ArticleDevelopmental biology2015
REST represses a subset of the pancreatic endocrine differentiation program.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- Mining the transcriptome of target tissues of autoimmune and degenerative pancreatic β-cell and brain diseases to discover therapies.iScience · 2022Article
- Pancreatic cell fate specification: insights into developmental mechanisms and their application for lineage reprogramming.Current opinion in genetics & development · 2021Review
- REST is a major negative regulator of endocrine differentiation during pancreas organogenesis.Genes & development · 2021Article
- Harnessing the Endogenous Plasticity of Pancreatic Islets: A Feasible Regenerative Medicine Therapy for Diabetes?International journal of molecular sciences · 2021Review
- Loss of RE-1 silencing transcription factor accelerates exocrine damage from pancreatic injury.Cell death & disease · 2020Article
- News about the Role of the Transcription Factor REST in Neurons: From Physiology to Pathology.International journal of molecular sciences · 2019Review
- Molecular Modelling of Islet β-Cell Adaptation to Inflammation in Pregnancy and Gestational Diabetes Mellitus.International journal of molecular sciences · 2019Review
- Patterns of differential gene expression in a cellular model of human islet development, and relationship to type 2 diabetes predisposition.Diabetologia · 2018Article
- The type 2 diabetes-associated HMG20A gene is mandatory for islet beta cell functional maturity.Cell death & disease · 2018Article
- Review
- Neuron-enriched RNA-binding Proteins Regulate Pancreatic Beta Cell Function and Survival.The Journal of biological chemistry · 2017Article
- The Importance of REST for Development and Function of Beta Cells.Frontiers in cell and developmental biology · 2017Review
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
To contribute to devise successful beta-cell differentiation strategies for the cure of Type 1 diabetes we sought to uncover barriers that restrict endocrine fate acquisition by studying the role of the transcriptional repressor REST in the developing pancreas. Rest expression is prevented in neurons and in endocrine cells, which is necessary for their normal function. During development, REST represses a subset of genes in the neuronal differentiation program and Rest is down-regulated as neurons differentiate. Here, we investigate the role of REST in the differentiation of pancreatic endocrine cells, which are molecularly close to neurons. We show that Rest is widely expressed in pancreas progenitors and that it is down-regulated in differentiated endocrine cells. Sustained expression of REST in Pdx1(+) progenitors impairs the differentiation of endocrine-committed Neurog3(+) progenitors, decreases beta and alpha cell mass by E18.5, and triggers diabetes in adulthood. Conditional inactivation of Rest in Pdx1(+) progenitors is not sufficient to trigger endocrine differentiation but up-regulates a subset of differentiation genes. Our results show that the transcriptional repressor REST is active in pancreas progenitors where it gates the activation of part of the beta cell differentiation program.
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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.