ArticleLeukemia research2014
The AML1/ETO target gene LAT2 interferes with differentiation of normal hematopoietic precursor cells.
Article in Leukemia research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.Oncogene · 2021Review
- NTAL is associated with treatment outcome, cell proliferation and differentiation in acute promyelocytic leukemia.Scientific reports · 2020Article
- Runx1t1 promotes the neuronal differentiation in rat hippocampus.Stem cell research & therapy · 2020Article
- Subtype-specific regulatory network rewiring in acute myeloid leukemia.Nature genetics · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The adaptor protein linker activator of T-cells 2 (LAT2) is a known AML1/ETO target gene whose function during normal hematopoiesis is unknown. We addressed the role of LAT2 during erythroid and myeloid differentiation of normal human CD34+ hematopoietic cells. LAT2 is expressed at low levels in CD34+ cells and upregulated during cytokine-induced myeloid and erythroid differentiation. Forced LAT2 expression leads to a delay of erythroid and myeloid differentiation keeping CD34+ cells in a more immature state, whereas LAT2 knockdown accelerates differentiation. It is tempting to speculate that by affecting the differentiation capacity of normal hematopoietic progenitors, LAT2 may contribute to the pathogenesis of AML.
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Registered trials
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