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. 2016 Feb 15;30(4):421–433. doi: 10.1101/gad.271452.115

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© 2016 Pauklin et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.

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Figure 1. — Cyclin D proteins can regulate cell fate decisions in hESCs independently of CDK4/6 activity. (A) Schematic overview of teratoma assay. (B) Histological sections of teratomas derived from GFP-overexpressing hESCs. (K) Kidney; (ME) mesoderm; (EN) endoderm; (NE) neuroectoderm. (C) Ratio of histological structures specific to each germ layer. X²= 152.5, Bonferroni corrected P < 6.6 × 10⁻¹⁶, χ² test. (D) Histological sections of teratomas derived from Cyclin D1 overexpressing hESCs. (E) CDK4/6 inhibition does not fully abolish Cyclin D function. Significant differences calculated by two-way ANOVA are marked. (F) Morphology of a CycD1-K112E mutant overexpressing hESCs. Representative colonies of hESCs overexpressing GFP and CycD1-K112E. (G) The CycD1-K112E mutant, which is not able to activate CDK4/6, can block endoderm genes and induce neuroectoderm. Significant differences compared with overexpressing GFP and calculated by t-test are marked. All data are shown as mean ± SD. n = 3.