A KLF4-DYRK2–mediated pathway regulating self-renewal in CML stem cells

Author:

Park Chun Shik1,Lewis Andrew H.12,Chen Taylor J.12,Bridges Cory S.1ORCID,Shen Ye12,Suppipat Koramit3,Puppi Monica1,Tomolonis Julie A.4,Pang Paul D.2,Mistretta Toni-Ann1,Ma Leyuan5,Green Michael R.5,Rau Rachel6ORCID,Lacorazza H. Daniel1ORCID

Affiliation:

1. Department of Pathology and Immunology and

2. Integrative Molecular and Biomedical Sciences Program, Baylor College of Medicine, Houston, TX;

3. Texas Children’s Cancer and Hematology Center, Texas Children’s Hospital, Houston, TX;

4. MD/PhD Program, Baylor College of Medicine, Houston, TX;

5. Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, MA;

6. Department of Pediatrics-Oncology, Baylor College of Medicine, Houston, TX

Abstract

Park et al describe a novel KLF4-mediated pathway that promotes chromic myeloid leukemia (CML) stem cell (LSC) survival. Deletion of KLF4 in a mouse model of CML decreases LSC survival through repression of Dyrk2, resulting in c-Myc depletion and increased p53 activity.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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