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| 1 | Differential stem cell aging kinetics in Hutchinson-Gilford progeria syndrome and Werner syndrome显示文摘Hutchinson-Gilford 早衰症候群(HGPS ) 和沃纳症候群(WS ) 是二最好描绘的人的 progeroid 症候群。HGPS 被一个点变化在 lamin A (LMNA ) 基因引起,导致截断的蛋白质 productprogerin 的生产。WS 被变化在 WRN 基因引起,编码 loss-of-function RecQ DNA helicase。这里,由基因编辑,我们创造了 isogenic 人的胚胎的干细胞(转换字符) 与异质接合(G608G/+) 或同型结合(G608G/G608G ) LMNA 变化和 biallelic WRN 大美人为为 HGPS 和 WS 致病建模,分别地。当转换字符和 endothelial 房间(EC ) 没介绍早熟的老朽的任何特征时, HGPS 间充质、 WS 间充质的干细胞(MSC ) 与不同动力学显示出联系老化的显型。当 HGPS-MSCs 展出了迟了发作的尖锐早衰 characterisitcs 时, WS-MSCs 有早发作的温和早衰显型。一起拿,我们的学习比较并且形成对照不同病理 underpinning 二早衰混乱,并且提供可靠干细胞为病理学、生理的老化识别新治疗学的策略的基于的模型。 | Zeming Wu Weiqi Zhang Moshi Song Wei Wang Gang Wei Wei Li Jinghui Lei Yu Huang Yanmei Sang Piu Chan Chang Chen Jing Qu Keiichiro Suzuki Juan Carlos Izpisua Belmonte Guang-Hui Liu | 2018 | Protein & Cell2018，9，4： | 15 |
| 2 | Genetic enhancement in cultured human adult stem cells conferred by a single nucleotide recoding显示文摘 | Jiping Yang Jingyi Li Keiichiro Suzuki Xiaomeng Liu Jun Wu Weiqi Zhang Ruotong Ren Weizhou Zhang Piu Chan Juan Carlos Izpisua Belmonte Jing Qu Fuchou Tang Guang-Hui Liu | 2017 | Cell Research2017，27，9： | 12 |
| 3 | Modeling xeroderma pigmentosum associated neurological pathologies with patients-derived iPSCs显示文摘干皮病 pigmentosum (XP ) 是联系 XP 的基因的变化引起的一组基因混乱,导致 DNA 修理的缺陷。XP 病人经常展出神经病学的退化,而是内在的机制是未知的,部分地由于合适的疾病模型的缺乏。这里,我们产生了包括 XPA, XPB, XPC, XPG,和 XPV 在五不同 XP 基因怀有变化的病人特定的导致的 pluripotent 干细胞(iPSCs ) 。这些 iPSCs 进一步被区分到神经房间,并且他们到 DNA 损坏应力的危险性被调查。在神经干细胞(NSC ) 或神经原的 XPA 的变化导致了严重 DNA 损坏修理缺点,并且有变异的 XPA 的这些神经房间对 DNA 导致损坏的 apoptosis 过分敏感。因此, XP 变异的神经房间代表珍贵工具在 XP 病人澄清神经病学的畸形的分子的机制。 | Lina Fu Xiuling Xu Ruotong Ren Jun Wu Weiqi Zhang Jiping Yang Xiaoqing Ren Si Wang Yang Zhao Liang Sun Yang Yu Zhaoxia Wang Ze Yang Yun Yuan Jie Qiao Juan Carlos Izpisua Belmonte Jing Qu Guang-Hui Liu | 2016 | Protein & Cell2016，7，3： | 11 |
| 4 | Single-cell transcriptomic atlas of primate cardiopulmonary aging显示文摘Aging is a major risk factor for many diseases,especially in highly prevalent cardiopulmonary comorbidities and infectious diseases including Coronavirus Disease 2019(COVID-19).Resolving cellular and molecular mechanisms associated with aging in higher mammals is therefore urgently needed.Here,we created young and old non-human primate single-nucleus/cell transcriptomic atlases of lung,heart and artery,the top tissues targeted by SARS-CoV-2.Analysis of cell type-specific aging-associated transcriptional changes revealed increased systemic inflammation and compromised virus defense as a hallmark of cardiopulmonary aging.With age,expression of the SARS-CoV-2 receptor angiotensin-converting enzyme 2(ACE2)was increased in the pulmonary alveolar epithelial barrier,cardiomyocytes,and vascular endothelial cells.We found that interleukin 7(IL7)accumulated in aged cardiopulmonary tissues and induced ACE2 expression in human vascular endothelial cells in an NF-κB-dependent manner.Furthermore,treatment with vitamin C blocked IL7-induced ACE2 expression.Altogether,our findings depict the first transcriptomic atlas of the aged primate cardiopulmonary system and provide vital insights into age-linked susceptibility to SARS-CoV-2,suggesting that geroprotective strategies may reduce COVID-19 severity in the elderly. | Shuai Ma Shuhui Sun Jiaming Li Yanling Fan Jing Qu Liang Sun Si Wang Yiyuan Zhang Shanshan Yang Zunpeng Liu Zeming Wu Sheng Zhang Qiaoran Wang Aihua Zheng Shuguang Duo Yang Yu Juan Carlos Izpisua Belmonte Piu Chan Qi Zhou Moshi Song Weiqi Zhang Guang-Hui Liu | 2021 | Cell Research2021，31，4： | 10 |
| 5 | CRISPR/Cas9-mediated targeted gene correction in amyotrophic lateral sclerosis patient iPSCs显示文摘 | Lixia Wang Fei Yi Lina Fu Jiping Yang Si Wang Zhaoxia Wang Keiichiro Suzuki Liang Sun Xiuling Xu Yang Yu Jie Qiao Juan Carlos Izpisua Belmonte Ze Yang Yun Yuan Jing Qu Guang-Hui Liu | 2017 | Protein & Cell2017，8，5： | 10 |
