Table 2.
Gene | log 2 FC | 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. |
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.