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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| Abstract | 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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| AbstractList | 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. 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.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. 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. |
| Author | Kefalas, George Larose, Louise |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29168198$$D View this record in MEDLINE/PubMed |
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| Copyright | 2017 Société Française des Microscopies and Société de Biologie Cellulaire de France. Published by John Wiley & Sons Ltd 2017 Société Française des Microscopies and Société de Biologie Cellulaire de France. Published by John Wiley & Sons Ltd. |
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| Keywords | Peptide hormones/insulin Pancreas Endoplasmic reticulum Apoptosis Diseases |
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| Snippet | 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... 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... |
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| SubjectTerms | Activating Transcription Factor 4 - genetics Activating Transcription Factor 4 - immunology Adult Animals Apoptosis Diabetes Mellitus, Experimental - enzymology Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - immunology Diabetes Mellitus, Experimental - pathology Diabetes Mellitus, Type 1 - enzymology Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - pathology Diabetes Mellitus, Type 2 - enzymology Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - immunology Diabetes Mellitus, Type 2 - pathology Diseases eIF-2 Kinase - deficiency eIF-2 Kinase - genetics eIF-2 Kinase - immunology Endoplasmic reticulum Epiphyses - abnormalities Epiphyses - enzymology Epiphyses - immunology Epiphyses - pathology Eukaryotic Initiation Factor-2 - genetics Eukaryotic Initiation Factor-2 - immunology Gene Expression Regulation, Developmental Homeostasis - genetics Homeostasis - immunology Humans Infant, Newborn Insulin-Secreting Cells - enzymology Insulin-Secreting Cells - immunology Insulin-Secreting Cells - pathology NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - immunology Osteochondrodysplasias - enzymology Osteochondrodysplasias - genetics Osteochondrodysplasias - immunology Osteochondrodysplasias - pathology Pancreas Peptide hormones/insulin Signal Transduction |
| Title | PERK leads a hub dictating pancreatic β cell homoeostasis |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fboc.201700059 https://www.ncbi.nlm.nih.gov/pubmed/29168198 https://www.proquest.com/docview/1967861278 |
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