The MADS transcription factor Mef2c is a pivotal modulator of myeloid cell fate.

@article{Schler2008TheMT,
  title={The MADS transcription factor Mef2c is a pivotal modulator of myeloid cell fate.},
  author={Andrea Sch{\"u}ler and Maike Schwieger and Afra Engelmann and Kristoffer Weber and Stefan Horn and Ursula M{\"u}ller and Michael A Arnold and Eric N. Olson and Carol Stocking},
  journal={Blood},
  year={2008},
  volume={111 9},
  pages={
          4532-41
        }
}
Mef2c is a MADS (MCM1-agamous-deficient serum response factor) transcription factor best known for its role in muscle and cardiovascular development. A causal role of up-regulated MEF2C expression in myelomonocytic acute myeloid leukemia (AML) has recently been demonstrated. Due to the pronounced monocytic component observed in Mef2c-induced AML, this study was designed to assess the importance of Mef2c in normal myeloid differentiation. Analysis of bone marrow (BM) cells manipulated to… 
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Dual roles for MEF2A and MEF2D during human macrophage terminal differentiation and c-Jun expression.
TLDR
Ch Chromatin immunoprecipitations demonstrate that MEF2A is present on the c-Jun promoter, both in undifferentiated and in macrophage-differentiated cells, and highlight for the first time the possible dual roles of MEf2A andMEF2D in human macrophages, as activators or as repressors of gene transcription.
1,25-Dihydroxyvitamin D3 induces monocytic differentiation of human myeloid leukemia cells by regulating C/EBPβ expression through MEF2C
Mef2C is a lineage-restricted target of Scl/Tal1 and regulates megakaryopoiesis and B-cell homeostasis.
TLDR
This work identifies Mef2C as an integral member of hematopoietic transcription factors with distinct upstream regulatory mechanisms and functional requirements in megakaryocyte and B-lymphoid lineages.
MEF2C and CEBPA: Possible co-regulators in chronic myeloid leukemia disease progression.
Homing and invasiveness of MLL/ENL leukemic cells is regulated by MEF2C.
TLDR
Mef2c-dependent targets included several genes encoding matrix metalloproteinases and chemokine ligands and receptors, providing a mechanistic link to increased homing and motility, and may be responsible for the aggressive nature of this leukemia subtype.
Regulation of lymphoid versus myeloid fate 'choice' by the transcription factor Mef2c
TLDR
An unexpected function for the myeloid oncogene product Mef2c in lymphoid development is described, which is a crucial component of the transcriptional network that regulates cell fate 'choice' in multipotent progenitors.
MEF2C Phosphorylation Is Required for Chemotherapy Resistance in Acute Myeloid Leukemia.
TLDR
Kinase-dependent dysregulation of this transcription factor confers susceptibility to MARK/SIK kinase inhibition in preclinical models, substantiating its clinical investigation for improved diagnosis and therapy of AML.
Identification of the Regulatory Elements and Target Genes of Megakaryopoietic Transcription Factor MEF2C.
TLDR
It is demonstrated that small deletions linked to a platelet count-associated single nucleotide polymorphism alter transcriptional activity, suggesting a mechanism by which genetic variation in MEF2C alters platelet production.
Frequent Derepression of the Mesenchymal Transcription Factor Gene FOXC1 in Acute Myeloid Leukemia.
Salt-Inducible Kinase inhibition suppresses acute myeloid leukemia progression in vivo.
TLDR
These findings validate Sik3 as a therapeutic target in MEF2C-addicted AML and provide a rationale for developing drug-like inhibitors of SIK3 for definitive pre-clinical investigation and for studies in human patients.
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