Pseudokinase tribbles (Trib) family, Trib1 and Trib2, but not Trib3, act as oncogene to drive acute leukemia by destabilizing the myeloid transcription factor CCAAT/enhancer-binding protein α (C/EBPα) and inhibiting myeloid differentiation. A recent study identifies pseudokinase TRIB3 as an important factor in acute promyelocytic leukemia (APL) progression and therapy resistance. Targeting TRIB3 may provide a novel therapeutic approach for APL.
Keywords: AML; UPS; protein quality control; protein-protein interactions; sumoylation; tribbles; α-helical peptide.