| 6 | A human circulating immune cell landscape in aging and COVID-19显示文摘Age-associated changes in immune cells have been linked to an increased risk for infection.However,a global and detailed characterization of the changes that human circulating immune cells undergo with age is lacking.Here,we combined scRNA-seq,mass cytometry and sCATAC-seq to compare immune cell types in peripheral blood collected from young and old subjects and patients with COVID-19.We found that the immune cell landscape was reprogrammed with age and was characterized by T cell polarization from naive and memory cells to effector,cytotoxic,exhausted and reg-ulatory cells,along with increased late natural killer cells,age-associated B cells,inflammatory monocytes and age-associated dendritic cells.In addition,the expression of genes,which were implicated in coron-avirus susceptibility,was upregulated in a cell subtype-specific manner with age.Notably,COVID-19 promoted age-induced immune cell polarization and gene expression related to inflammation and cellular senes-cence.Therefore,these findings suggest that a dysreg-ulated immune system and increased gene expression associated with SARS-CoV-2 susceptibility may at least partially account for COVID-19 vulnerability in the elderly. | Yingfeng Zheng Xiuxing Liu Wenqing Le Lihui Xie He Li Wen Wen Si Wang Shuai Ma Zhaohao Huang Jinguo Ye Wen Shi Yanxia Ye Zunpeng Liu Moshi Song Weiqi Zhang Jing-Dong J.Han Juan Carlos lzpisua Belmonte Chuanle Xiao Jing Qu Hongyang Wang Guang-Hui Liu Wenru Su | 2020 | Protein & Cell2020，11，10： | 10 |
| 7 | Stabilization of heterochromatin by CLOCK promotes stem cell rejuvenation and cartilage regeneration显示文摘Accumulating evidence indicates an association between the circadian clock and the aging process.However,it remains elusive whether the deregulation of circadian clock proteins underlies stem cell aging and whether they are targetable for the alleviation of aging-associated syndromes.Here,we identified a transcription factor-independent role of CLOCK,a core component of the molecular circadian clock machinery,in counteracting human mesenchymal stem cell(hMSC)decay.CLOCK expression was decreased during hMSC aging.In addition,CLOCK deficiency accelerated hMSC senescence,whereas the overexpression of CLOCK,even as a transcriptionally inactive form,rejuvenated physiologically and pathologically aged hMSCs.Mechanistic studies revealed that CLOCK formed complexes with nuclear lamina proteins and KAP1,thus maintaining heterochromatin architecture and stabilizing repetitive genomic sequences.Finally,gene therapy with lentiviral vectors encoding CLOCK promoted cartilage regeneration and attenuated age-related articular degeneration in mice.These findings demonstrate a noncanonical role of CLOCK in stabilizing heterochromatin,promoting tissue regeneration,and mitigating aging-associated chronic diseases. | Chuqian Liang Zunpeng Liu Moshi Song Wei Li Zeming Wu Zehua Wang Qiaoran Wang Si Wang Kaowen Yan Liang Sun Tomoaki Hishida Yanning Cai Juan Carlos lzpisua Belmonte Pedro Guillen Piu Chan Qi Zhou Weiqi Zhang Jing Qu Guang-Hui Liu | 2021 | Cell Research2021，31，2： | 8 |
| 8 | Modeling CADASIL vascular pathologies with patient-derived induced pluripotent stem cells显示文摘Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy(CADASIL)is a rare hereditary cerebrovascular disease caused by a NOTCH3 mutation.However,the underlying cellular and molecular mechanisms remain unidentified.Here,we generated non-integrative induced pluripotent stem cells(iPSCs)from fibroblasts of a CADASIL patient harboring a heterozygous NOTCH3 mutation(c.3226C>T,p.R1076C).Vascular smooth muscle cells(VSMCs)differentiated from CADASIL-specific iPSCs showed gene expression changes associated with disease phenotypes,including activation of the NOTCH and NF-kB signaling pathway,cytoskeleton disorganization,and excessive cell proliferation.In comparison,these abnormalities were not observed in vascular