Alternative splicing encodes functional intracellular CD59 isoforms that mediate insulin secretion and are down-regulated in diabetic islets
(2022) In Proceedings of the National Academy of Sciences of the United States of America 119(24).- 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.
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https://lup.lub.lu.se/record/4d6470f2-6d77-47f2-b366-aea95a54bc43
- author
- organization
- publishing date
- 2022-06-14
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Alternative Splicing, CD59 Antigens/genetics, Diabetes Mellitus/genetics, Humans, Insulin Secretion, Protein Isoforms/genetics
- in
- Proceedings of the National Academy of Sciences of the United States of America
- volume
- 119
- issue
- 24
- article number
- e2120083119
- pages
- 10 pages
- publisher
- National Academy of Sciences
- external identifiers
-
- scopus:85131345386
- pmid:35666870
- ISSN
- 1091-6490
- DOI
- 10.1073/pnas.2120083119
- language
- English
- LU publication?
- yes
- id
- 4d6470f2-6d77-47f2-b366-aea95a54bc43
- date added to LUP
- 2022-06-20 16:43:47
- date last changed
- 2024-09-18 18:13:20
@article{4d6470f2-6d77-47f2-b366-aea95a54bc43, abstract = {{<p>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.</p>}}, author = {{Golec, Ewelina and Ekström, Alexander and Noga, Maciej and Omar-Hmeadi, Muhmmad and Lund, Per-Eric and Villoutreix, Bruno O and Krus, Ulrika and Wozniak, Katarzyna and Korsgren, Olle and Renström, Erik and Barg, Sebastian and King, Ben C and Blom, Anna M}}, issn = {{1091-6490}}, keywords = {{Alternative Splicing; CD59 Antigens/genetics; Diabetes Mellitus/genetics; Humans; Insulin Secretion; Protein Isoforms/genetics}}, language = {{eng}}, month = {{06}}, number = {{24}}, publisher = {{National Academy of Sciences}}, series = {{Proceedings of the National Academy of Sciences of the United States of America}}, title = {{Alternative splicing encodes functional intracellular CD59 isoforms that mediate insulin secretion and are down-regulated in diabetic islets}}, url = {{http://dx.doi.org/10.1073/pnas.2120083119}}, doi = {{10.1073/pnas.2120083119}}, volume = {{119}}, year = {{2022}}, }