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Table 2 Genes deregulated by MLL-AF9 and prioritized as potentially druggable targets in MLL-AF9 leukemia

From: RNAi-mediated silencing of MLL-AF9 reveals leukemia-associated downstream targets and processes

Gene log2FC Protein class Official full name
Biological role
AHR 0.44 Nuclear receptor Aryl hydrocarbon receptor
Upregulated by AML associated fusion gene AML1-ETO. Differentiation of myeloblastic leukemia cells. Estrogen receptor degradation. AHR knockout mice display CML.
ATP2B2 −0.69 Transporter ATPase, Ca++ transporting, plasma membrane 2
Lowers intracellular calcium; protects from apoptosis.
DRD5 −0.96 Receptor Dopamine receptor D5
Raised after G-CSF treatment; dopamine receptor agonists activate Wnt signaling, induce migration and increase clonogenic capacity and repopulation of CD34+ cells.
HIPK2 0.5 Enzyme Homeodomain interacting protein kinase 2
Phosphorylates transcription (co-) factors (e.g. c-Myb); may trigger (myeloid) differentiation and apoptosis. Mutations found in AML cases.
PARP8 −0.63 Enzyme Poly (ADP-ribose) polymerase family, member 8
Phosphorylated upon DNA damage. Upregulated in MLL rearranged AML patients.
ROR2 0.81 Receptor/enzyme Receptor tyrosine kinase-like orphan receptor 2
Mediates noncanonical Wnt signaling. Putative tumor suppressor in leukemia, presumably via inhibition of Wnt canonical signaling.
TAS1R3 −2.01 Receptor Taste receptor, type 1, member 3
Glucose absorption/energy supply. Heterodimers sense extracellular amino acids, activate MTORC1 and inhibit autophagy.
  1. Details to biological roles and references are given in Additional file 3: Table S2. Log2FC: log2 fold change in MLL-AF9 knockdown relative to control.