M C Wapenaar

Summary

Affiliation: University Medical Center Groningen
Country: The Netherlands

Publications

  1. ncbi request reprint Associations with tight junction genes PARD3 and MAGI2 in Dutch patients point to a common barrier defect for coeliac disease and ulcerative colitis
    M C Wapenaar
    Genetics Department, University Medical Center Groningen, PO Box 30001, 9700 RB Groningen, The Netherlands
    Gut 57:463-7. 2008
  2. pmc The SPINK gene family and celiac disease susceptibility
    Martin C Wapenaar
    Complex Genetics Section, DBG Department of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands
    Immunogenetics 59:349-57. 2007
  3. doi request reprint Intestinal barrier gene variants may not explain the increased levels of antigliadin antibodies, suggesting other mechanisms than altered permeability
    Victorien M Wolters
    Department of Pediatric Gastroenterology, UMC Utrecht, Utrecht, The Netherlands
    Hum Immunol 71:392-6. 2010
  4. ncbi request reprint Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect
    Alienke J Monsuur
    Complex Genetics Section, DBG Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands
    Nat Genet 37:1341-4. 2005
  5. ncbi request reprint No genetic association of the human prolyl endopeptidase gene in the Dutch celiac disease population
    Begona Diosdado
    Complex Genetics Section, Dept of Biomedical Genetics, Univ Medical Centre Utrecht, Utrecht, The Netherlands
    Am J Physiol Gastrointest Liver Physiol 289:G495-500. 2005
  6. ncbi request reprint Genetic and functional analysis of pyroglutamyl-peptidase I in coeliac disease
    Alienke J Monsuur
    Complex Genetics Section, DBG Department of Medical Genetics, University Medical Centre, Utrecht, The Netherlands
    Eur J Gastroenterol Hepatol 18:637-44. 2006
  7. pmc A microarray screen for novel candidate genes in coeliac disease pathogenesis
    B Diosdado
    Complex Genetics Group, Department of Biomedical Genetics, University Medical Centre, Utrecht, The Netherlands
    Gut 53:944-51. 2004
  8. ncbi request reprint The interferon gamma gene in celiac disease: augmented expression correlates with tissue damage but no evidence for genetic susceptibility
    Martin C Wapenaar
    Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands
    J Autoimmun 23:183-90. 2004
  9. ncbi request reprint Neutrophil recruitment and barrier impairment in celiac disease: a genomic study
    Begona Diosdado
    Department of Medical Genetics, Division of Biomedical Genetics, University Medical Center, Utrecht, The Netherlands
    Clin Gastroenterol Hepatol 5:574-81. 2007
  10. ncbi request reprint Inflammatory bowel disease and celiac disease: overlaps in the pathology and genetics, and their potential drug targets
    Eleonora A M Festen
    Department of Genetics, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands
    Endocr Metab Immune Disord Drug Targets 9:199-218. 2009

