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. 2022 Sep 17;12:15636. doi: 10.1038/s41598-022-19654-y

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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CHD2 haploinsufficiency alters the efficiency of the proliferation to differentiation transition during hcIN differentiation. (A) RT-qPCR was used to define the expression in WT and CHD2^+/− cultures at D35 of 6 significantly down-regulated DEGs (as obtained by RNA-seq analysis), that are associated with cell cycle progression. (B) Comparison of the numbers of SST immunopositive hcINs in WT versus CHD2^+/− cultures, after plating equivalent numbers of progenitors. Earlier and more efficient differentiation of progenitors resulted in a reduction in the total number of hcINs generated. n = 3 biological replicate experiments. (C) Representative images of SST and MAP2 staining in WT and CHD2^+/− D35 cultures. (D) The percentage of nuclei that were immunopositive for Ki-67 in the WT versus CHD2^+/− model at D35 of differentiation were defined. n = 3 biological replicate experiments. (E) Representative images of D35 cells immunostained for Ki-67. Scale bars = 100 µm. Data is represented as mean ± SEM and was analyzed by Students t-test: **P < 0.01 ***P < 0.001 ****P < 0.0001 versus control.