endothelial cells(VECs)derived from the patients iPSCs.Importantly,the abnormal upregulation of NF-kB target genes in CADASIL VSMCs was diminished by a NOTCH pathway inhibitor,providing a potential therapeutic strategy for CADASIL.Overall,using this iPSCbased disease model,our study identified clues for studying the pathogenic mechanisms of CADASIL and developing treatment strategies for this disease. | Chen Ling Zunpeng Liu Moshi Song Weiqi Zhang Si Wang Xiaoqian Liu Shuai Ma Shuhui Sun Lina Fu Qun Chu Juan Carlos Izpisua Belmonte Zhaoxia Wang Jing Qu Yun Yuan Guang-Hui Liu | 2019 | Protein & Cell2019，10，4： | 7 |
| 9 | Effects of glutamine supplementation on gut barrier,glutathione content and acute phase response in malnourished rats during inflammatory shock显示文摘AIM: To evaluate the effect of glutamine on intestinal mucosa integrity,glutathione stores and acute phase response in protein-depleted rats during an inflammatory shock. METHODS: Plasma acute phase proteins (APP),jejunal APP mRNA levels,liver and jejunal glutathione concentrations were measured before and one,three and seven days after turpentine injection in 4 groups of control,protein-restricted,protein-restricted rats supplemented with glutamine or protein powder. Bacterial translocation in mesenteric lymph nodes and intestinal morphology were also assessed. RESULTS: Protein deprivation and turpentine injection significantly reduced jejunal villus height,and crypt depths. Mucosal glutathione concentration significantly decreased in protein-restricted rats. Before turpentine oil,glutamine supplementation restored villus heights and glutathione concentration (3.24 ± 1.05 vs 1.72 ± 0.46 μmol/g tissue,P < 0.05) in the jejunum,whereas in the liver glutathione remained low. Glutamine markedly increased jejunal α1-acid glycoprotein mRNA level after turpentine oil but did not affect its plasma concentration. Bacterial translocation in protein-restricted rats was not prevented by glutamine or protein powder supplementation. CONCLUSION: Glutamine restored gut glutathione stores and villus heights in malnourished rats but had no preventive effect on bacterial translocation in our model. | Liliana Belmonte Mose Co■ffier Florence Le Pessot Olga Miralles-Barrachina Martine Hiron Antony Leplingard Jean-Franois Lemeland Bernadette Hecketsweiler Maryvonne Daveau Philippe Ducrotté Pierre Déchelotte | 2007 | World Journal of Gastroenterology2007，13，20： | 6 |
| 10 | Analysis of hepatitis B virus preS1 variability and prevalence of the rs2296651 polymorphism in a Spanish population显示文摘AIM To determine the variability/conservation of the domain of hepatitis B virus(HBV) pre S1 region that interacts with sodium-taurocholate cotransporting polypeptide(hereafter, NTCP-interacting domain) and the prevalence of the rs2296651 polymorphism(S267 F, NTCP variant) in a Spanish population. METHODS Serum samples from 246 individuals were included and divided into 3 groups: patients with chronic HBV infection(CHB)(n = 41, 73% Caucasians), patients with resolved HBV infection(n = 100, 100% Caucasians) and an HBV-uninfected control group(n = 105, 100% Caucasians). Variability/conservation of the amino acid(aa) sequences of the NTCPinteracting domain,(aa 2-48 in viral genotype D) and a highly conserved pre S1 domain associated with virion morphogenesis(aa 92-103 in viral genotype D) were analyzed by next-generation sequencing and compared in 18 CHB patients with viremia > 4 log IU/mL. The rs2296651 polymorphism was determined in all individuals in all 3 groups using an in-house real-time PCR melting curve analysis.RESULTS The HBV pre S1 NTCP-interacting domain showed a high degree of conservation among the examined viral genomes especially between aa 9 and 21(in the genotype D consensus sequence). As compared with the virion morphogenesis domain, the NTCPinteracting domain had a smaller proportion of HBV genotype-unrelated changes comprising > 1% of the quasispecies(25.5% vs 