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Biol Open. 2017 Apr 15;6(4):511-517. doi: 10.1242/bio.022426.

Depletion of .

Biology open

Shoudong Ye, Tao Zhang, Chang Tong, Xingliang Zhou, Kan He, Qian Ban, Dahai Liu, Qi-Long Ying

Affiliations

  1. Center for Stem Cell and Translational Medicine, School of Life Sciences, Anhui University, Hefei 230601, People's Republic of China.
  2. Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  3. Center for Stem Cell and Translational Medicine, School of Life Sciences, Anhui University, Hefei 230601, People's Republic of China [email protected] [email protected].
  4. Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA [email protected] [email protected].

PMID: 28288968 PMCID: PMC5399551 DOI: 10.1242/bio.022426

Abstract

Mouse and rat embryonic stem cell (ESC) self-renewal can be maintained by dual inhibition of glycogen synthase kinase 3 (GSK3) and mitogen-activated protein kinase kinase (MEK). Inhibition of GSK3 promotes ESC self-renewal by abrogating T-cell factor 3 (TCF3)-mediated repression of the pluripotency network. How inhibition of MEK mediates ESC self-renewal, however, remains largely unknown. Here, we show that inhibition of MEK can significantly suppress lymphoid enhancer factor 1 (LEF1) expression in mouse ESCs. Knockdown or knockout of

© 2017. Published by The Company of Biologists Ltd.

Keywords: Differentiation; Embryonic stem cells; LEF1; Self-renewal; TCF3

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