These authors contributed equally to this work.
Autoimmune, Cholestatic and Biliary Disease
Version of Record online: 23 APR 2012
Copyright © 2011 American Association for the Study of Liver Diseases
Volume 55, Issue 6, pages 1912–1921, June 2012
How to Cite
Ehmer, U., Kalthoff, S., Fakundiny, B., Pabst, B., Freiberg, N., Naumann, R., Manns, M. P. and Strassburg, C. P. (2012), Gilbert syndrome redefined: A complex genetic haplotype influences the regulation of glucuronidation. Hepatology, 55: 1912–1921. doi: 10.1002/hep.25561
Potential conflict of interest: Nothing to report.
Supported by the Deutsche Forschungsgemeinschaft SFB621 project C3 (to C.P.S.).
- Issue online: 29 MAY 2012
- Version of Record online: 23 APR 2012
- Accepted manuscript online: 27 DEC 2011 01:48AM EST
- Manuscript Accepted: 3 DEC 2011
- Manuscript Received: 10 AUG 2011
Additional Supporting Information may be found in the online version of this article.
|HEP_25561_sm_suppinfofig.tif||5844K||Supporting Information Figure: Western blot analyses demonstrate reduced UGT1A (all UGT1A proteins using antibody directed against common sequence), UGT1A3, UGT1A4, UGT1A6 protein in the humanized tgUGT1A SNP mice. Note that the UGT1A and UGT1A6 antibodies used display cross-reactivity with mouse proteins. However, protein levels in htgUGT1A SNP mice are lower than in the wild type counterparts indicating lower UGT1A protein expression in the presence of UGT1A SNPs.|
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