We characterized transcriptional regulatory modes related to HSCs

Thus, our method can systematically infer the regulation modes exerted by TFs that are probably necessary for gene expression, as well as suggesting synergistic TF modules. Using our transcriptome profiles and this novel method, we characterized transcriptional regulatory modes related to HSCs, which suggested the functional importance of TFs expressed at steady-state or low levels. Remarkably, we identified 24 differentially expressed TFs that targeted 21 Varlitinib putative TF-binding sites in LT-HSCs. These TFs might be essential for maintaining the HSC capacity during the early stage of hematopoiesis. HSC fate is controlled tightly by extrinsic and intrinsic factors. The identification and characterization of these factors may lead to more effective clinical therapies for acquired and congenital blood disorders. Owing to recent advances in experimental and computational techniques, many recent studies have begun to move beyond the traditional beliefs regarding hematopoiesis. However, the determination of the upstream regulatory elements that are responsible for the development of the hematopoietic system remains far from adequate and requires the application of various approaches. In the present study, we established novel transcriptome profiles from mouse LT- and ST-HSCs using an RNA-seq assay and developed a computational method for exploring the potential modes of transcriptional regulation based on these profiles. Our RNA-seq assay confirmed the transcriptionally active state of ST-HSCs with markedly high numbers of DEGs. These DEGs included 77 cell-surface molecules and 57 TFs, which indicates that specific extrinsic and intrinsic regulators respond actively during the transition between LT and ST-HSCs. During this transition, we observed that many previously annotated lineage-specific genes were up- and downregulated. In particular, lymphoid potential genes that preferentially Aciclovir undergo upregulation in ST-HSCs and potential megakaryocyte/erythroid genes had opposite patterns, suggesting that lymphoid priming occurs during this early stage.

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