31.8%), but a larger proportion of genotype-associated viral polymorphisms(34% vs 27.3%), according to consensus sequences from Gen Bank patterns of HBV genotypes A to H. Variation/conservation in both domains depended on viral genotype, with genotype C being the most highly conserved and genotype E the most variable(limited finding, only 2 genotype E included). Of note, proline residues were highly conserved in both domains, and serine residues showed changes only to threonine or tyrosine in the virion morphogenesis domain. The rs2296651 polymorphism was not detected in any participant.CONCLUSION In our CHB population, the NTCP-interacting domain was highly conserved, particularly the proline residues and essential amino acids related with the NTCP interaction, and the prevalence of rs2296651 was low/null. | Rosario Casillas David Tabernero Josep Gregori Irene Belmonte Maria Francesca Cortese Carolina González Mar Riveiro-Barciela Rosa Maria López Josep Quer Rafael Esteban Maria Buti Francisco Rodríguez-Frías | 2018 | World Journal of Gastroenterology2018，24，6： | 5 |
| 11 | Cut and Paste: restoring cellular function by gene correction显示文摘 | Guang-Hui Liu Ignacio Sancho-Martinez Juan Carlos Izpisua Belmonte | 2012 | Cell Research2012，22，2： | 5 |
| 12 | A widely adaptable approach to generate integration-free iPSCs from non-invasively acquired human somatic cells显示文摘 | Zhichao Ding Lina Sui Ruotong Ren Yanjun Liu Xiuling Xu Lina Fu Ruijun Bai Tingting Yuan Ying Hao Weiqi Zhang Huize Pan Wensu Liu Han Yu Concepcion Rodriguez Esteban Xiaobing Yu Ze Yang Jian Li Xiaomin Wang Juan Carlos Izpisua Belmonte Guang-Hui Liu Fei Yi Jing Qu | 2015 | Protein & Cell2015，6，5： | 5 |
| 13 | Smashing Tissue Extraction and GC Analysis of Active Fatty Acids from Oil Cake of Perilla Seeds显示文摘Objective To optimize the extraction technology of perilla seeds oil from the oil cake of perilla seeds(OCPS)by using the contents of active fatty acids as evaluation standard.Methods The fatty acids were extracted from OCPS,the residue of perilla seeds after cold-press,by smashing tissue extraction(STE),the new technology selected through comparing with classical leaching extraction(LE),Soxhlet extraction(SE),ultrasonic extraction(UE),and supercritical-CO2 fluid extraction(SFE).For optimized condition of STE,orthogonal test was designed and completed.The contents of five fatty acids in extracted oil and OCPS were determined by GC.Results The optimized extraction parameters were smashing for 1.5 min under extraction power of 150 W and 1:6 of the material/solvent ratio.The contents of five fatty acids in the oils extracted by five techniques from OCPS and determined by GC were as follows:α-linolenic acid(41.12%-51.81%),linoleic acid(15.38%-16.43%),oleic acid (18.93%-27.28%),stearic acid(2.56%-4.01%),and palmitic acid(7.38%-10.77%).Conclusion The results show that STE is the most efficient technology with the highest yield(LE:0.57%;SE:1.03%;UE:0.61%;SFE:0.80%;STE: 1.17%)and shortest time(LE:720 min;SE:360 min;UE:30 min;SFE:120 min;STE:1.5 min)among five tested extraction technologies.It is first reported using STE to extract herbal oil enriched with active fatty acids. | SUN Yan-ling1,LIU Yan-ze2,3,XIAO Han4,WEI Ying-feng4,ZHAO Yu-qing1,5 1.Shenyang Pharmaceutical University,Shenyang 110006,China 2.Bio-organic and Natural Product Laboratory,MRC 311,McLean Hospital/Harvard Medical School,Belmont,MA 02478,USA 3.Institute of Medicinal Plant Development,Chinese Academy of Medical Sciences,Beijing 100193,China 4.Liaoning Jiashi Nutritional Plant Oil Development Co.Ltd.,Shenyang 110035,China 5.Key Laboratory of Structure-Based Drug Design&Discovery,Shenyang Pharmaceutical University,Ministry of Education,Shenyang 110016,China | 2011 | Chinese Herbal Medicines2011，3，1： | 5 |
