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Lysine 117 Residue is Essential for the Function of the Hepatocyte nuclear factor 1α

ABSTRACT: Lysine 117 Residue is Essential for the Function of the Hepatocyte nuclear factor 1α

PROVIDER: PRJNA857016 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20048058_1.fastq.gz	Fastqsanger.gz
	SRR20048058_2.fastq.gz	Fastqsanger.gz
	SRR20048059_1.fastq.gz	Fastqsanger.gz
	SRR20048059_2.fastq.gz	Fastqsanger.gz
	SRR20048060_1.fastq.gz	Fastqsanger.gz

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Lysine 117 Residue is Essential for the Function of the Hepatocyte nuclear factor 1α

Project description:Hepatocyte nuclear factor 1α (HNF1α) play essential roles in controlling development and metabolism, its mutations are clearly linked to the occurrence of maturity-onset diabetes of the young (MODY3) in human. 117 lysine to glutamic acid (E117) mutation in the HNF1α gene was clinically associated with MOYD3, but no functional data on this variant is available. Here, we generated a knock-in mouse model in which the lysine 117 is replaced with glutamic acid in the endogenous murine HNF1α locus. The HNF1αE117/E117 mice reproduced HNF1-null phenotypes including dwarfism, hepatic dysfunction, renal Fanconi syndrome, diabetes and die from a progressive wasting syndrome, but no hyperphenylalaninemia. Moreover, HNF1αE117/E117 mice shared similar hepatic gene expression profiles with HNF1 deficient mice. In vitro experiments showed that HNF1 mutants in which the lysine 117 residue were replaced by glutamic acid, arginine or glutamine residues, respectively, had a significant decreased in overall transactivation and DNA binding capacity. K117 mutants had no effect on its protein stabilities and nuclear localization, but significantly blocked its own association. Our results clearly demonstrate that the lysine 117 residue is essential for the function of the HNF1a, and prove important to identify the molecular basis for diseases associated with defects in HNF1α We then performed gene expression profiling analysis using data obtained from RNA-seq of liver tissue of 3 WT mice and 3 KI mice.

2023-01-01 | GSE207758 | GEO

Lysine 117 residue is essential for the function of the hepatocyte nuclear factor 1α in pancreas

Project description:Lysine 117 residue is essential for the function of the hepatocyte nuclear factor 1α in pancreas

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Lysine 117 residue is essential for the function of the hepatocyte nuclear factor 1α in pancreas

Project description:To determine the impact of K117E mutation on HNF1α functions, we generated a C57BL/6J knock-in mouse model wherein the lysine 117 (K117) was replaced with glutamic acid (E117) in the endogenous murine HNF1α locus by CRISPR/Cas9. We then performed gene expression profiling analysis using data obtained from RNA-seq of pancreas of WT and HNF1αK1117E Hom mice of 9 weeks old (n=3/group)

2023-11-23 | GSE232242 | GEO

MYLIP attenuates hypoxia tolerance by inducing K27-linked polyubiquitination and subsequent proteasomal degradation of HIF-α

Project description:Hypoxia tolerance is mainly controlled by the hypoxia signaling pathway and HIF-1α/2α serve as master regulators in this pathway. Here we identify MYLIP, an E3 ubiquitin ligase thought to specifically target lipoprotein receptors, as a negative regulator of HIF-1α/2α. MYLIP interacts with HIF-1α/2α and catalyzes K27-linked polyubiquitination at lysine 118/442 (HIF-1α) or lysine 117 (HIF-2α). This modification induces proteasomal degradation of HIF-1α, resulting in inhibition of hypoxia signaling. Furthermore, Mylip-deficient bluntsnout bream, zebrafish and mice are more tolerant to hypoxia. These findings reveal a role for MYLIP in regulating hypoxia signaling and identify a target for developing fish strains with high hypoxia tolerance for the benefit of the

2024-12-04 | GSE283363 | GEO

Bosea sp. 117

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Epigenetic analysis of hepatocyte-like cells from MSC-Ucs.

Project description:Global DNA methylation profiling of hepatocyte-like cells. We established a protein-based artificial transcription system and successfully engineered human hepatocyte-like cells from human umbilical cord-derived mesenchymal stem cells (MSC-UCs). We utilized four artificial transcription factors (ATFs) that targeted hepatocyte nuclear factor (HNF)1α, HNF3γ, HNF4α and GATA4 (4F), and found that treatment with 4F for 3 (4Fd3) or 5 (4Fd5) days converted MSC-UCs to hepatocyte-like cells. We then examined global DNA methylation profiles of 4Fd3, 4Fd5, NTP-EGFP protein treated cells (NE) and non-treated cells (NC).

2022-06-09 | GSE205546 | GEO

Loss of Hepatocyte-Nuclear-Factor-1α Impacts on Adult Mouse Intestinal Epithelial Cell Growth and Cell Lineages Differentiation

Project description:Although hepatocyte-nuclear-factor-1α (Hnf1α) is crucial for pancreas and liver functions, it is believed to play a limited functional role for intestinal epithelial functions. The aim of this study was to assess the consequences of abrogating Hnf1α on the maintenance of adult small intestinal epithelial functions. Methodology/Principal Findings An Hnf1α knockout mouse model was used. Assessment of histological abnormalities, crypt epithelial cell proliferation, epithelial barrier, glucose transport and signalling pathways were measured in these animals. Changes in global gene expression were also analyzed. Mice lacking Hnf1α displayed increased crypt proliferation and intestinalomegaly as well as a disturbance of intestinal epithelial cell lineages production during adult life. This phenotype was associated with a decrease of the mucosal barrier function and lumen-to-blood glucose delivery. The mammalian target of rapamycin (mTOR) signalling pathway was found to be overly activated in the small intestine of adult Hnf1α mutant mice. The intestinal epithelium of Hnf1α null mice displayed a reduction of the enteroendocrine cell population. An impact was also observed on proper Paneth cell differentiation with abnormalities in the granule exocytosis pathway. Conclusions/Significance Together, these results unravel a functional role for Hnf1α in regulating adult intestinal growth and sustaining the functions of intestinal epithelial cell lineages. HNF1alpha was knocked out. A total of 3 control and 3 mutant littermate individuals were sacrificed at 4 months of age. The jejunum was harvested and total RNA was isolated from each individual. Each RNA sample was independently used to generate probes to screen Affymetrix chips.

2011-01-01 | E-GEOD-23040 | biostudies-arrayexpress

Cyanophage MED4-117

Project description:Cyanophage MED4-117 genome sequencing project

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Bradyrhizobium elkanii strain:USDA 117 | isolate:USDA 117

Project description:Bradyrhizobium elkanii USDA 117 genome sequencing

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Bosea sp. 117

Project description:Bosea sp. 117 Genome sequencing and assembly

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