Extensive NEUROG3 occupancy in the human pancreatic endocrine gene regulatory network.
Fiche publication
Date publication
août 2021
Journal
Molecular metabolism
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BIRCK Catherine, Dr GRADWOHL Gérard, Dr SCHREIBER Valérie
Tous les auteurs :
Schreiber V, Mercier R, Jiménez S, Ye T, García-Sánchez E, Klein A, Meunier A, Ghimire S, Birck C, Jost B, Honnens de Lichtenberg K, Honoré C, Serup P, Gradwohl G
Lien Pubmed
Résumé
Mice lacking the bHLH transcription factor (TF) Neurog3 do not form pancreatic islet cells, including insulin secreting beta cells, causing diabetes. In human, homozygous mutations of NEUROG3 manifest with neonatal or childhood diabetes. Despite this critical role in islet cell development, the precise function and downstream genetic programs regulated directly by NEUROG3 remain elusive. Therefore, we mapped genome-wide NEUROG3 occupancy in human induced pluripotent stem cell (iPSC)-derived endocrine progenitors and determined NEUROG3 dependency of associated genes to uncover direct targets.
Mots clés
CUT&RUN, NEUROG3, SNPs, T2DM, iPSC, islet progenitors
Référence
Mol Metab. 2021 Aug 2;:101313