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  • 1
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    Switching cell fate, ncRNAs coming to play (2013)
    Springer Nature
    Details
    Publication Date: 2013-01-18
    Description: Switching cell fate, ncRNAs coming to play Cell Death and Disease 4, e464 (January 2013). doi:10.1038/cddis.2012.196 Authors: D Guan, W Zhang, W Zhang, G-H Liu & J C Izpisua Belmonte
    Keywords: ncRNAslncRNAsmicroRNAsreprogrammingtrans-differentiation
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 2
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    Zebrafish heart regeneration occurs by cardiomyocyte dedifferentiation and proliferation (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-26
    Description: Although mammalian hearts show almost no ability to regenerate, there is a growing initiative to determine whether existing cardiomyocytes or progenitor cells can be coaxed into eliciting a regenerative response. In contrast to mammals, several non-mammalian vertebrate species are able to regenerate their hearts, including the zebrafish, which can fully regenerate its heart after amputation of up to 20% of the ventricle. To address directly the source of newly formed cardiomyocytes during zebrafish heart regeneration, we first established a genetic strategy to trace the lineage of cardiomyocytes in the adult fish, on the basis of the Cre/lox system widely used in the mouse. Here we use this system to show that regenerated heart muscle cells are derived from the proliferation of differentiated cardiomyocytes. Furthermore, we show that proliferating cardiomyocytes undergo limited dedifferentiation characterized by the disassembly of their sarcomeric structure, detachment from one another and the expression of regulators of cell-cycle progression. Specifically, we show that the gene product of polo-like kinase 1 (plk1) is an essential component of cardiomyocyte proliferation during heart regeneration. Our data provide the first direct evidence for the source of proliferating cardiomyocytes during zebrafish heart regeneration and indicate that stem or progenitor cells are not significantly involved in this process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846535/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846535/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jopling, Chris -- Sleep, Eduard -- Raya, Marina -- Marti, Merce -- Raya, Angel -- Izpisua Belmonte, Juan Carlos -- R33 HL088293/HL/NHLBI NIH HHS/ -- R33 HL088293-01A1/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Mar 25;464(7288):606-9. doi: 10.1038/nature08899.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center of Regenerative Medicine in Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20336145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle Proteins/metabolism ; *Cell Dedifferentiation ; Cell Lineage ; Cell Proliferation ; Gene Expression Regulation ; Heart/*physiology ; Myocytes, Cardiac/*cytology/enzymology ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Regeneration/genetics/*physiology ; Sarcomeres/metabolism ; Zebrafish/genetics/metabolism/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Disease-corrected haematopoietic progenitors from Fanconi anaemia induced pluripotent stem cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-06-02
    Description: The generation of induced pluripotent stem (iPS) cells has enabled the derivation of patient-specific pluripotent cells and provided valuable experimental platforms to model human disease. Patient-specific iPS cells are also thought to hold great therapeutic potential, although direct evidence for this is still lacking. Here we show that, on correction of the genetic defect, somatic cells from Fanconi anaemia patients can be reprogrammed to pluripotency to generate patient-specific iPS cells. These cell lines appear indistinguishable from human embryonic stem cells and iPS cells from healthy individuals. Most importantly, we show that corrected Fanconi-anaemia-specific iPS cells can give rise to haematopoietic progenitors of the myeloid and erythroid lineages that are phenotypically normal, that is, disease-free. These data offer proof-of-concept that iPS cell technology can be used for the generation of disease-corrected, patient-specific cells with potential value for cell therapy applications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720823/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720823/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raya, Angel -- Rodriguez-Piza, Ignasi -- Guenechea, Guillermo -- Vassena, Rita -- Navarro, Susana -- Barrero, Maria Jose -- Consiglio, Antonella -- Castella, Maria -- Rio, Paula -- Sleep, Eduard -- Gonzalez, Federico -- Tiscornia, Gustavo -- Garreta, Elena -- Aasen, Trond -- Veiga, Anna -- Verma, Inder M -- Surralles, Jordi -- Bueren, Juan -- Izpisua Belmonte, Juan Carlos -- R01 HL053670/HL/NHLBI NIH HHS/ -- R01 HL053670-14/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Jul 2;460(7251):53-9. doi: 10.1038/nature08129. Epub 2009 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Regenerative Medicine in Barcelona, Dr. Aiguader 88, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19483674" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cellular Reprogramming ; Fanconi Anemia/*pathology/*therapy ; Health ; Hematopoietic Stem Cells/*cytology/metabolism ; Humans ; Pluripotent Stem Cells/*cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Linking the p53 tumour suppressor pathway to somatic cell reprogramming (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-08-12
