Ontology highlight
ABSTRACT:
PROVIDER: PRJNA755208 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ATAC-seq in precursor and differentiated ER-Hoxb8 cells
2022-05-12 | GSE200730 | GEO
Project description:ATAC-seq in precursor and differentiated ER-Hoxb8 cells
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Project description:Gene expression profiling of progenitor and neutrophil-derived HoxB8-ER cells (WT and Ezh2-/-) and neutrophil-derived HOXB8-ER treated with GSK343 and vehicle for 9 days. Ezh2 loss might lead to effective cytopenias caused by dysfunctional mature cells. To test this hypothesis, we examined Ezh2-null murine myeloid cell lines capable of neutrophilic differentiation. Bone marrow cells from Ezh2-/- and controls were immortalized with a HoxB8-estrogen receptor fusion and could be differentiated into mature neutrophils by removing estrogen from the culture medium.Gene expression profiling showed upregulation of oxidative phosphorylation pathway genes and ectopic expression of Gata1 and its associated erythroid gene targets. Functional and gene expression differences observed in Ezh2-/- derived neutrophils could be replicated in controls by treatment with the Ezh2-specific inhibitor GSK343. In conclusion, we demonstrate that Ezh2 loss allows for differentiation of normal appearing, but dysfunctional mature neutrophils characterized by ectopic gene expression and elevated levels of reactive oxygen species. These defects could contribute to the inflammatory bone marrow microenvironment and clinical phenotypes observed in patients with MDS.
2017-11-18 | GSE107061 | GEO
Project description:Progenitor cells of yolk sac and bone marrow origin were transduced with an estrogen receptor Hoxb8 fusion protein to generate stable cell lines. Macrophages were differentiated with M-CSF in the absence of estrogen, and then stimulated with IL-4 or LPS. Hoxb8 progenitor cells and differentiated macrophages were analyzed by RNA sequencing.
2022-01-10 | GSE176409 | GEO
Project description:The impact of LPS and LTA stimulation on differentiated bone marrow and Yolk sac Hoxb8 macrophages in comparison to untreated control cells was studied by global protein profiling using a bottom-up approach.
2022-02-04 | PXD026922 | Pride
Project description:<p>The efficacy of the adaptive immune response declines dramatically with age, but the cell-intrinsic mechanisms driving the changes characteristic of immune aging in humans remain poorly understood. One hallmark of immune aging is the loss of self-renewing naive cells and the accumulation of differentiated but dysfunctional cells within the CD8 T cell compartment. Using ATAC-seq, we first inferred the transcription factor binding activities that maintain the naive and central and effector memory CD8 T cell states in young adults. Integrating our results with RNA-seq, we determined that BATF, ETS1, Eomes, and Sp1 govern transcription networks associated with specific CD8 T cell subset properties, including activation and proliferative potential. Extending our analysis to aged humans, we found that the differences between memory and naive CD8 T cells were largely preserved across age, but that naive and central memory cells from older individuals exhibited a shift toward a more differentiated pattern of chromatin openness. Additionally, aged naive cells displayed a loss in chromatin openness at gene promoters, a phenomenon that appears to be due largely to a loss in binding by NRF1, leading to a marked drop-off in the ability of the naive cell to initiate transcription of mitochondrial genes. Our findings identify BATF- and NRF1-driven gene regulation as targets for delaying CD8 T cell aging and restoring T cell function.</p>
| phs001187 | dbGaP
Project description:We used an ex vivo system of murine ER-Hoxb8 neutrophils that phenotypically and morphologically recapitulate neutrophil maturation stages during five days of in vitro culture in the presence of G-CSF. To investigate the development of the ROS system in neutrophils during their development, we compared transcriptomes of D0, D1, D3 and D5 Hoxb8 neutrophils.
2020-09-15 | GSE147910 | GEO
Project description:Investigation of immune cell differentiation and function is limited by shortcomings of suitable and scalable experimental systems. Although forced expression of certain Hox genes allows immortalization of hematopoietic progenitor cells, their differentiation potential is limited to select myeloid lineages. Here we show that an estrogen-regulated form of Hoxb8 that is retrovirally delivered into bone marrow cells can be used along with FLT3 ligand to conditionally immortalize early hematopoietic progenitor cells (Hoxb8-FL). Hoxb8-FL cells have lost self-renewal capacity and the ability to adopt megakaryocyte/ erythroid lineage fates, but sustain myeloid and lymphoid differentiation potential. Hoxb8-FL cells differentiate in vitro and in vivo into different myeloid and lymphoid cell types, including macrophages, granulocytes, dendritic cells and B- and T-lymphocytes, which are phenotypically and functionally indistinguishable from their primary counterparts. Given the simplicity to generate Hoxb8-FL cells and their unlimited proliferative capacity, this system provides unique opportunities to investigate cell differentiation and immune cell functions. Hoxb8 expressing immortalized cells
2013-06-05 | E-GEOD-45759 | biostudies-arrayexpress
Project description:HOXB8 functions as a transcription factor, but its genomic targets remains unknown. Thus, we profiled HOXB8 binding loci across the genome using ChIP-seq.
2019-10-04 | GSE121208 | GEO
Project description:We recently identified CCDC134 as a novel regulator of TLR responses. To gain a comprehensive understanding of the effects of CCDC134 loss, we conducted total proteome analysis on control sgRen and sgCCDC134 Hoxb8 immortalized murine myeloid progenitors that were differentiated into macrophages. Interestingly, we observed that plasma membrane and endolysosomal TLRs, along with their associated chaperone Gp96, were among the most significantly downregulated proteins. Our findings further demonstrated that CCDC134 is essential for the proper folding and stability of Gp96. As a result, the deletion of CCDC134 in various cell lines and Hoxb8-derived macrophages results in altered TLR folding and trafficking.
2024-11-14 | PXD053042 | Pride