ArticleBMC cell biology2007
PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice.
Article in BMC cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Frequency and spectrum of Wolcott-Rallison syndrome in Saudi Arabia: a systematic review.The Libyan journal of medicine · 2013Pooled it
- The PERK inhibitor GSK2606414 evokes developmental defects in zebrafish consistent with Wolcott-Rallison syndrome phenotypes.Pharmacological reports : PR · 2026Article
- The transcription factors Tfeb and Tfe3 are required for survival and embryonic development of pancreas and liver in zebrafish.PLoS genetics · 2025Article
- Predicting cellular adaptation proteins dependent on eIF2α regulation under stress conditions: Physiological and pathophysiological implications in neuronal function.Computational and structural biotechnology journal · 2025Article
- The Integrated Stress Response in Pancreatic Development, Tissue Homeostasis, and Cancer.Gastroenterology · 2024Review
- Targeting Endoplasmic Reticulum Stress as an Effective Treatment for Alcoholic Pancreatitis.Biomedicines · 2022Review
- A possible connection between reactive oxygen species and the unfolded protein response in lens development: From insight to foresight.Frontiers in cell and developmental biology · 2022Review
- Co-opting regulation bypass repair as a gene-correction strategy for monogenic diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- PERK in POMC neurons connects celastrol with metabolism.JCI insight · 2021Article
- Targeting the integrated stress response in ophthalmology.Current eye research · 2021Review
- Article
- Downregulation of ceramide synthase 1 promotes oral cancer through endoplasmic reticulum stress.International journal of oral science · 2021Article
- Review
- ATF4-mediated histone deacetylase HDAC1 promotes the progression of acute pancreatitis.Cell death & disease · 2021Article
- PERK Signaling Controls Myoblast Differentiation by Regulating MicroRNA Networks.Frontiers in cell and developmental biology · 2021Article
- Perfluorooctanoic acid activates the unfolded protein response in pancreatic acinar cells.Journal of biochemical and molecular toxicology · 2020Article
- Translational induction of ATF4 during integrated stress response requires noncanonical initiation factors eIF2D and DENR.Nature communications · 2020Article
- Lessons from animal models of endocrine disorders caused by defects of protein folding in the secretory pathway.Molecular and cellular endocrinology · 2020Review
- ER-associated degradation in health and disease - from substrate to organism.Journal of cell science · 2019Review
- What makes a good new therapeutic L-asparaginase?World journal of microbiology & biotechnology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDeficiency of the PERK eIF2 alpha kinase in humans and mice results in postnatal exocrine pancreatic atrophy as well as severe growth and metabolic anomalies in other organs and tissues. To determine if the exocrine pancreatic atrophy is due to a cell-autonomous defect, the Perk gene was specifically ablated in acinar cells of the exocrine pancreas in mice.
resultsWe show that expression of PERK in the acinar cells is required to maintain their viability but is not required for normal protein synthesis and secretion. Exocrine pancreatic atrophy in PERK-deficient mice was previously attributed to uncontrolled ER-stress followed by apoptotic cell death based on studies in cultured fibroblasts. However, we have found no evidence for perturbations in the endoplasmic reticulum or ER-stress and show that acinar cells succumb to a non-apoptotic form of cell death, oncosis, which is associated with a pronounced inflammatory response and induction of the pancreatitis stress response genes. We also show that mice carrying a knockout mutation of PERK's downstream target, ATF4, exhibit pancreatic deficiency caused by developmental defects and that mice ablated for ATF4's transcriptional target CHOP have a normal exocrine pancreas.
conclusionWe conclude that PERK modulates secretory capacity of the exocrine pancreas by regulating cell viability of acinar cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.