scholarly journals Pancreatic β Cell Identity Is Maintained by DNA Methylation-Mediated Repression of Arx

2011 ◽  
Vol 20 (4) ◽  
pp. 419-429 ◽  
Author(s):  
Sangeeta Dhawan ◽  
Senta Georgia ◽  
Shuen-ing Tschen ◽  
Guoping Fan ◽  
Anil Bhushan
Keyword(s):  
Dna Methylation ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity

scholarly journals Multiomic Profiling Identifies cis-Regulatory Networks Underlying Human Pancreatic β Cell Identity and Function

Cell Reports ◽  
2019 ◽  
Vol 26 (3) ◽  
pp. 788-801.e6 ◽  
Author(s):  
Nathan Lawlor ◽  
Eladio J. Márquez ◽  
Peter Orchard ◽  
Narisu Narisu ◽  
Muhammad Saad Shamim ◽  
...  
Keyword(s):  
Regulatory Networks ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity ◽  
And Function

scholarly journals Transcription factor ATF4 maintains pancreatic β-cell identity during ER stress

2021 ◽  
Vol 94 (0) ◽  
pp. 2-Y-E2-1
Author(s):  
Keisuke Kitakaze ◽  
Miho Oyadomari ◽  
Jun Zhang ◽  
Yoshimasa Hamada ◽  
Yasuhiro Takenouchi ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Er Stress ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity

scholarly journals A point mutation in the Pdia6 gene results in loss of pancreatic β-cell identity causing overt diabetes

2021 ◽  
pp. 101334
Author(s):  
Nirav Florian Chhabra ◽  
Anna-Lena Amend ◽  
Aimée Bastidas-Ponce ◽  
Sibylle Sabrautzki ◽  
Marta Tarquis-Medina ◽  
...  
Keyword(s):  
Point Mutation ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity ◽  
Overt Diabetes

scholarly journals Epigenetic Regulation of β Cell Identity and Dysfunction

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaoqiang Sun ◽  
Liu Wang ◽  
S. M. Bukola Obayomi ◽  
Zong Wei
Keyword(s):  
Dna Methylation ◽  
Histone Modification ◽  
Driving Forces ◽  
Β Cells ◽  
Β Cell ◽  
Cell Identity ◽  
Potential Implication ◽  
Postnatal Maturation ◽  
Cell Dysfunction ◽  
Epigenetic Signatures

β cell dysfunction and failure are driving forces of type 2 diabetes mellitus (T2DM) pathogenesis. Investigating the underlying mechanisms of β cell dysfunction may provide novel targets for the development of next generation therapy for T2DM. Epigenetics is the study of gene expression changes that do not involve DNA sequence changes, including DNA methylation, histone modification, and non-coding RNAs. Specific epigenetic signatures at all levels, including DNA methylation, chromatin accessibility, histone modification, and non-coding RNA, define β cell identity during embryonic development, postnatal maturation, and maintain β cell function at homeostatic states. During progression of T2DM, overnutrition, inflammation, and other types of stress collaboratively disrupt the homeostatic epigenetic signatures in β cells. Dysregulated epigenetic signatures, and the associating transcriptional outputs, lead to the dysfunction and eventual loss of β cells. In this review, we will summarize recent discoveries of the establishment and disruption of β cell-specific epigenetic signatures, and discuss the potential implication in therapeutic development.

scholarly journals Pancreatic β-cell specific loss of E2f1 impairs insulin secretion and β-cell identity through the epigenetic repression of non β-cell programs

2020 ◽  
Author(s):  
Frédérik Oger ◽  
Cyril Bourouh ◽  
Xavier Gromada ◽  
Maeva Moreno ◽  
Charlène Carney ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Histone Deacetylase Inhibitors ◽  
Molecular Mechanisms ◽  
Human Islets ◽  
Gene Promoters ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity ◽  
Specific Loss ◽  
Epigenetic Repression

AbstractThe loss of pancreatic β-cell identity emerges as an important feature of type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore the cell-autonomous role of the cell cycle regulator and transcription factor E2F1 in the maintenance of β-cell identity and insulin secretion. We show that the β-cell-specific loss of E2f1 function in mice triggers glucose intolerance associated with defective insulin secretion, an altered α-to-β-cell ratio, a downregulation of many β-cell genes and a concomitant increase of non-β-cell markers. Mechanistically, the epigenomic profiling of non-beta cell upregulated gene promoters identified an enrichment of bivalent H3K4me3/H3K27me3 or H3K27me3 marks. Conversely, downregulated genes were enriched in active chromatin H3K4me3 and H3K27ac histone marks. We find that histone deacetylase inhibitors modulate E2F1 transcriptional and epigenomic signatures associated with these β-cell dysfunctions. Finally, the pharmacological inhibition of E2F transcriptional activity in human islets also impairs insulin secretion and the expression of β-cell identity genes. Our data suggest that E2F1 is critical for maintaining β-cell identity through a sustained repression of non β-cell transcriptional programs.

scholarly journals LKB1 and AMPK differentially regulate pancreatic β‐cell identity

2014 ◽  
Vol 28 (11) ◽  
pp. 4972-4985 ◽  
Author(s):  
Marina Kone ◽  
Timothy J. Pullen ◽  
Gao Sun ◽  
Mark Ibberson ◽  
Aida Martinez‐Sanchez ◽  
...  
Keyword(s):  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity

scholarly journals Pancreatic β-cell identity in diabetes

2016 ◽  
Vol 18 ◽  
pp. 110-116 ◽  
Author(s):  
M. S. Remedi ◽  
C. Emfinger
Keyword(s):  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity

scholarly journals The transcription factorPax6is required for pancreatic β cell identity, glucose-regulated ATP synthesis, and Ca2+dynamics in adult mice

2017 ◽  
Vol 292 (21) ◽  
pp. 8892-8906 ◽  
Author(s):  
Ryan K. Mitchell ◽  
Marie-Sophie Nguyen-Tu ◽  
Pauline Chabosseau ◽  
Rebecca M. Callingham ◽  
Timothy J. Pullen ◽  
...  
Keyword(s):  
Atp Synthesis ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Identity ◽  
Adult Mice
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