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通过过表达Sall4从小鼠成纤维细胞重编程获得多能性。

Reconstitution of pluripotency from mouse fibroblast through Sall4 overexpression.

作者信息

Xiao Lizhan, Huang Zifen, Wu Zixuan, Yang Yongzheng, Zhang Zhen, Kumar Manish, Wu Haokaifeng, Mao Huiping, Lin Lihui, Lin Runxia, Long Jingxian, Zeng Lihua, Guo Jing, Luo Rongping, Li Yi, Zhu Ping, Liao Baojian, Wang Luqin, Liu Jing

机构信息

Center for Development and Regeneration, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.

Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, Guangdong-Hong Kong Joint Laboratory for Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.

出版信息

Nat Commun. 2024 Dec 30;15(1):10787. doi: 10.1038/s41467-024-54924-5.

Abstract

Somatic cells can be reprogrammed into pluripotent stem cells (iPSCs) by overexpressing defined transcription factors. Specifically, overexpression of OCT4 alone has been demonstrated to reprogram mouse fibroblasts into iPSCs. However, it remains unclear whether any other single factor can induce iPSCs formation. Here, we report that SALL4 alone, under an optimized reprogramming medium iCD4, is capable of reprogramming mouse fibroblasts into iPSCs. Mechanistically, SALL4 facilitates reprogramming by inhibiting somatic genes and activating pluripotent genes, such as Esrrb and Tfap2c. Furthermore, we demonstrate that co-overexpressing SALL4 and OCT4 synergistically enhances reprogramming efficiency. Specifically, the activation of Rsk1/Esrrb/Tfap2c by SALL4, alongside OCT4's activation of Sox2 and the suppression of Mndal by SALL4 and Sbsn by OCT4, cooperate to facilitate SALL4+OCT4-mediated reprogramming. Overall, our study not only establishes an efficient method for iPSCs induction using the SALL4 single factor but also provides insights into the synergistic effects of SALL4 and OCT4 in reprogramming.

摘要

通过过表达特定的转录因子,体细胞可被重编程为多能干细胞(诱导多能干细胞,iPSCs)。具体而言,已证明单独过表达OCT4可将小鼠成纤维细胞重编程为iPSCs。然而,尚不清楚是否有任何其他单一因子能诱导iPSCs形成。在此,我们报告,在优化的重编程培养基iCD4条件下,单独的SALL4能够将小鼠成纤维细胞重编程为iPSCs。从机制上讲,SALL4通过抑制体细胞基因并激活多能性基因(如Esrrb和Tfap2c)来促进重编程。此外,我们证明共同过表达SALL4和OCT4可协同提高重编程效率。具体来说,SALL4对Rsk1/Esrrb/Tfap2c的激活,以及OCT4对Sox2的激活,再加上SALL4对Mndal的抑制和OCT4对Sbsn的抑制,共同促进了SALL4+OCT4介导的重编程。总体而言,我们的研究不仅建立了一种使用SALL4单一因子诱导iPSCs的有效方法,还深入了解了SALL4和OCT4在重编程中的协同作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3cc/11686038/56db50b37a3a/41467_2024_54924_Fig1_HTML.jpg

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