| 14 | Single-nucleus transcriptomic landscape of primate hippocampal aging显示文摘The hippocampus plays a crucial role in learning and memory,and its progressive deterioration with age is functionally linked to a variety of human neurodegenerative diseases.Yet a systematic profiling of the aging effects on various hippocampal cell types in primates is still missing.Here,we reported a variety of new aging-associated phenotypic changes of the primate hippocampus.These include,in particular,increased DNA damage and heterochromatin erosion with time,alongside loss of proteostasis and elevated inflammation.To understand their cellular and molecular causes,we established the first single-nucleus transcriptomic atlas of primate hippocampal aging.Among the 12 identified cell types,neural transiently amplifying progenitor cell(TAPC)and microglia were most affected by aging.In-depth dissection of gene-expression dynamics revealed impaired TAPC division and compromised neuronal function along the neurogenesis trajectory;additionally elevated pro-inflammatory responses in the aged microglia and oligodendrocyte,as well as dysregulated coagulation pathways in the aged endothelial cells may contribute to a hostile microenvironment for neurogenesis.This rich resource for understanding primate hippocampal aging may provide potential diagnostic biomarkers and therapeutic interventions against age-related neurodegenerative diseases. | Hui Zhang Jiaming Li Jie Ren Shuhui Sun Shuai Ma Weiqi Zhang Yang Yu Yusheng Cai Kaowen Yan Wei Li Baoyang Hu Piu Chan Guo-Guang Zhao Juan Carlos Izpisua Belmonte Qi Zhou Jing Qu Si Wang Guang-Hui Liu | 2021 | Protein & Cell2021，12，9： | 5 |
| 15 | Safety and Efficacy of Antigen-Specific Regulatory T-Cell Therapy for Patients With Refractory Crohn’s Disease显示文摘 | Pierre Desreumaux Arnaud Foussat Matthieu Allez Laurent Beaugerie Xavier Hébuterne Yoram Bouhnik Maria Nachury Valérie Brun Hervé Bastian Nathalie Belmonte Michel Ticchioni Agnès Duchange Patricia Morel–Mandrino Virginie Neveu Nathalie Clerget–Chossat Mig | 2012 | Gastroenterology2012，，5： | 4 |
| 16 | Induced neural stem cells: a new tool for studying neural development and neurological disorders显示文摘 | Guang-Hui Liu Fei Yi Keiichiro Suzuki Jing Qu Juan Carlos Izpisua Belmonte | 2012 | Cell Research2012，22，7： | 4 |
| 17 | Human induced pluripotent stem cells derived hepatocytes:rising promise for disease modeling,drug development and cell therapy显示文摘Recent advances in the study of human hepatocytes derived from induced pluripotent stem cells(iPSC)represent new promises for liver disease study and drug discovery.Human hepatocytes or hepatocyte-like cells differentiated from iPSC recapitulate many func-tional properties of primary human hepatocytes and have been demonstrated as a powerful and efficient tool to model human liver metabolic diseases and fa-cilitate drug development process.In this review,we summarize the recent progress in this field and discuss the future perspective of the application of human iPSC derived hepatocytes. | Fei Yi Guang-Hui Liu Juan Carlos Izpisua Belmonte | 2012 | Protein & Cell2012，3，4： | 3 |
| 18 | A single-cell transcriptomic atlas of primate pancreatic islet aging显示文摘Aging-related degeneration of pancreatic islet cells contributes to impaired glucose tolerance and diabetes.Endocrine cells age heterogeneously,complicating the efforts to unravel the molecular drivers underlying endocrine aging.To overcome these obstacles,we undertook single-cell RNA sequencing of pancreatic islet cells obtained from young and aged non-diabetic cynomolgus monkeys.Despite sex differences and increased transcriptional variations,agedβ-cells showed increased unfolded protein response(UPR)along with the accumulation of protein aggregates.We observed transcriptomic dysregulation of UPR components linked to canonical ATF6 and IRE1 signaling pathways,comprising adaptive UPR during pancreatic aging.Notably,we found aging-relatedβ-cell-specific upregulation of HSP90 B1,an endoplasmic reticulum-located chaperone,impeded high glucose-induced insulin secretion.Our work decodes aging-associated transcriptomic changes that underlie pancreatic islet functional decay at single-cell resolution and indicates that targeting UPR components may prevent loss of proteostasis,suggesting an avenue to delayingβ-cell aging and preventing aging-related diabetes. | Jingyi Li Yuxuan Zheng Pengze Yan Moshi Song Si Wang Liang Sun Zunpeng Liu Shuai Ma Juan Carlos Izpisua Belmonte Piu Chan Qi Zhou Weiqi Zhang Guang-Hui Liu Fuchou Tang Jing Qu | 2021 | National Science Review2021，8，2： | 3 |
