Gerd A. Kullak-Ublick
University of Zurich
256 Papers
1.4K Citations
Gerd A. Kullak-Ublick is an academic researcher from University of Zurich. The author has contributed to research in topics: Medicine & Bile acid. The author has an hindex of 61, co-authored 245 publications. Previous affiliations of Gerd A. Kullak-Ublick include Novartis & National Patient Safety Foundation.
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Papers
Constitutive rat multidrug-resistance protein 2 gene transcription is down-regulated by Y-box protein 1.
Andreas Geier,Peter R. Mertens,Thomas Gerloff,Christoph G. Dietrich,Abdelaziz En-Nia,Gerd A. Kullak-Ublick,S.J Karpen,Siegfried Matern,Carsten Gartung +8 more
TL;DR: Constitutive Mrp2 gene expression is conferred through the proximal -186 bp of the minimal promoter sequence, and YB-1 acts as a repressor in vitro by specific binding to a defined element in the proxy promoter sequence.
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Diagnosis of melanoma under concomitant natalizumab therapy.
TL;DR: A 41-year-old woman who had been treated with natalizumab for 15 months for multiple sclerosis was found to have a superficial spreading melanoma in situ pTis (SSM-type) on the basis of a dysplastic nevus of a compound type, which could explain the potential of melanoma cells to spread.
Glucocorticoid receptor gene haplotype structure and steroid therapy outcome in IBD patients.
TL;DR: NR3C1 haplotypes are not related to steroid therapy outcome and were not included in the association analysis of the influence of haplotype on steroid therapy outcomes or IBD activity.
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Low allopurinol doses are sufficient to optimize azathioprine therapy in inflammatory bowel disease patients with inadequate thiopurine metabolite concentrations
Ivanka Curkovic,Katharina Rentsch,Pascal Frei,Michael Fried,Gerhard Rogler,Gerd A. Kullak-Ublick,Alexander Jetter +6 more
TL;DR: Combination therapy with only 50 mg allopurinol and 50-mg azathioprine daily is sufficient, efficacious and safe in most IBD patients with inadequate thiopurine metabolite concentrations to optimize azathyprine-based IBD therapy.
Regulation of the gene encoding the intestinal bile acid transporter ASBT by the caudal-type homeobox proteins CDX1 and CDX2.
TL;DR: The human ASBT promoter is activated transcriptionally by CDX1 and CDX2, which provides a possible explanation for the reported observation that ASBT is aberrantly expressed in esophageal metaplasia that also expresses CDX transcription factors.