{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang X"],"funding":["European Research Council"],"pagination":["3235-3250"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8630008"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["28(12)"],"pubmed_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<sup>-/-</sup> hematopoietic stem and progenitor cells released reduced amounts of G-CSF while retaining their capacity for CSF"],"journal":["Cell death and differentiation"],"pubmed_title":["MLKL promotes cellular differentiation in myeloid leukemia by facilitating the release of G-CSF."],"pmcid":["PMC8630008"],"funding_grant_id":["682473"],"pubmed_authors":["Keller EC","Shi R","Mishra R","Herold T","Shen B","Agrawal D","Bassermann F","Jost PJ","Garcia-Saez AJ","Dill V","Belka C","Wang X","Slotta-Huspenina J","Ros U"],"additional_accession":[]},"is_claimable":false,"name":"MLKL promotes cellular differentiation in myeloid leukemia by facilitating the release of G-CSF.","description":"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<sup>-/-</sup> hematopoietic stem and progenitor cells released reduced amounts of G-CSF while retaining their capacity for CSF","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2026-05-08T05:28:45.57Z","creation":"2022-02-11T13:43:52.616Z"},"accession":"S-EPMC8630008","cross_references":{"pubmed":["34079078"],"doi":["10.1038/s41418-021-00811-1"]}}