Collaborators

Detail Information

Publications16

  1. ncbi request reprint Associations with tight junction genes PARD3 and MAGI2 in Dutch patients point to a common barrier defect for coeliac disease and ulcerative colitis
    M C Wapenaar
    Genetics Department, University Medical Center Groningen, PO Box 30001, 9700 RB Groningen, The Netherlands
    Gut 57:463-7. 2008
    ..Previous studies showed the association of both diseases with variants in MYO9B, presumably involved in epithelial permeability...
  2. pmc The SPINK gene family and celiac disease susceptibility
    Martin C Wapenaar
    Complex Genetics Section, DBG Department of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands
    Immunogenetics 59:349-57. 2007
    ..SPINK4 exhibits CD pathology-related differential gene expression, likely derived from altered goblet cell activity. All of the four SPINK genes tested do not contribute to the genetic risk for CD in the Dutch population...
  3. doi request reprint Intestinal barrier gene variants may not explain the increased levels of antigliadin antibodies, suggesting other mechanisms than altered permeability
    Victorien M Wolters
    Department of Pediatric Gastroenterology, UMC Utrecht, Utrecht, The Netherlands
    Hum Immunol 71:392-6. 2010
    ..Thus, other immunologic phenomena play a role in the increased prevalence of elevated AGA in patients with Down syndrome, possibly involving altered induction and/or maintenance of tolerance...
  4. ncbi request reprint Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect
    Alienke J Monsuur
    Complex Genetics Section, DBG Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands
    Nat Genet 37:1341-4. 2005
    ..55 x 10(-5)). This result is suggestive of a primary impairment of the intestinal barrier in the etiology of celiac disease, which may explain why immunogenic gluten peptides are able to pass through the epithelial barrier...
  5. ncbi request reprint No genetic association of the human prolyl endopeptidase gene in the Dutch celiac disease population
    Begona Diosdado
    Complex Genetics Section, Dept of Biomedical Genetics, Univ Medical Centre Utrecht, Utrecht, The Netherlands
    Am J Physiol Gastrointest Liver Physiol 289:G495-500. 2005
    ..These are further supported by the activity determinations in which we observed no differences in PREP activity between CD patients and controls...
  6. ncbi request reprint Genetic and functional analysis of pyroglutamyl-peptidase I in coeliac disease
    Alienke J Monsuur
    Complex Genetics Section, DBG Department of Medical Genetics, University Medical Centre, Utrecht, The Netherlands
    Eur J Gastroenterol Hepatol 18:637-44. 2006
    ..We also determined the enzymatic activity of PGPEPI in duodenal biopsies. Our results uniformly indicate that PGPEP1 is not involved in the aetiology and pathology of CD...
  7. pmc A microarray screen for novel candidate genes in coeliac disease pathogenesis
    B Diosdado
    Complex Genetics Group, Department of Biomedical Genetics, University Medical Centre, Utrecht, The Netherlands
    Gut 53:944-51. 2004
    ..The causative molecular pathways underlying the pathogenesis of coeliac disease are poorly understood. To unravel novel aspects of disease pathogenesis, we used microarrays to determine changes in gene expression of duodenal biopsies...
  8. ncbi request reprint The interferon gamma gene in celiac disease: augmented expression correlates with tissue damage but no evidence for genetic susceptibility
    Martin C Wapenaar
    Department of Biomedical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands
    J Autoimmun 23:183-90. 2004
    ..Likewise, all alleles were randomly transmitted to affected children in parents-case trios. There is no evidence for IFNG as a predisposing gene in CD, despite its enhanced expression in patients in complete remission...
  9. ncbi request reprint Neutrophil recruitment and barrier impairment in celiac disease: a genomic study
    Begona Diosdado
    Department of Medical Genetics, Division of Biomedical Genetics, University Medical Center, Utrecht, The Netherlands
    Clin Gastroenterol Hepatol 5:574-81. 2007
    ..To assess the contribution of either immune response we performed global gene expression profiling of the regenerating mucosa...
  10. ncbi request reprint Inflammatory bowel disease and celiac disease: overlaps in the pathology and genetics, and their potential drug targets
    Eleonora A M Festen
    Department of Genetics, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands
    Endocr Metab Immune Disord Drug Targets 9:199-218. 2009
    ..We describe the details and overlaps in the pathomechanism and genetics of inflammatory bowel disease and celiac disease, and discuss potential drug targets for intervention...
  11. ncbi request reprint Association analysis of MYO9B gene polymorphisms with celiac disease in a Swedish/Norwegian cohort
    Silja S Amundsen
    Institute of Immunology, University of Oslo, Rikshospitalet University Hospital, Oslo, Norway
    Hum Immunol 67:341-5. 2006
    ..Alternatively, it might be due to variable linkage disequilibria in distinct populations in the tested SNPs and a causative mutation yet to be identified or to false positive findings (type I error) in the Dutch study...
  12. pmc A genome-wide association study for celiac disease identifies risk variants in the region harboring IL2 and IL21
    David A van Heel
    Centre for Gastroenterology, Institute of Cell and Molecular Science, Queen Mary University of London, London E1 2AT, UK
    Nat Genet 39:827-9. 2007
    ..3 x 10(-14), odds ratio = 0.63), suggesting that genetic variation in this region predisposes to celiac disease...
  13. pmc Newly identified genetic risk variants for celiac disease related to the immune response
    Karen A Hunt
    Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, 4 Newark Street, London E1 2AT, UK
    Nat Genet 40:395-402. 2008
    ..Type 1 diabetes and celiac disease share HLA-DQ, IL2-IL21, CCR3 and SH2B3 risk regions. Thus, this extensive genome-wide association follow-up study has identified additional celiac disease risk variants in relevant biological pathways...
  14. ncbi request reprint A functional candidate screen for coeliac disease genes
    Christine R Curley
    The Broad Institute, Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA
    Eur J Hum Genet 14:1215-22. 2006
    ..The findings in coeliac disease need to be replicated. Expanding genetic association studies of these cytochrome genes to other inflammatory conditions should reveal whether their causative influence extends beyond coeliac disease...
  15. ncbi request reprint A novel splicing mutation in KCNQ2 in a multigenerational family with BFNC followed for 25 years
    Gerrit Jan de Haan
    Epilepsy Institute of The Netherlands, Heemstede, Netherlands
    Epilepsia 47:851-9. 2006
    ..A large multigenerational family with benign familial neonatal convulsions (BFNC) was revisited to identify the disease-causing mutation and to assess long-term outcome...
  16. ncbi request reprint A combined genetics and genomics approach to unravelling molecular pathways in coeliac disease
    Martin C Wapenaar
    Complex Genetics Group, Department of Biomedical Genetics, University Medical Centre Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands
    Novartis Found Symp 267:113-34; discussion 134-44. 2005
    ..Furthermore, expression data will point to the molecular pathways involved in the disease pathogenesis...