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

Chun Shik Park | Zendy; Andrew Henry Lewis | Zendy; Taylor J Chen | Zendy; Cory Seth Bridges | Zendy; Shen Ye | Zendy; Koramit Suppipat | Zendy; Monica Puppi | Zendy; Julie Tomolonis | Zendy; Paul Pang | Zendy; ToniAnn Mistretta | Zendy; Leyuan Ma | Zendy; Michael R. Green | Zendy; Rachel E. Rau | Zendy; H. Daniel Lacorazza | Zendy

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

Author(s) -

Chun Shik Park,

Andrew Henry Lewis,

Taylor J Chen,

Cory Seth Bridges,

Shen Ye,

Koramit Suppipat,

Monica Puppi,

Julie Tomolonis,

Paul Pang,

ToniAnn Mistretta,

Leyuan Ma,

Michael R. Green,

Rachel E. Rau,

H. Daniel Lacorazza

Publication year - 2019

Publication title -

blood

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.515

H-Index - 465

eISSN - 1528-0020

pISSN - 0006-4971

DOI - 10.1182/blood.2018875922

Subject(s) - klf4 , stem cell , biology , cancer research , medicine , microbiology and biotechnology , sox2 , genetics , embryonic stem cell , gene

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.

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