PERK leads a hub dictating pancreatic β cell homoeostasis
In humans, the pathogenesis of diabetes is characterised by two major pancreatic β cell defects: a reduction in β cell mass and the failure of β cells to produce enough insulin. Over the past two decades, multiple studies involving cell cultures, animal models and human subjects have established the...
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Published in | Biology of the cell Vol. 110; no. 2; pp. 27 - 32 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
01.02.2018
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Subjects | |
Online Access | Get full text |
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Summary: | In humans, the pathogenesis of diabetes is characterised by two major pancreatic β cell defects: a reduction in β cell mass and the failure of β cells to produce enough insulin. Over the past two decades, multiple studies involving cell cultures, animal models and human subjects have established the importance of the protein kinase RNA‐like endoplasmic reticulum kinase (PERK) in the adaptive functional capacity of pancreatic β cells during embryonic development and into adulthood. In this review, we will highlight major findings identifying PERK as a crucial player in β cell physiology and in diabetes.
Review
Protein kinase RNA‐like endoplasmic reticulum kinase (PERK) is a crucial player in pancreatic β cell physiology and in diabetes. Through multiple independent pathways, PERK maintains β cell homeostasis by promoting β cell proliferation, insulin processing and insulin secretion. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 0248-4900 1768-322X 1768-322X |
DOI: | 10.1111/boc.201700059 |