Related Experiment Video
Updated: Jul 2, 2026

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
Published on: September 1, 2019
Pim-1 kinase phosphorylates and stabilizes RUNX3 and alters its subcellular localization
Hye-Ryun Kim1, Byung-Chul Oh, Joong-Kook Choi
1Department of Biochemistry, School of Medicine, Institute for Tumor Research, Chungbuk National University, Cheongju 361-763, South Korea.
Abstract:
The loci of the Pim and Runx gene families have been identified as targets for viral insertions in CD2-myc mice. Synergistic cooperation between Pim and RUNX was also found in the CD2-Runx2 transgenic mouse lymphoma model. RUNX genes have come to prominence recently because of their roles as essential regulators of cell fate in development. Paradoxically, they appear to function either as tumor-suppressor genes or dominant oncogenes according to the cellular context. However, the molecular mechanism of the ambiguous roles played by this family of transcription factors in cancer has remained largely uninvestigated. Here we demonstrate that Pim-1 phosphorylates four Ser/Thr residues within the Runt domain and stabilizes RUNX3 protein. In addition, Pim-1 markedly altered the cellular localization of RUNX3 from the nucleus to the cytoplasm. Our results demonstrate that the subcellular localization of RUNX3 is altered by phosphorylation. We propose that RUNX family members may behave as oncogenes if mislocalized to a cellular micro-compartment.
Related Concept Videos
Abnormal Proliferation
PI3K/mTOR/AKT Signaling Pathway
The JAK-STAT Signaling Pathway
Negative Regulator Molecules
MAPK Signaling Cascades
Covalently Linked Protein Regulators
These groups modify specific amino acids in a protein.
