Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 205, Issue 7, Pages 1529-1534Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20072080
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Funding
- Medical Research Council (UK)
- Papworth NHS Trust
- Wellcome Trust Intermediate Clinical Fellow
- Medical Research Council [G0500306] Funding Source: researchfish
- MRC [G0500306] Funding Source: UKRI
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Members of the serpin (serine proteinase inhibitor) superfamily play a central role in the control of inflammatory, coagulation, and fibrinolytic cascades. Point mutations that cause abnormal conformational transitions in these proteins can trigger disease. Recent work has defined three pathways by which these conformers cause tissue damage. Here, we describe how these three mechanisms can be integrated into a new model of the pathogenesis of emphysema caused by mutations in the serpin alpha(1)-antitrypsin.
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