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GenomicsLoss-of-function due to MODY1/HNF4A mutation abrogates liver and pancreas differentiation from MODY1-hiPSCs
Loss-of-function due to MODY1/HNF4A mutation abrogates liver and pancreas differentiation from MODY1-hiPSCs
PRJNA416326 | ENA
TranscriptomicsLoss-of-function due to MODY1/HNF4A mutation abrogates liver and pancreas differentiation from MODY1-hiPSCs
Purpose: To investigate the impact of MODY1/HNF4A mutation on foregut development using differentiated control and MODY1-hiPSCs Methods: RNA-Seq was performed on foregut/hepato-pancreatic progenitors obtained on day 14 of the directed differentiation of hiPSCs from MODY1 patients (3 clones from iN90...
ORGANISM(S): Homo sapiens 
2019-06-01 | GSE106335 | GEO
UnknownHNF4A Haploinsufficiency in MODY1 Abrogates Liver and Pancreas Differentiation from Patient-Derived Induced Pluripotent Stem Cells.
Not available
S-EPMC6562146 | biostudies-literature
UnknownDouble heterozygous mutations involving both HNF1A/MODY3 and HNF4A/MODY1 genes: a case report.
Not available
S-EPMC2963490 | biostudies-literature
UnknownHypoxia reduces HNF4α/MODY1 protein expression in pancreatic β-cells by activating AMP-activated protein kinase.
Not available
S-EPMC5448099 | biostudies-literature
UnknownThe MODY1 gene for hepatocyte nuclear factor 4alpha and a feedback loop control COUP-TFII expression in pancreatic beta cells.
Not available
S-EPMC2447131 | biostudies-literature
GenomicsDrosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults [ChIP-seq]
Although mutations in the nuclear receptor HNF4A were identified as the cause of Maturity Onset Diabetes of the Young 1 (MODY1) nearly two decades ago, the mechanisms by which HNF4A regulates glucose homeostasis remain unclear. Here we report that loss of Drosophila HNF4 recapitulates hallmark sympt...
ORGANISM(S): Drosophila melanogaster 
2015-11-28 | GSE73675 | GEO
TranscriptomicsDrosophila HNF4 promotes glucose-stimulated insulin secretion and increased mitochondrial function in adults [RNA-seq]
Although mutations in the nuclear receptor HNF4A were identified as the cause of Maturity Onset Diabetes of the Young 1 (MODY1) nearly two decades ago, the mechanisms by which HNF4A regulates glucose homeostasis remain unclear. Here we report that loss of Drosophila HNF4 recapitulates hallmark sympt...
ORGANISM(S): Drosophila melanogaster 
2015-11-28 | GSE73523 | GEO
ProteomicsLC-MSMS study of hiPSC-derived β-like cells in different 3D Eevironments
In this project hiPSC-derived β-like cells were studied in two different 3D enviromnets; size-adjusted cell aggregates (using Aggrewell™ plates) and inside alginate capsules. The hiPSC derived from a patient with maturity-onset diabetes of the young 1 (MODY1), which is a monogenic diabetes form, cau...
ORGANISM(S): Homo sapiens (Human) 
2022-05-20 | PXD025054 | Pride
Nf4a Cell aggregates Tmt quantification Β-cell differentiation Global proteomics Crispr/cas9 Mody1 Hipsc Alginate encapsulation 
UnknownNovel presentations of congenital hyperinsulinism due to mutations in the MODY genes: HNF1A and HNF4A.
Not available
S-EPMC3674296 | biostudies-literature
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