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- W2081736209 abstract "Targeted disruption of a highly conserved distal enhancer reduces expression of the PU.1 transcription factor by 80% and leads to acute myeloid leukemia (AML) with frequent cytogenetic aberrations in mice. Here we identify a SNP within this element in humans that is more frequent in AML with a complex karyotype, leads to decreased enhancer activity, and reduces PU.1 expression in myeloid progenitors in a development-dependent manner. This SNP inhibits binding of the chromatin-remodeling transcriptional regulator special AT-rich sequence binding protein 1 (SATB1). Overexpression of SATB1 increased PU.1 expression, and siRNA inhibition of SATB1 downregulated PU.1 expression. Targeted disruption of the distal enhancer led to a loss of regulation of PU.1 by SATB1. Interestingly, disruption of SATB1 in mice led to a selective decrease of PU.1 RNA in specific progenitor types (granulocyte-macrophage and megakaryocyte-erythrocyte progenitors) and a similar effect was observed in AML samples harboring this SNP. Thus we have identified a SNP within a distal enhancer that is associated with a subtype of leukemia and exerts a deleterious effect through remote transcriptional dysregulation in specific progenitor subtypes." @default.
- W2081736209 created "2016-06-24" @default.
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- W2081736209 date "2007-09-04" @default.
- W2081736209 modified "2023-10-13" @default.
- W2081736209 title "A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia" @default.
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- W2081736209 doi "https://doi.org/10.1172/jci30525" @default.
- W2081736209 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1937499" @default.
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