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. 2018 Jun 30;75(18):3339–3351. doi: 10.1007/s00018-018-2862-4

Fig. 1.

Fig. 1

Signaling pathways in human pluripotency maintenance. In hPSCs: a Activin/Nodal signaling molecules induce SMAD2/3 phosphorylation and interaction with SMAD4. The SMAD2/3–SMAD4 complex then translocates to the nucleus, where it promotes NANOG expression. NANOG cooperates with OCT4 and SOX2 to maintain pluripotency in hPSCs. b FGF2 activates phosphorylation of PI3K/AKT or MAPK/ERK signaling cascades, which cooperate with SMAD2/3–SMAD4 complexes to promote pluripotency in hPSCs. c Canonical Wnts inhibit the activity of the APC/AXIN/GSK-3β complex, by which β-catenin is protected from degradation. β-Catenin translocates to the nucleus, where it cooperates with TCF/LEF family members to regulate expression of target genes. Whether the canonical Wnt/β-catenin cascade maintains pluripotency or promotes differentiation of hESCs remains controversial