Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

15 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HNF1A, H3K4me3 and H3K27ac ChIP-seq in control and Haster-deficient mouse livers

ABSTRACT: The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed HNF1A, H3K4me3 and H3K27ac ChIP-seq to assess the impact of HNF1A upregulation on the chromatin landscape of Haster KO liver.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Anthony Beucher

PROVIDER: E-MTAB-11471 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

UMI-4C in control and HASTER-deficient EndoC-betaH3 cells overexpressing HNF1A

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription HNF1A. If HASTER is deleted after beta cells have been formed and HNF1A is already stably expressed, HASTER is not required to maintain HNF1A activity, and is only required to provide negative feedback on HNF1A. HNF1A binding to the HASTER promoter mediates the repression of the HNF1A gene itself. To determine whether HNF1A binding to the HASTER promoter remodels 3D chromatin interactions of the HNF1A promoter, we performed UMI-4C experiments in wild type and HASTER-promoter KO EndoC-betaH3 cells with or without doxycycline-induced HNF1A overexpression using the HNF1A promoter as viewpoint.

2022-05-01 | E-MTAB-11473 | biostudies-arrayexpress

UMI-4C in control and Haster-deficient mouse livers

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed UMI-4C experiments to assess how Haster inactivation remodel 3D chromatin interactions of the Hnf1a promoter using the Hnf1a promoter as viewpoint (V1, Hnf1a promoter upstream CTCF site viewpoint; V2, Hnf1a promoter VP).

2022-05-01 | E-MTAB-11472 | biostudies-arrayexpress

HNF1A, UTX, H3K27me3 and H3K27ac ChIP-seq in wild-type and UTX- or HNF1A-deficient mouse pancreas

Project description:HNF1A and UTX are putative tumor suppressors in pancreatic cancer. In this study, we have combined mouse genetics, transcriptomics and genome binding studies to link HNF1A and UTX in a molecular mechanism that suppresses pancreatic cancer. In this session, we have profiled UTX, HNF1A, H3K27me3 and H3K27ac in normal and UTX- or HNF1A-deficient mouse pancreas by ChIP-seq experiments. We show that HNF1A recruits UTX to its genomic targets in pancreatic acinar cells, which results in remodeling of the chromatin landscape and activation of a broad transcriptional program of differentiated acinar cells, which in turn indirectly suppresses tumor suppressor pathways.

2019-12-20 | E-MTAB-7944 | biostudies-arrayexpress

Strain-specific RNA-seq in Haster Stop/+ C57BL/6;PWK/PhJ F1 mice

Project description:Germ-line deletion of the Haster promoter region results in overexpression of Hnf1a in liver, while a variegated phenotype is observed in pancreatic islets, with overexpression or silencing of the Hnf1a gene in different cells. Mouse hybrid experiments show that both activation and silencing mechanisms occur in cis. To assess whether HASTER transcription or RNA transcripts are involved in the regulation of Hnf1a, we have generated a mouse model where the 4xSV40 polyA signal has been inserted downstream of Haster promoters (Haster-Stop allele) to terminate Haster transcription, but leaving the Haster promoter intact. Haster Stop/+ F1 mice with the Haster Stop allele from C57BL/6 origin and wild type allele from the PWK/PhJ origin were used for stain-specific RNA-seq in pancreatic islets and liver. Allele-specific quantification of Hnf1a exon 1 were used to assess the requirement of the Haster transcripts/transcription for Hnf1a expression.

2022-05-01 | E-MTAB-11475 | biostudies-arrayexpress

scRNA-seq of pancreatic islets from control and Haster-pKO mice

Project description:Pancreas specific deletion of the Haster promoter region results in a variegated phenotype in pancreatic islets with overexpression or silencing of the Hnf1a gene. To determine the transcriptional consequence of the overexpression or silencing of Hnf1a is islet cells from the Haster pKO mice (Haster loxP/loxP;Pdx1-Cre), we performed scRNA-seq of pancreatic islets from control and adult female Haster pKO mice.

2022-05-01 | E-MTAB-11477 | biostudies-arrayexpress

RNA-seq in control and Haster-deficient mouse livers

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed RNA-seq from control and KO livers to assess the transcriptional impact of the HNF1A upregulation in the Haster KO liver.

2022-05-01 | E-MTAB-11463 | biostudies-arrayexpress

ChIP-seq analysis of Esrrb, Nanog, Oct4, and Sox2 in EpiSCs undergoing reprogramming

Project description:To investigate the molecular mechanisms underlying the reprogramming of epiblast stem cells (EpiSCs) into embryonic stem cells (ESCs) induced by Esrrb, we performed ChIP-seq analysis of Esrrb, Nanog, Oct4, and Sox2 in Tet-on Esrrb EpiSCs after treatment with doxycycline (Dox).

2018-06-01 | E-MTAB-5342 | biostudies-arrayexpress

Tissue- and Stage-specific ChIP for H3K27ac, CTCF, Beaf and Su(Hw) in D. melanogaster embryos

Project description:This study contains a series of ChIP-seq experiments performed on nuclear material similar to what was used in Tissue- and Stage-specific Capture-C for selected TSS and CRM (BioStudies/ArrayExpress collection E-MTAB-9310). ChIP-seq with chromatin isolated from nuclei isolated from 2-3h whole embryos samples or Mef2-/Elav-sorted nuclei from 6-8h and 10-12h embryo samples was performed using anti-H3K27ac (Anti-Histone H3 (acetyl K27) antibody, Abcam #ab4729, purified polyclonal), anti-CTCF (rabbit anti Drosophila CTCF antibody, Reinkawitz lab, purified polyclonal), anti-Beaf (mouse anti Drosophila BEAF antibody, DSHB #1553420, monoclonal) and anti-Su(Hw) (goat anti Drosophila Su(Hw) antibody, Geyer lab, purified polyclonal) antibodies.

2023-06-30 | E-MTAB-12639 | biostudies-arrayexpress

ChIP-seq experiment of SMC-FLAG binding to Streptomyces venezuelae chromosome in wild type and parB knockout strain

Project description:We studied the binding of SMC protein to Streptomyces venezuelae chromosome during development of aerial hyphae (14 hour of growth) using SMC-FLAG protein. Additionally investigated the role of ParB protein in SMC DNA binding using parB deletion strain.

2021-05-28 | E-MTAB-9822 | biostudies-arrayexpress

ChIP-seq of tumour associated macrophages derived from high grade ovarian serous carcinoma patient ascites

Project description:Tumor associated macrophages of one patient were assayed for histone modifications, methylation (MIRA) and CEBP.

2018-08-13 | E-MTAB-6297 | biostudies-arrayexpress