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- W4380185909 abstract "The chromosomal translocation t(4;11) results in the expression of MLL-AF4 and AF4-MLL, and is associated with the onset of pro B-ALL in infant, children and adults. Although this particular translocation is the most frequent MLL-rearrangement, the precise cancer mechanism is still unclear, and a satisfactory in vivo model for pro B-ALL only exists in CRISPR/Cas9 model systems. Given the fact that MLL-AF4 alone is unable to transform hematopoietic cells, other possibilities have been discussed, e.g. specific cells-of-origin need for cellular transformation, or that the reciprocal fusion is the true driver of leukemogenesis. Experimental evidence is pointing to another mechanism, namely the impact of post-transcriptional mechanisms via RNA-binding proteins (RBPs) for the abundance of the MLL-AF4 fusion transcript. Here, we present first data on RBPs and potential binding motifs which differ in mouse and human AF4 sequences. As a consequence, human MLL-AF4 could only be expressed at low levels, because otherwise this transcript is too toxic for mammalian cells." @default.
- W4380185909 created "2023-06-11" @default.
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- W4380185909 date "2023-05-01" @default.
- W4380185909 modified "2023-09-26" @default.
- W4380185909 title "Impact of posttranscriptional regulations of MLL-AF4 and its target Genes in pro B-ALL" @default.
- W4380185909 doi "https://doi.org/10.1055/s-0043-1768519" @default.
- W4380185909 hasPublicationYear "2023" @default.
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