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Electronic Letters to:

Brief Communications:
Daniel R. Johnson, Jason C. O'Connor, Matthew E. Hartman, Richard I. Tapping, and Gregory G. Freund
Acute Hypoxia Activates the Neuroimmune System, Which Diabetes Exacerbates
J. Neurosci. 2007; 27: 1161-1166 [Abstract] [Full text] [PDF]
*eLetters: Submit a response to this article

Electronic letters published:

[Read eLetter] Metabolic mediator in diabetic acidosis
Heikki Savolainen   (1 February 2007)

Metabolic mediator in diabetic acidosis 1 February 2007
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Heikki Savolainen,
Professor
Department of Occupational Safety and Health, FIN-33101 Tampere, Finland

Send letter to journal:
Re: Metabolic mediator in diabetic acidosis

heikki.savolainen{at}stm.fi Heikki Savolainen

Signal transmission from plasma membrane to nucleus is one of the functions of Raf-1 protein ser/thr kinase. Its activity is greatly diminished in diabetic metabolism because of an accumulation of methylglyoxal from the excessive glucose. Methylglyoxal seems to activate the proteasome-mediated peptide degradation through increased ubiquitination (1). Thus, the exacerbation in diabetes could be effected through enhanced degradation of low-molecular-weight regulatory protein species.

1. Du J, Zen J, Ou X, Ren X, Cai S. (2006) Methylglyoxal downregulates Raf-1 protein through a ubiquitination-mediated mechanism. Int J Biochem Cell Biol 38, 1084-91.

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