Similar Datasets
Project description:ChIP-seq of NRF1 in skeletal muscle
| PRJNA1060641 | ENA
Project description:Determine AR cistrome in skeletal muscle and correlate it with the presence of H3K4me2.
2023-05-25 | GSE216373 | GEO
Project description:To investigate the role of NRF1 in regulating primordial germ cell development, We established conditional knockout mice of Nrf1 in primordial germ cell to observe the effect of Nrf1 knockout on the development of primordial germ cell. At the same time, we utilized a pluripotent stem cell differentiation system in vitro to obtain PGCL cells for chip_ Seq, analyze which genes Nrf1 directly binds to. Meanwhile, we established a pluripotent stem cell line induced by Nrf1 overexpression and performed RNA_seq analysis on PGCL cells overexpressing Nrf1 obtained in vitro
2023-08-05 | GSE231661 | GEO
Project description:To elucidate the function of Nrf1-small Maf heterodimer, we constructed a tethered Nrf1-MafG (T-N1G) heterodimer using a flexible linker peptide and examined its function in the small Maf-deficient mouse embryonic fibroblast (MEF).
2022-01-30 | GSE188785 | GEO
Project description:Eukaryotic transcription factors (TFs) are key determinants of gene activity, yet they bind only a fraction of their corresponding DNA sequence motifs in any given cell type. Chromatin has the potential to restrict accessibility of binding sites; however, in which context chromatin states are instructive for TF binding remains mainly unknown. To explore the contribution of DNA methylation to constrained TF binding, we mapped DNase-I-hypersensitive sites in murine stem cells in the presence and absence of DNA methylation. Methylation-restricted sites are enriched for TF motifs containing CpGs, especially for those of NRF1. In fact, the TF NRF1 occupies several thousand additional sites in the unmethylated genome, resulting in increased transcription. Restoring de novo methyltransferase activity initiates remethylation at these sites and outcompetes NRF1 binding. This suggests that binding of DNA-methylationsensitive TFs relies on additional determinants to induce local hypomethylation. In support of this model, removal of neighbouring motifs in cis or of a TF in trans causes local hypermethylation and subsequent loss of NRF1 binding. This competition between DNA methylation and TFs in vivo reveals a case of cooperativity between TFs that acts indirectly via DNA methylation. Methylation removal by methylation-insensitive factors enables occupancy of methylation-sensitive factors, a principle that rationalizes hypomethylation of regulatory regions. DNase-seq (2 replicates) in mouse embryonic stem cells with (WT) and without DNA methylation (DNMT TKO). RNA-seq (3 replicates) in WT and DNMT TKO cells and in DNMT TKO cells after treatment with control siRNA or siRNA targeting Nrf1. H3K27ac ChIP-seq (2 replicates) in WT and DNMT TKO cells. NRF1 ChIP-seq (2 replicates) in WT and DNMT TKO cells, in WT upon culture in different conditions (adaptation to 2i and back to serum), upon transient overexpression of NRF1 and after differentiation into neuronal progenitor cells (NP). Whole-genome bisulfite sequencing in DNMT TKO cells and in WT upon culture in different conditions (adaptation to 2i and back to serum). NRF1 ChIP-seq (2 replicates) in human HMEC and HCC1954 cells.
2015-12-16 | E-GEOD-67867 | biostudies-arrayexpress
Project description:Analysis of binding of the transcriptional factor Nrf1 in mouse embryonic stem cells by ChIP-Seq
2017-12-15 | E-MTAB-3475 | biostudies-arrayexpress
Project description:GATA4 occupancy on the mouse genome of satellite cell-derived primary myoblasts. Proliferating myoblasts cultured in growth medium were immunoprecipitated with anti-GATA4 antibody or control IgG. Precipitated genomic DNAs were subjected to next generation sequencing. Paired-end 150 bp sequence reads of GATA4-ChIP and IgG-ChIP using mouse skeletal muscle myoblasts.
2015-04-10 | E-GEOD-67703 | biostudies-arrayexpress
Project description:Heart disease can be caused by ischemic coronary artery injury, hypertension, and chemotherapy, all of which lead to loss or dysfunction of cardiac muscle. The adult mammalian heart lacks the ability to regenerate. In contrast, the heart of neonatal mice, within the first week after birth, possesses a unique ability to regenerate lost myocardium following injury, mediated by proliferation of cardiomyocytes. The mechanisms whereby neonatal cardiomyocytes adapt to injury-induced stress conditions and activate regenerative cellular programs remain to be defined. Here, we show that Nrf1, an endoplasmic reticulum (ER) bound transcription factor, is expressed in regenerating cardiomyocytes. Genetic deletion of Nrf1 prevented cardiomyocytes from activating a transcriptional program required for heart regeneration, revealed by single-nucleus RNA sequencing (snRNA-seq). Conversely, adeno-associated virial (AAV) overexpression of Nrf1 protected the adult mouse heart from ischemia/reperfusion (I/R) injury. Nrf1 also protected human induced pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) from doxorubicin-induced cardiotoxicity. The protective function of Nrf1 is mediated by a dual stress response mechanism involving activation of the proteasome and redox balance. Our findings reveal a mechanistic interplay between adaptive stress responses and heart regeneration, and highlight the central role of Nrf1 in these processes.
2021-05-01 | GSE163630 | GEO
Project description:Heart disease can be caused by ischemic coronary artery injury, hypertension, and chemotherapy, all of which lead to loss or dysfunction of cardiac muscle. The adult mammalian heart lacks the ability to regenerate. In contrast, the heart of neonatal mice, within the first week after birth, possesses a unique ability to regenerate lost myocardium following injury, mediated by proliferation of cardiomyocytes. The mechanisms whereby neonatal cardiomyocytes adapt to injury-induced stress conditions and activate regenerative cellular programs remain to be defined. Here, we show that Nrf1, an endoplasmic reticulum (ER) bound transcription factor, is expressed in regenerating cardiomyocytes. Genetic deletion of Nrf1 prevented cardiomyocytes from activating a transcriptional program required for heart regeneration, revealed by single-nucleus RNA sequencing (snRNA-seq). Conversely, adeno-associated virial (AAV) overexpression of Nrf1 protected the adult mouse heart from ischemia/reperfusion (I/R) injury. Nrf1 also protected human induced pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) from doxorubicin-induced cardiotoxicity. The protective function of Nrf1 is mediated by a dual stress response mechanism involving activation of the proteasome and redox balance. Our findings reveal a mechanistic interplay between adaptive stress responses and heart regeneration, and highlight the central role of Nrf1 in these processes.
2021-05-01 | GSE163628 | GEO
Project description:This study will reveal the importance of nrf1 in revealing the translational control of Fe homeostasis
2019-12-30 | E-MTAB-8158 | biostudies-arrayexpress