Autophagy activation by rapamycin eliminates mouse Mallory-Denk bodies and blocks their proteasome inhibitor-mediated formation†
Article first published online: 21 FEB 2008
Copyright © 2008 American Association for the Study of Liver Diseases
Volume 47, Issue 6, pages 2026–2035, June 2008
How to Cite
Harada, M., Hanada, S., Toivola, D. M., Ghori, N. and Omary, M. B. (2008), Autophagy activation by rapamycin eliminates mouse Mallory-Denk bodies and blocks their proteasome inhibitor-mediated formation. Hepatology, 47: 2026–2035. doi: 10.1002/hep.22294
Potential conflict of interest: Nothing to report.
- Issue published online: 28 MAY 2008
- Article first published online: 21 FEB 2008
- Accepted manuscript online: 21 FEB 2008 12:00AM EST
- Manuscript Accepted: 11 FEB 2008
- Manuscript Received: 9 OCT 2007
- National Institutes of Health (NIH). Grant Number: DK52951
- Department of Veterans Affairs
- NIH Digestive Disease Center institutional. Grant Number: DK56339
Supplementary material for this article can be found on the H EPATOLOGY Web site ( http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html ).
|hep22294-SupplementaryFigure1.tif||5512K||Supplementary Fig. 1: Effect of bortezomib on K18-null livers.K18-null (-/-) mice [3 months old (4 mice) and 12 months old (3 mice)] were given bortezomib (Bort) as described in Experimental Procedures followed by double-staining for ubiquitin (green) or K8 (red). Control mice (-Bort) were also similarly stained, and representative images are shown. Note that livers from 3 months old K18-null mice, which rarely possess inclusions under basal condition (A-C), develop scattered inclusions as the mice age (G-I) as shown previously. 21Treatment with bortezomib for 2 weeks results in MDB formation in the young mice (D-F) but the formation of inclusions is far more robust in the older mice (J-L). Arrows highlight the inclusions. Bar=50 microns.|
|hep22294-SupplementaryTable1.doc||44K||Supplementary Table 1|
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