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. 2018 Nov 21;26(9):1716–1734. doi: 10.1038/s41418-018-0241-1

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© The Author(s) 2018

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — The schematic model for mechanism of BICD1-mediated HIF1α nuclear translocation in UCB-MSCs under hypoxia. Hypoxia induces GSK3β phosphorylation at Ser9 residue via Akt activation. Silencing of GSK3β induces the interaction between BICD1 and HIF1α. BICD1 regulation by Akt activation or GSK3β silencing stimulates HIF1α nuclear translocation. BICD1-mediated HIF1α nuclear translocation is critical for hypoxia adaptation, enhances regenerative potential of UCB-MSCs transplantation