be synthesized de novo. Identification of a powerful extrahepatic regulatory enhancer for arginase I provides potential to manipulate arginase I activity in immune cells while sparing liver urea cycle function.




Pauleau, A.-L., Rutschman, R., Lang, R., Pernis, A., Watowich, S. S., & Murray, P. J. (2014). Enhancer-Mediated Control of Macrophage-Specific Arginase I Expression. The Journal of Immunology, 172(12), 7565–7573. https://doi.org/10.4049/jimmunol.172.12.7565

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free