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Leuk Res. 2014 Mar;38(3):340-5. doi: 10.1016/j.leukres.2013.12.014. Epub 2013 Dec 25.

The AML1/ETO target gene LAT2 interferes with differentiation of normal hematopoietic precursor cells.

Author information

1
Department of Hematology and Oncology, University of Freiburg, Medical Center, Freiburg, Germany. Electronic address: aitomi.essig@charite.de.
2
Department of Hematology and Oncology, University of Freiburg, Medical Center, Freiburg, Germany.

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.

KEYWORDS:

Acute myeloid leukemia; Adaptor molecule; Erythroid differentiation; Myeloid differentiation

PMID:
24456692
PMCID:
PMC4135084
DOI:
10.1016/j.leukres.2013.12.014
[Indexed for MEDLINE]
Free PMC Article

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