Alternative splicing encodes functional intracellular CD59 isoforms that mediate insulin secretion and are down-regulated in diabetic islets-Reference-Cited by-同舟云学术

Alternative splicing encodes functional intracellular CD59 isoforms that mediate insulin secretion and are down-regulated in diabetic islets

Published:2022-06-06 Issue:24 Volume:119 Page:
ISSN:0027-8424
Container-title:Proceedings of the National Academy of Sciences
language:en
Short-container-title:Proc. Natl. Acad. Sci. U.S.A.

Author:

Golec Ewelina¹,Ekström Alexander¹^ORCID,Noga Maciej¹,Omar-Hmeadi Muhmmad²,Lund Per-Eric²,Villoutreix Bruno O.³,Krus Ulrika⁴,Wozniak Katarzyna¹,Korsgren Olle⁵^ORCID,Renström Erik⁴,Barg Sebastian²^ORCID,King Ben C.¹^ORCID,Blom Anna M.¹^ORCID

Affiliation:

1. Section of Medical Protein Chemistry, Department of Translational Medicine, Lund University, 214-28 Malmö, Sweden

2. Department of Medical Cell Biology, Uppsala University, BMC 571, 75123 Uppsala, Sweden

3. Université Paris Cité, Department of Neuroscience, NeuroDiderot, Inserm U1141, Paris, F-75019 France

4. Lund University Diabetes Centre, Department of Clinical Sciences Malmö, Lund University, 214-28 Malmö, Sweden

5. Department of Immunology, Genetics, and Pathology, Uppsala University, 751 85 Uppsala, Sweden

Abstract

Significance This project describes the existence of previously unknown non–GPI-anchored CD59 isoforms required for insulin secretion, named CD59–IRIS-1 and CD59–IRIS-2, and finds reduced expression of CD59-IRIS isoforms in human diabetic islets, showing a link between dysregulation of IRIS isoforms and defects in insulin secretion in diabetic patients. These data open a path for future studies into CD59-IRIS expression and function in additional cell types capable of regulated secretion. Identification of additional specific CD59-IRIS binding partners within the cell could provide therapeutic targets for enhancement of insulin secretion in T2D.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Link

https://pnas.org/doi/pdf/10.1073/pnas.2120083119

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