Targets of this post-translational regulatory mechanism include VHL, PML, MDM2, RelA, HAND1 and hTERT, among many others.
Dr. Pandolfi and colleagues characterized the function of the fusion oncoproteins of APL, of the genes involved in the chromosomal translocations of APL, as well as of major tumor suppressors such PTEN, PML, and p53.
The most frequent translocation is t(15,17)(q21;q22), which fuses the RARA gene with the PML gene.
Two proteins, sp100 and promyelocytic leukemia (PML) factor are localized to punctate domains in the nucleus (nuclear dots or nuclear bodies).
protein | leukemia | Protein subunit | Protein-protein interaction | Hfq protein | protein domain | Leukemia & Lymphoma Society | Protein-protein_interaction | Leukemia | Protein Data Bank | RNA-binding protein | Acute lymphoblastic leukemia | Promyelocytic leukemia protein | G protein | Wiskott–Aldrich syndrome protein | Protein G | protein dimer | Protein A | C-reactive protein | Bone morphogenetic protein 2 | AMP-activated protein kinase | Acute myeloid leukemia | Transmembrane protein | Tau protein | Sterol regulatory element-binding protein | SR protein | Rab escort protein | Protein structure | protein structure | Protein phosphatase 2 |