| 19 | Compound screening platform using human induced pluripotent stem cells to identify small molecules that promote chondrogenesis显示文摘Articular cartilage,which is mainly composed of collagen Ⅱ,enables smooth skeletal movement.Degeneration of collagen Ⅱ can be caused by various events,such as injury,but degeneration especially increases over the course of normal aging.Unfortunately,the body does not fully repair itself from this type of degeneration,resulting in impaired movement.Microfracture,an articular cartilage repair surgical technique,has been commonly used in the clinic to induce the repair of tissue at damage sites.Mesenchymal stem cells(MSC)have also been used as cell therapy to repair degenerated cartilage.However,the therapeutic outcomes of all these techniques vary in different patients depending on their age,health,lesion size and the extent of damage to the cartilage.The repairing tissues either form fibrocartilage or go into a hypertrophic stage,both of which do not reproduce the equivalent functionality of endogenous hyaline cartilage.One of the reasons for this is inefficient chondrogenesis by endogenous and exogenous MSC.Drugs that promote chondrogenesis could be used to induce self-repair of damaged cartilage as a non-invasive approach alone,or combined with other techniques to greatly assist the therapeutic outcomes.The recent development of human induced pluripotent stem cell(iPSCs),which are able to self-renew and differentiate into multiple cell types,provides a potentially valuable cell resource for drug screening in a“more relevant”cell type.Here we report a screening platform using human iPSCs in a multi-well plate format to identify compounds that could promote chondrogenesis. | Sheng-Lian Yang Erica Harnish Thomas Leeuw Uwe Dietz Erika Batchelder Paul SWright Jane Peppard Paul August Cecile Volle-Challier Francoise Bono Jean-Marc Herbert Juan Carlos Izpisua Belmonte | 2012 | Protein & Cell2012，3，12： | 3 |
| 20 | Establishment of hepatic and neural differentiation platforms of Wilson’s disease specific induced pluripotent stem cells显示文摘The combination of disease-specific human induced pluripotent stem cells(iPSC)and directed cell differentiation offers an ideal platform for modeling and studying many inherited human diseases.Wilson’s disease(WD)is a monogenic disorder of toxic copper accumulation caused by pathologic mutations of the ATP7B gene.WD affects multiple organs with primary manifestations in the liver and central nervous system(CNS).In order to better investigate the cellular pathogenesis of WD and to develop novel therapies against various WD syndromes,we sought to establish a comprehensive platform to differentiate WD patient iPSC into both hepatic and neural lineages.Here we report the generation of patient iPSC bearing a Caucasian population hotspot mutation of ATP7B.Combining with directed cell differentiation strategies,we successfully differentiated WD iPSC into hepatocyte-like cells,neural stem cells and neurons.Gene expression analysis and cDNA sequencing confirmed the expression of the mutant ATP7B gene in all differentiated cells.Hence we established a platform for studying both hepatic and neural abnormalities of WD,which may provide a new tool for tissue-specific disease modeling and drug screening in the future. | Fei Yi Jing Qu Mo Li Keiichiro Suzuki Na Young Kim Guang-Hui Liu Juan Carlos Izpisua Belmonte | 2012 | Protein & Cell2012，3，11： | 3 |
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