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| 1 | Rescue of premature aging defects in Cockayne syndrome stem cells by CRISPR/Cas9-mediated gene correction显示文摘Cockayne syndrome(CS)is a rare autosomal recessive inherited disorder characterized by a variety of clinical features,including increased sensitivity to sunlight,progressive neurological abnormalities,and the appearance of premature aging.However,the pathogenesis of CS remains unclear due to the limitations of current disease models.Here,we generate integration-free induced pluripotent stem cells(iPSCs)from fibroblasts from a CS patient bearing mutations in CSB/ERCC6 gene and further derive isogenic genecorrected CS-iPSCs(GC-iPSCs)using the CRISPR/Cas9 system.CS-associated phenotypic defects are recapitulated in CS-iPSC-derived mesenchymal stem cells(MSCs)and neural stem cells(NSCs),both of which display increased susceptibility to DNA damage stress.Premature aging defects in CS-MSCs are rescued by the targeted correction of mutant ERCC6.We next map the transcriptomic landscapes in CS-iPSCs and GC-iPSCs and their somatic stem cell derivatives(MSCs and NSCs)in the absence or presence of ultraviolet(UV)and replicative stresses,revealing that defects in DNA repair account for CS pathologies.Moreover,we generate autologous GC-MSCs free of pathogenic mutation under a cGMP(Current Good Manufacturing Practice)-compliant condition,which hold potential for use as improved biomaterials for future stem cell replacement therapy for CS.Collectively,our models demonstrate novel disease features and molecular mechanisms and lay a foundation for the development of novel therapeutic strategies to treat CS. | Si Wang Zheying Min Qianzhao Ji Lingling Geng Yao Su Zunpeng Liu Huifang Hu Lixia Wang Weiqi Zhang Keiichiro Suzuiki Yu Huang Puyao Zhang Tie-Shan Tang Jing Qu Yang Yu Guang-Hui Liu Jie Qiao | 2020 | Protein & Cell2020，11，1： | 7 |
| 2 | Neuroendocrine characteristics of induced pluripotent stem cells from polycystic ovary syndrome women显示文摘Dear Editor, Polycystic ovary syn drome (PCOS) is a comm on female reproductive endocrinopathy that afflicts up to 10%-15% of women in reproductive age worldwide (Nestler, 2016). Women with PCOS exhibit hyperandrogenism, intermittent/ absent menstrual cycles, and polycystic ovaries on ultrasound (Rotterdam, 2004). The pathophysiology of PCOS extends beyond infertility and hirsutism to hypothalamic neuroendocrine dysfunotion (Goodarzi et al., 2011). Most wome n with PCOS exhibit in creased luteinizing horm one (LH) levels, resulting from high-frequency gonadotropin-releasing hormone (GnRH) secretion (Cimino et al., 2016). Pren ata I testostero ne (T) treatment in sheep results in disrupted steroid feedback on gonadotropin release, which in creases pituitary sen sitivity to GnRH and subseque ntly leads to LH hypersecretion (Sullivan and Moenter, 2004;Cardoso et al., 2016). A recent study shows that GnRHdependent LH pulsatility and secretion are elevated by anti- Mullerian hormone (AMH) in PCOS disease. The increased prenatal AMH reprograms fetus and induces PCOS in adults (Tata et al., 2018). Furthermore, the androgen receptor (AR) plays a role in hyperandrogenism and ovarian folliculoge esis in PCOS (Wang et al., 2015;Abbott, 2017). However, the disease mechanism behind PCOS remains unclear, and current management focuses on treating the symptoms but not the mechanism (Chen et al., 2016;Shi et al., 2018). A further understanding of this disease is necessary to uncover the pathology of PCOS and develop new potential therapeutic avenues and drugs. | Zheying Min Yue Zhao Jing Hang Yun Ren Tao Tan Yong Fan Yang Yu | 2019 | Protein & Cell2019，10，7： | 4 |
| 3 | Correction to: Neuroendocrine characteristics of induced pluripotent stem cells from polycystic ovary syndrome women显示文摘In the original publication the Fig.2 and the Supplementary Material 1 was incorrect.The correct version of Fig.2 and the Supplementary Material are provided in this correction article.NESTIN should be corrected to PAX6 in Fig.2C legend and at page 528 and Supplementary Material 1.NANOG should be corrected to PAX6 in Fig.2C picture. | Zheying Min Yue Zhao Jing Hang Yun Ren Tao Tan Yong Fan Yang Yu | 2020 | Protein & Cell2020，11，3： | 2 |
| 4 | IFN-γ-mediated IRF1/miR-29b feedback loop suppresses colorectal cancer cell growth and metastasis by repressing IGF1显示文摘 | Li Yuan Chang Zhou Yanxia Lu Min Hong Zuoyang Zhang Zheying Zhang Yaya Chang Chao Zhang Xuenong Li | 2015 | Cancer Letters2015，，： | 1 |
| 5 | Correction to:Rescue of premature aging defects in Cockayne syndrome stem cells by CRISPR/Cas9-mediated gene correction显示文摘CORRECTION TO:PROTEIN CELL HTTPS://DOI.ORG/10.1007/S13238-019-0623-2 In Fig.7C,we used the ERCC6mut.iPSCs(CS iPSCs)as NANOG positive control pluripotent cells in the upper pan-els.However,these cells were inadvertently labeled as ERCC6^(GC)-iPSCs.In the revised version of Fig.7C,we have updated the high-quality images along with the corrected mark.In addition,we have also made corresponding chan-ges in the figure legend. | Si Wang Zheying Min Qianzhao Ji Lingling Geng Yao Su Zunpeng Liu Huifang Hu Lixia Wang Weiqi Zhang Keiichiro Suzuiki Yu Huang Puyao Zhang Tie-Shan Tang Jing Qu Yang Yu Guang-Hui Liu Jie Qiao | 2022 | Protein & Cell2022，13，8： | 0 |
| 6 | Ascl1 represses the mesendoderm induction in Xenopus显示文摘 | ZheYing Min Hao Lin Xuechen Zhu Li Gao Aftab A. Khand Qinghua Tao | 2016 | Acta Biochimica et Biophysica Sinica2016，48，11： | 0 |
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