Targeting pseudokinase TRIB3 brings about a new therapeutic option for acute promyelocytic leukemia

Abstract

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

• α-helical peptide
• aml
• protein-protein interactions
• protein quality control
• sumoylation
• tribbles
• ups