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Role of the intracellular receptor domain of gp130 (exon 17) in human inflammatory bowel disease
Christoph J. Auernhammer, Kathrin Zitzmann, Fabian Schnitzler, Julia Seiderer, George Vlotides, Dieter Engelhardt, Michael Sackmann, Burkhard Göke, Thomas Ochsenkühn, Department of Internal Medicine II - Grosshadern, Ludwig-Maximilians-University, D-81377 Munich, Germany
Peter Lohse, Department of Clinical Chemistry - Grosshadern, Ludwig-Maximilians-University, D-81377 Munich, Germany
Author contributions: All authors contributed equally to the work.
Supported by the Department of Clinical Chemistry - Grosshadern, Ludwig-Maximilians-University
Correspondence to: Christoph Auernhammer, M.D., Department of Internal Medicine II, Klinikum Grosshadern, Ludwig-Maximilians-University, Marchioninistr 15, D-81377 Munich, Germany. email@example.com
Telephone: +49-89-7095-0 Fax: +49-89-700-4418
Received: June 8, 2004
Revised: June 10, 2004
Accepted: July 27, 2004
Published online: February 28, 2005
AIM: To study the role of the intracellular receptor domain of gp130 in human inflammatory bowel disease (IBD).
METHODS: We amplified and sequenced the complete exon 17 of the human gp130 gene in 146 patients with IBD. According to clinical and histopathological signs, the 146 patients with IBD were classified as having Crohn’s disease (n = 73) or ulcerative colitis (n = 63), or as indeterminate status (n = 10).
RESULTS: No mutations in exon 17 of the gp130 gene could be detected in any of the 146 patients with IBD examined.
CONCLUSION: There is no evidence that mutations in exon 17 of the gp130 gene are involved in the pathogenesis of human IBD.