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Intestinal expression of SHIP in inflammatory bowel diseases
  1. Ingrid Arijs1,
  2. Gert De Hertogh2,
  3. Bart Lemmens2,
  4. Jan Van der Goten1,
  5. Séverine Vermeire1,
  6. Frans Schuit3,
  7. Paul Rutgeerts1
  1. 1Department of Gastroenterology, Translational Research Center for Gastrointestinal Disorders (TARGID), University Hospital Gasthuisberg, Catholic University Leuven, Leuven, Belgium
  2. 2Department of Morphology and Molecular Pathology, University Hospital Gasthuisberg, Leuven, Belgium
  3. 3Gene Expression Unit, Department of Molecular Cell Biology, Catholic University Leuven, Leuven, Belgium
  1. Correspondence to Professor Dr Paul Rutgeerts, Department of Gastroenterology, University Hospital Gasthuisberg, Herestraat 49, mailbox 7003, B-3000 Leuven, Belgium; paul.rutgeerts{at}uzleuven.be

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We read with interest the recent paper in Gut by Kerr and colleagues1 describing a new mouse model of Crohn's disease (CD)-like ileitis caused by Src homology 2 domain-containing inositol-5′-phosphatase (SHIP) deficiency. The human SHIP protein, encoded by the INPP5D gene on chromosome 2q37.1, is an enzyme that hydrolyses the 5′-phosphate of phosphatidylinositol-(3,4,5)-trisphosphate so that it counteracts stimulatory pathways such as phosphoinositide 3-kinase. The enzyme is regulated by tyrosine phosphorylation in haematopoietic cells following activation of surface receptors for various cytokines or in response to B cell antigen receptor cross-linking or T cell activation. In previous studies, the authors showed that SHIP signalling plays …

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