A dual role of Erk signaling in embryonic stem cells Xinwei Ma, Haixia Chen, Lingyi Chen  Experimental Hematology  Volume 44, Issue 3, Pages 151-156 (March 2016) DOI: 10.1016/j.exphem.2015.12.008 Copyright © 2016 ISEH - International Society for Experimental Hematology Terms and Conditions

Figure 1 Schematic illustration of Erk signaling in ESCs. Conventional Ras/Mek/Erk signaling activates the expression of Elk1, c-Fos, p53, c-Jun, and so on, consequently promoting cell proliferation, cell cycle progression, and telomere maintenance. Erk signaling also suppresses the expression of pluripotency genes, such as Nanog, Krdm14, Tbx3, and Klf4. In additional to Erk, Mek may fulfill its function through an unidentified factor to repress pluripotency genes, including Nanog, Tbx3, and Klf4. Experimental Hematology 2016 44, 151-156DOI: (10.1016/j.exphem.2015.12.008) Copyright © 2016 ISEH - International Society for Experimental Hematology Terms and Conditions

Figure 2 Dual role of Erk signaling in mouse ESCs. A minimal level of Erk signaling (marked by a green dashed line) is required for cell proliferation, cell cycle progression, suppression of apoptosis, telomere length maintenance, and genomic stability. Above a certain threshold (represented by a red dashed line), Erk signaling represses the expression of pluripotency genes and activates the expression of developmental genes. Thus, an intermediate Erk signaling strength is optimal for pluripotency maintenance. Experimental Hematology 2016 44, 151-156DOI: (10.1016/j.exphem.2015.12.008) Copyright © 2016 ISEH - International Society for Experimental Hematology Terms and Conditions