Transcriptome profiling of Dek over-expressed quiescent muscle stem cells in vivo
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ABSTRACT:
PROVIDER: PRJNA494565 | ENA |
REPOSITORIES: ENA
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Project description:To understand the molecular signatures of Dek over-expressed quiescent muscle stem cells in vivo, we isolated quiescent muscle stem cells by fixation using perfusion technique and profiled the transcriptome by RNA-Seq.
2020-05-22 | GSE120799 | GEO
Project description:To identify Dek-associated RNA in muscle stem cells during quiescence to activation transition, we used Dek antibody to immunoprecipitated Dek-associated RNA from fresh-isolated quiescent muscle stem cell and profiled pull down by RNA-Seq.
2020-05-22 | GSE143412 | GEO
Project description:We find that the DEK oncoprotein preferentially binds close to the transcription start sites of highly and ubiquitously expressed genes. Sequencing of DNA precipitated by an antibofy against the DEK oncoprotein (ChIP-seq).
2014-09-26 | E-GEOD-60692 | biostudies-arrayexpress
Project description:Many stem cell populations exist in a quiescent state in vivo, exiting quiescence and entering the cell cycle in response to specific stimuli. In the case of skeletal muscle, the muscle stem cells (MuSCs, or “satellite cells”) are quiescent under normal homeostatic conditions and undergo activation and cell cycle entry in response to muscle fiber damage. Quiescent MuSCs are also much more potent than their proliferating progeny in assays of stem cell transplantation. In recent years, it has become increasingly apparent that the quiescent state is both actively maintained and dynamically regulated. However, most of the analyses of quiescent MuSCs have come from cells that have been removed from their niche in vivo, purified by fluorescence activated cell sorting, and then assay ex vivo. Although such cells are still in the quiescent state under these conditions, there is no doubt that significant biochemical changes will occur during the isolation and purification process. Thus, we have sought to examine the true in vivo quiescent state by analyzing the transcriptome of MuSCs. To achieve that, we have used techniques to label actively transcribing RNA in vivo using nucleoside analogs. In mice in which the enzyme uracil phosphoribosyltransferase (UPRT) is expressed specifically in MuSCs, administration of 4-thiouracil (4TU), which is converted to thiouridine (TU) by UPRT, resulted in labelling of MuSC transcripts, and the transcriptome could be analyzed following pull-down of TU-tagged RNA. Varying the timing of 4TU administration revealed the dynamic regulation of different subsets of transcripts. Notably, labeling transcripts during the isolation procedure revealed very active transcription of specific subsets of genes. Nevertheless, the ex vivo transcriptome remained largely reflective of the in vivo transcriptome. Using the transcriptional inhibitor, α-amanitin, we were also able to show that there was little difference between the steady-state transcript levels of the most highly expressed genes when comparing the ex vivo transcriptome with the in vivo transcriptome. Together, these data provide a novel view of the molecular regulation of the quiescent state at the transcriptional level, demonstrate the utility of these tools for probing transcriptional dynamics in vivo, and provide an invaluable resource for understanding stem cell state transitions.
2017-11-12 | GSE97399 | GEO
Project description:Nuclear protein DEK is an endogenous DNA-binding chromatin factor regulating hematopoiesis. DEK is one of only two known secreted nuclear chromatin factors, but whether and how extracellular DEK regulates hematopoiesis is not known. We demonstrate that extracellular DEK greatly enhances ex vivo expansion of cytokine-stimulated human and mouse hematopoietic stem cells, and regulates hematopoiesis in vivo and in vitro. These effects are mediated through chemokine receptor CXCR2 and heparan sulfate proteoglycans, and are associated with enhanced phosphorylation of ERK1/2, AKT and p38 MAPK. Thus, DEK acts as a hematopoietic cytokine, with potential for clinical applicability.
2019-02-22 | GSE126875 | GEO
Project description:To understand the molecular signatures of quiescent muscle stem cells in vivo, we isolated quiescent muscle stem cells by fixation using perfusion technique and profiled the transcriptome by RNA-Seq.
2020-05-22 | GSE113631 | GEO
Project description:Introduction: Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer, exhibiting rapid progression and is unresponsive to hormone therapy. Reliable prognostic assays and more effective treatments are critically required. However, the research of NEPC has been hampered by a lack of clinically relevant in vivo models. Recently, we successfully developed a first-in-field patient tissue-derived xenograft model of complete neuroendocrine transdifferentiation from prostate adenocarcinoma. By comparing gene expression profiles of the parental adenocarcinoma line (LTL331) and the NEPC subline (LTL331R), we identified DEK, a gene not previously reported in prostate cancer, as a potential biomarker and target for NEPC. Methods: DEK protein expression in patient tissue-derived xenograft models and clinical samples was assessed by immunohistochemistry. The function of DEK was determined by siRNA-induced reduction of DEK expression in PC-3 cells, a cell line with NEPC characteristics, followed by functional assays and gene expression profiling analysis. Results: Elevated DEK protein expression was observed in all clinical NEPC cases, which is distinct from their benign counterparts (0%), hormonal naïve prostate cancer (2.45%) and castration resistant prostate cancer (29.55%). Increased DEK expression is an independent clinical risk factor and is associated with shorter disease free survival in hormonal naïve prostate cancer patients. Reduction of DEK expression in PC-3 cells led to a marked reduction in cell proliferation, cell migration and invasion. Conclusions: The results suggest that DEK may play an important role in the progression of prostate cancer, especially NEPC and provide a potential biomarker to aid risk stratification of prostate cancer and a novel therapeutic target for treating NEPC. The function of DEK was determined by siRNA-induced reduction of DEK expression in PC-3 cells, a cell line with NEPC characteristics, followed by functional assays and gene expression profiling analysis.
2015-01-15 | E-GEOD-61214 | biostudies-arrayexpress
Project description:Gene expression profiling of U937 cells upon knockdown of the DEK oncogene by two different shRNAs (shDEK14 and shDEK17). The DEK oncogene was knocked down by shRNA to study the changes in gene expression.
2014-09-26 | E-GEOD-60732 | biostudies-arrayexpress
Project description:Among most of leukemogenic fusion proteins the aberrant localization that the translocation partners are forced in when compared to their wt counterparts contributes to leukemogenesis most likely by a sequester of interaction partners. The aim was to disclose the role of localization of DEK/NUP214 and the related sequester of proteins interacting with DEK/NUP214 for the induction t(6;9)- AML. The pathways indispensable for the induction of the leukemogenic phenotype were worked out by comparing the interactome of the full-length fusion protein to that of biologiaclly-dead mutants.
2022-10-14 | PXD031885 | Pride
Project description:We find that the DEK oncoprotein preferentially binds close to the transcription start sites of highly and ubiquitously expressed genes.
2014-09-26 | GSE60692 | GEO