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PS2 - 5. Insulin degradation via the ERAD pathway; the production of auto-antigens in type 1 diabetes

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Nederlands Tijdschrift voor Diabetologie Aims and scope

Abstract

A high insulin demand requires efficient folding and oxidation of proinsulin molecules in the ER lumen of pancreatic β-cells. When molecules fail to fold, either due to ER stress or because of a mutation within the amino acid sequence, proteins are targeted for degradation.

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Authors and Affiliations

  1. Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands

    Hanneke Hoelen & Emmanuel Wiertz

  2. Department of Molecular Cell Biology, LUMC, Leiden, The Netherlands

    Arnaud Zaldumbide & Rob Hoeben

  3. http://www.bsl.nl

    Maaike Ressing, Eelco de Koning & Bart Roep

Authors
  1. Hanneke Hoelen
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  2. Arnaud Zaldumbide
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  3. Maaike Ressing
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  4. Eelco de Koning
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  5. Rob Hoeben
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  6. Bart Roep
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  7. Emmanuel Wiertz
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Additional information

1 Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands, 2 Department of Molecular Cell Biology, LUMC, Leiden, The Netherlands, 3 Department of Immunohematology and Blood Transfusion, LUMC, Leiden, The Netherlands.

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Hoelen, H., Zaldumbide, A., Ressing, M. et al. PS2 - 5. Insulin degradation via the ERAD pathway; the production of auto-antigens in type 1 diabetes. NED. TIJDSCHR. DIABET. 11, 139 (2013). https://doi.org/10.1007/s12467-013-0073-z

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  • DOI: https://doi.org/10.1007/s12467-013-0073-z

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