Publications by authors named "Felicia Kathrine Bratt Lauridsen"
Article Synopsis
- * Gene expression analysis indicated that RA-CFP-dim HSCs had higher levels of RA-target genes, although both subtypes reacted similarly to RA stimuli in lab tests.
- * Advanced techniques like single-cell RNA sequencing highlighted that variations in cell cycle activity are key to the differences seen in HSCs, revealing that these cells often display low-level expressions of genes related to different lineages
Article Synopsis
- Transcription factors PU.1 and CEBPA are crucial for coordinating enhancer activity during the differentiation of granulocytic-monocytic cells into myeloid cells, but their specific roles are not fully understood.
- The study analyzes changes in enhancer dynamics, transcription factor binding, and gene expression in mouse models to reveal how PU.1 and CEBPA regulate these processes differently, with CEBPA showing a pioneering role in enhancer accessibility.
- Findings indicate that CEBPA influences PU.1 levels and is essential for proper differentiation, as its absence leads to an early block in the differentiation process, highlighting their collaborative roles in GM-lineage development.
Within the bone marrow, stem cells differentiate and give rise to diverse blood cell types and functions. Currently, hematopoietic progenitors are defined using surface markers combined with functional assays that are not directly linked with in vivo differentiation potential or gene regulatory mechanisms. Here, we comprehensively map myeloid progenitor subpopulations by transcriptional sorting of single cells from the bone marrow.
View Article and Find Full Text PDFMLL-fusion proteins are potent inducers of oncogenic transformation, and their expression is considered to be the main oncogenic driving force in ∼10% of human acute myeloid leukemia (AML) patients. These oncogenic fusion proteins are responsible for the initiation of a downstream transcriptional program leading to the expression of factors such as MEIS1 and HOXA9, which in turn can replace MLL-fusion proteins in overexpression experiments. To what extent MLL fusion proteins act on their own during tumor initiation, or if they collaborate with other transcriptional regulators, is unclear.
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