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A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1 - Nature Genetics

  • ️Schreiber, Stefan
  • ️Sun Dec 31 2006

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Acknowledgements

We thank all affected individuals, families and physicians for their cooperation. We acknowledge the cooperation of the German Crohn and Colitis Patient Association (Deutsche Morbus Crohn und Colitis Vereinigung) and the contributing gastroenterologists. The authors thank T. Wesse, B. Petersen, L. Bossen, T. Henke, S. Ehlers, A. Dietsch, T. Kaacksteen and D. Soars for technical help. The ongoing technical and logistic support and helpful discussions with A. Toeppel, C.R. Scafe, A. Kejariwal, H.M. Wenz, M. Rhodes, S. Short, T. Woodage and D.A. Gilbert from Applied Biosystems is especially acknowledged. We thank C.-C. Chiang for preparing the submission of new SNPs to dbSNP. T.H. Karlsen (Rikshospitalet) is acknowledged for helpful discussions. We thank A. Forbes, J. Sanderson and S. Fisher for case ascertainment and establishment of the UK Crohn disease database. We acknowledge use of genotype data from the British 1958 Birth Cohort DNA collection, funded by Medical Research Council grant G0000934 and Wellcome Trust grant 068545/Z/02. This study was supported by the German Ministry of Education and Research (BMBF) through the National Genome Research Network (environmental diseases network and SMP-GEM), the POPGEN biobank, the analysis infrastructure and methods of the MediGrid project and the German Research Council (Ha 3091/1-1, 2-1), Applied Biosystems, TECAN, the Wellcome Trust and CORE (UK).

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Author notes

  1. Jochen Hampe and Andre Franke: These authors contributed equally to this work.

Authors and Affiliations

  1. Institute for Clinical Molecular Biology, Christian-Albrechts University Kiel, University Hospital Schleswig-Holstein, Kiel, 24105, Germany

    Jochen Hampe, Andre Franke, Philip Rosenstiel, Andreas Till, Markus Teuber, Robert Häsler & Stefan Schreiber

  2. First Department of Medicine, Christian-Albrechts University Kiel, University Hospital Schleswig-Holstein, Kiel, 24105, Germany

    Jochen Hampe, Ulrich R Fölsch & Stefan Schreiber

  3. Genome Analysis Group, Leibniz Institute for Age Research, Fritz Lipmann Institute, Beutenbergstrasse 11, Jena, 07745, Germany

    Klaus Huse & Matthias Platzer

  4. Max Planck Institute for Informatics, Stuhlsatzenhausweg 85, Saarbrücken, 66123, Germany

    Mario Albrecht, Gabriele Mayr & Thomas Lengauer

  5. Applied Biosystems, 850 Lincoln Center Drive, Foster City, 94404, California, USA

    Francisco M De La Vega, Jason Briggs & Simone Günther

  6. Department of Medical and Molecular Genetics, King's College London School of Medicine, London, SE1 9RT, UK

    Natalie J Prescott, Clive M Onnie & Christopher G Mathew

  7. Department of Pathology, Christian-Albrechts University Kiel, University Hospital Schleswig-Holstein, Kiel, 24105, Germany

    Bence Sipos

  8. Institute of Medical Informatics and Statistics, Christian-Albrechts University Kiel, University Hospital Schleswig-Holstein, Kiel, 24105, Germany

    Michael Krawczak

  9. Max-Planck Institute for Molecular Genetics, Ihnestr. 63, Berlin, 14195, Germany

    Philip Rosenstiel

Authors

  1. Jochen Hampe

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  2. Andre Franke

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  3. Philip Rosenstiel

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  4. Andreas Till

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  5. Markus Teuber

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  6. Klaus Huse

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  7. Mario Albrecht

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  8. Gabriele Mayr

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  9. Francisco M De La Vega

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  10. Jason Briggs

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  11. Simone Günther

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  12. Natalie J Prescott

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  13. Clive M Onnie

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  14. Robert Häsler

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  15. Bence Sipos

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  16. Ulrich R Fölsch

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  17. Thomas Lengauer

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  18. Matthias Platzer

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  19. Christopher G Mathew

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  20. Michael Krawczak

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  21. Stefan Schreiber

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Contributions

J.H. and A.F. established the genotyping and analysis methodology; A.F. performed the genotyping and association analysis and contributed to the writing of the manuscript; S.S. supervised the patient recruitment; J.H. recruited the German patients and drafted the manuscript; P.R., A.T., A.F., K.H., R.H., B.S. and M.P. performed the protein, immunohistochemistry and cDNA experiments; M.T. provided LIMS programming support; M.A., G.M. and T.L. performed in silico protein analysis and contributed to writing the manuscript; F.D.L.V. designed the cSNP panel and genotyping assays and contributed to the manuscript; J.B. and S.G. helped establish the SNPlex automation system; N.P., C.O. and C.M. performed the replication experiment in the UK samples; U.F. contributed to the design and the writing of the paper; M.K. provided genetic epidemiology consulting, performed the interaction analysis and helped draft the manuscript; and J.H. and S.S. jointly designed and supervised the experiment.

Corresponding authors

Correspondence to Jochen Hampe or Stefan Schreiber.

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Competing interests

A patent application has been filed regarding ATG16L1 as a susceptibility gene for Crohn disease.

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Hampe, J., Franke, A., Rosenstiel, P. et al. A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat Genet 39, 207–211 (2007). https://doi.org/10.1038/ng1954

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  • Received: 31 July 2006

  • Accepted: 05 December 2006

  • Published: 31 December 2006

  • Issue Date: 01 February 2007

  • DOI: https://doi.org/10.1038/ng1954