Similar Datasets
Project description:Mouse retina CUT&Tag for ATF4 and BACH1 proteins.
| PRJNA1392547 | ENA
Project description:Gene expression of single cells from mouse retina in knockdown using shRNA of Atf4 and Bach1.
2026-06-18 | GSE314867 | GEO
Project description:Mouse retina scRNA in Atf4 and Bach1 knock-down
| PRJNA1393018 | ENA
Project description:c-Fos and c-Jun form activator protein 1 (AP-1) transcription factors that regulate gene expression by binding to specific motifs on the genome. To investigate c-Fos regulating genes in OIR rod photoreceptor cells, we performed CUT&Tag subjecting normoxia P14 and OIR P14 retina using c-Fos, H3K27ac (enhancer maker), H3K4me3 (active promoter maker), and H3K27me3 ( gene repression maker) antibodies.
2024-03-14 | GSE245456 | GEO
Project description:To elucidate the biological role of ATF4 in regulating downstream target genes, we conducted a CUT&Tag assay in primarily cultured neurons.
2024-09-13 | GSE263464 | GEO
Project description:To comprehensively profile cell types in the human retina, we performed single cell RNA-sequencing on 20,009 cells obtained post-mortem from three donors and compiled a reference transcriptome atlas. Using unsupervised clustering analysis, we identified 18 transcriptionally distinct clusters representing all known retinal cells: rod photoreceptors, cone photoreceptors, Müller glia cells, bipolar cells, amacrine cells, retinal ganglion cells, horizontal cells, retinal astrocytes and microglia.
2019-08-21 | E-MTAB-7316 | biostudies-arrayexpress
Project description:To determine the biological function of ATF4 in the modulation of downstream target genes, we performed Tagmentation (CUT&Tag) assay in HCT 116 (Human colorectal cancer) cells
2022-11-29 | GSE218559 | GEO
Project description:Multiple myeloma (MM) is a B-cell malignancy accounting for 20% of all blood-associated cancers. MM patients with a poorer prognosis and high-risk stratification were previously observed to be causally linked to the constitutive activation of non-canonical NF-kB (ncNF-kB) pathway. Consistent with this, the ncNF-kB p52 transcription factor was earlier found to regulate the enhancer landscape of MM to potentiate oncogenic transcription. However, the mechanism by which aberrant p52 expression is involved in coordinating enhancer activity has not been well explored. In this study, we analysed H3K27ac ChIP-seq and ATAC-seq data from MM cell lines and patient samples to screen for putative transcription factors that cooperate with p52 to regulate enhancers activated in MM. We report that ATF4 interacts with p52 and together, this complex mediates the activity of a subset of MM-associated enhancers through the recruitment of histone acetyltransferases (HATs), p300 and CBP (CREB-binding protein). We also identified a novel ATF4:p52 regulated target gene BACH1 under the regulation of a proximal super-enhancer, which was found to drive oncogenesis in MM by promoting cell cycle progression and proliferation. Together, our findings provide further mechanistic insights into how aberrant enhancer activation observed in MM tumours could lead to disease progression.
2025-04-21 | GSE292455 | GEO
Project description:Multiple myeloma (MM) is a B-cell malignancy accounting for 20% of all blood-associated cancers. MM patients with a poorer prognosis and high-risk stratification were previously observed to be causally linked to the constitutive activation of non-canonical NF-kB (ncNF-kB) pathway. Consistent with this, the ncNF-kB p52 transcription factor was earlier found to regulate the enhancer landscape of MM to potentiate oncogenic transcription. However, the mechanism by which aberrant p52 expression is involved in coordinating enhancer activity has not been well explored. In this study, we analysed H3K27ac ChIP-seq and ATAC-seq data from MM cell lines and patient samples to screen for putative transcription factors that cooperate with p52 to regulate enhancers activated in MM. We report that ATF4 interacts with p52 and together, this complex mediates the activity of a subset of MM-associated enhancers through the recruitment of histone acetyltransferases (HATs), p300 and CBP (CREB-binding protein). We also identified a novel ATF4:p52 regulated target gene BACH1 under the regulation of a proximal super-enhancer, which was found to drive oncogenesis in MM by promoting cell cycle progression and proliferation. Together, our findings provide further mechanistic insights into how aberrant enhancer activation observed in MM tumours could lead to disease progression.
2025-04-21 | GSE292454 | GEO
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.
2011-05-13 | E-GEOD-28051 | biostudies-arrayexpress