Smads as intracellular mediators of airway inflammation.

Groneberg, David A., Witt, Heiko, Adcock, Ian M., Hansen, Gesine and Springer, Jochen (2004) Smads as intracellular mediators of airway inflammation. Experimental Lung Research, 30 (3). pp. 223-250. ISSN 0190-2148

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Abstract

Transforming growth factor-beta (TGF-beta) plays an important role in the pathogenesis of allergic asthma and other airway diseases. Signals from the activated TGF-beta receptor complex are transduced to the nucleus of airway cells by Smad proteins, which represent a family of transcription factors that have recently been implicated to play a major role as intracellular mediators of inflammation. The Smad family consists of the receptor-regulated Smads, a common pathway Smad, and inhibitory Smads. Receptor-regulated Smads (R-Smads) are phosphorylated by the TGF-beta type Ireceptor. They include Smad2 and Smad3, which are recognized by TGF-beta and activin receptors, and Smads 1, 5, 8, and 9, which are recognized by bone morphogenetic protein (BMP) receptors. Smad4 is a common pathway Smad, which is also defined as cooperating Smad (co-Smad) and is not phosphorylated by the TGF-beta type I receptor. Inhibitory Smads(anti-Smads) include Smad6 and Smad7, which down-regulate TGF-beta signaling. To date, the Smads are the only TGF-beta receptor substrates with a demonstrated ability to propagate signals and with regard to the growing number of investigations of Smad-mediated effects in the airways, Smads may prove to be an important target for future development of new therapeutic strategies for asthma and chronic obstructive pulmonary disease.

Item Type: Article
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
University of East Anglia > Faculty of Medicine and Health Sciences > Research Groups > Gastroenterology and Gut Biology
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Depositing User: Rhiannon Harvey
Date Deposited: 09 Jun 2011 16:39
Last Modified: 25 Jul 2018 06:44
URI: https://ueaeprints.uea.ac.uk/id/eprint/32179
DOI: 10.1080/01902140490276320

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