MLKL promotes cellular differentiation in myeloid leukemia by facilitating the release of G-CSF.

ABSTRACT: The blockade of cellular differentiation represents a hallmark of acute myeloid leukemia (AML), which is largely attributed to the dysfunction of lineage-specific transcription factors controlling cellular differentiation. However, alternative mechanisms of cellular differentiation programs in AML remain largely unexplored. Here we report that mixed lineage kinase domain-like protein (MLKL) contributes to the cellular differentiation of transformed hematopoietic progenitor cells in AML. Using gene-targeted mice, we show that MLKL facilitates the release of granulocyte colony-stimulating factor (G-CSF) by controlling membrane permeabilization in leukemic cells. Mlkl^-/- hematopoietic stem and progenitor cells released reduced amounts of G-CSF while retaining their capacity for CSF

SUBMITTER: Wang X 

PROVIDER: S-EPMC8630008 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature