Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA399717 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sequencing files provided here include mouse liver ChIP-seq for CTCF and the cohesin subunit Rad21, and 4C-seq analyses in male and female mouse liver centered at an Albumin promoter viewpoint. These files are part of a larger study where we describe features of Topologically Associating Domains (TADs) and their impact on liver gene expression, then use these features to computationally predict subTAD structures not otherwise readily identifiable due to the low resolution of Hi-C. Our findings reveal that CTCF-based subTAD loops maintain key insulating properties of TADs, and support the proposal that subTADs are formed by the same loop extrusion mechanism and contribute to nuclear architecture as intra-TAD scaffolds that further constrain enhancer-promoter interactions. This allows high expression of super enhancer target genes and individual genes within inactive TADs, and may be a broadly conserved mechanism of genomic regulation.
2018-05-11 | GSE102998 | GEO
Project description:Quantitative analysis of chromatin interactions upon copy number variation at mouse 4E2 [4C-seq]
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Project description:4C-seq data was generated for regions of interest to confirm enhancer-gene promoter interactions
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Project description:Robust 4C-seq data analysis to screen for regulatory DNA interactions
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Project description:Robust 4C-seq data analysis to screen for regulatory DNA interactions
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Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
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
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Sex differences in liver gene expression are dictated by sex-differences in circulating growth hormone (GH) profiles. Presently, the pituitary hormone dependence of mouse liver gene expression was investigated on a global scale to discover sex-specific early GH response genes that might contribute to sex-specific regulation of downstream GH targets and to ascertain whether intrinsic sex-differences characterize hepatic responses to plasma GH stimulation. RNA expression analysis using 41,000-feature microarrays revealed two distinct classes of sex-specific mouse liver genes: genes subject to positive regulation (class-I) and genes subject to negative regulation by pituitary hormones (class-II). Genes activated or repressed in hypophysectomized (Hypox) mouse liver within 30-90min of GH pulse treatment at a physiological dose were identified as direct targets of GH action (early response genes). Intrinsic sex-differences in the GH responsiveness of a subset of these early response genes were observed. Notably, 45 male-specific genes, including five encoding transcriptional regulators that may mediate downstream sex-specific transcriptional responses, were rapidly induced by GH (within 30min) in Hypox male but not Hypox female mouse liver. The early GH response genes were enriched in 29 male-specific targets of the transcription factor Mef2, whose activation in hepatic stellate cells is associated with liver fibrosis leading to hepatocellular carcinoma, a male-predominant disease. Thus, the rapid activation by GH pulses of certain sex-specific genes is modulated by intrinsic sex-specific factors, which may be associated with prior hormone exposure (epigenetic mechanisms) or genetic factors that are pituitary-independent, and could contribute to sex-differences in predisposition to liver cancer or other hepatic pathophysiologies.
2010-01-27 | GSE17644 | GEO