    Description: Reprogramming somatic cells to induced pluripotent stem (iPS) cells has been accomplished by expressing pluripotency factors and oncogenes, but the low frequency and tendency to induce malignant transformation compromise the clinical utility of this powerful approach. We address both issues by investigating the mechanisms limiting reprogramming efficiency in somatic cells. Here we show that reprogramming factors can activate the p53 (also known as Trp53 in mice, TP53 in humans) pathway. Reducing signalling to p53 by expressing a mutated version of one of its negative regulators, by deleting or knocking down p53 or its target gene, p21 (also known as Cdkn1a), or by antagonizing reprogramming-induced apoptosis in mouse fibroblasts increases reprogramming efficiency. Notably, decreasing p53 protein levels enabled fibroblasts to give rise to iPS cells capable of generating germline-transmitting chimaeric mice using only Oct4 (also known as Pou5f1) and Sox2. Furthermore, silencing of p53 significantly increased the reprogramming efficiency of human somatic cells. These results provide insights into reprogramming mechanisms and suggest new routes to more efficient reprogramming while minimizing the use of oncogenes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735889/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735889/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawamura, Teruhisa -- Suzuki, Jotaro -- Wang, Yunyuan V -- Menendez, Sergio -- Morera, Laura Batlle -- Raya, Angel -- Wahl, Geoffrey M -- Izpisua Belmonte, Juan Carlos -- 5 R01 CA061449/CA/NCI NIH HHS/ -- 5 R01 CA100845/CA/NCI NIH HHS/ -- R01 CA061449/CA/NCI NIH HHS/ -- R01 CA061449-30/CA/NCI NIH HHS/ -- R01 CA100845/CA/NCI NIH HHS/ -- R01 CA100845-05/CA/NCI NIH HHS/ -- R33 HL088293/HL/NHLBI NIH HHS/ -- R33 HL088293-03/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Aug 27;460(7259):1140-4. doi: 10.1038/nature08311. Epub 2009 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19668186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cellular Reprogramming/*physiology ; Cyclin-Dependent Kinase Inhibitor p21/deficiency/genetics/metabolism ; Down-Regulation ; Embryo, Mammalian/cytology ; Female ; Fibroblasts/cytology/metabolism ; Humans ; Keratinocytes ; Male ; Mice ; Mice, Inbred C57BL ; Pluripotent Stem Cells/*cytology/*metabolism ; Tumor Suppressor Protein p53/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Distinct WNT pathways regulating AER formation and dorsoventral polarity in the chick limb bud (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: The apical ectodermal ridge (AER) is an essential structure for vertebrate limb development. Wnt3a is expressed during the induction of the chick AER, and misexpression of Wnt3a induces ectopic expression of AER-specific genes in the limb ectoderm. The genes beta-catenin and Lef1 can mimic the effect of Wnt3a, and blocking the intrinsic Lef1 activity disrupts AER formation. Hence, Wnt3a functions in AER formation through the beta-catenin/LEF1 pathway. In contrast, neither beta-catenin nor Lef1 affects the Wnt7a-regulated dorsoventral polarity of the limb. Thus, two related Wnt genes elicit distinct responses in the same tissues by using different intracellular pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kengaku, M -- Capdevila, J -- Rodriguez-Esteban, C -- De La Pena, J -- Johnson, R L -- Izpisua Belmonte, J C -- Tabin, C J -- New York, N.Y. -- Science. 1998 May 22;280(5367):1274-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596583" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Avian Proteins ; Base Sequence ; *Body Patterning ; Chick Embryo ; Cloning, Molecular ; Cytoskeletal Proteins/genetics/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Ectoderm/*metabolism ; Fibroblast Growth Factor 4 ; Fibroblast Growth Factor 8 ; Fibroblast Growth Factors/biosynthesis/genetics ; *Gene Expression Regulation, Developmental ; Glucosyltransferases ; Growth Substances/biosynthesis/genetics ; Homeodomain Proteins/genetics ; Intercellular Signaling Peptides and Proteins ; Limb Buds/embryology/*metabolism ; Lymphoid Enhancer-Binding Factor 1 ; Mesoderm/metabolism ; Molecular Sequence Data ; Morphogenesis ; Protein Biosynthesis ; Proteins/*genetics/physiology ; Proto-Oncogene Proteins/biosynthesis/*genetics/physiology ; Signal Transduction ; *Trans-Activators ; Transcription Factors/genetics/metabolism ; Up-Regulation ; Wnt Proteins ; Wnt3 Protein ; Wnt3A Protein ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Somatic coding mutations in human induced pluripotent stem cells (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-04
    Description: Defined transcription factors can induce epigenetic reprogramming of adult mammalian cells into induced pluripotent stem cells. Although DNA factors are integrated during some reprogramming methods, it is unknown whether the genome remains unchanged at the single nucleotide level. Here we show that 22 human induced pluripotent stem (hiPS) cell lines reprogrammed using five different methods each contained an average of five protein-coding point mutations in the regions sampled (an estimated six protein-coding point mutations per exome). The majority of these mutations were non-synonymous, nonsense or splice variants, and were enriched in genes mutated or having causative effects in cancers. At least half of these reprogramming-associated mutations pre-existed in fibroblast progenitors at low frequencies, whereas the rest occurred during or after reprogramming. Thus, hiPS cells acquire genetic modifications in addition to epigenetic modifications. Extensive genetic screening should become a standard procedure to ensure hiPS cell safety before clinical use.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074107/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074107/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gore, Athurva -- Li, Zhe -- Fung, Ho-Lim -- Young, Jessica E -- Agarwal, Suneet -- Antosiewicz-Bourget, Jessica -- Canto, Isabel -- Giorgetti, Alessandra -- Israel, Mason A -- Kiskinis, Evangelos -- Lee, Je-Hyuk -- Loh, Yuin-Han -- Manos, Philip D -- Montserrat, Nuria -- Panopoulos, Athanasia D -- Ruiz, Sergio -- Wilbert, Melissa L -- Yu, Junying -- Kirkness, Ewen F -- Izpisua Belmonte, Juan Carlos -- Rossi, Derrick J -- Thomson, James A -- Eggan, Kevin -- Daley, George Q -- Goldstein, Lawrence S B -- Zhang, Kun -- K08 HL089150/HL/NHLBI NIH HHS/ -- R01 HL094963/HL/NHLBI NIH HHS/ -- R01 HL094963-01/HL/NHLBI NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- U01 HL100001/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 3;471(7336):63-7. doi: 10.1038/nature09805.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of California at San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368825" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Cellular Reprogramming/*genetics ; DNA Mutational Analysis ; Epistasis, Genetic/genetics ; Fibroblasts/cytology/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology/*metabolism ; Male ; Middle Aged ; Models, Genetic ; Mutagenesis/*genetics ; Open Reading Frames/genetics ; Point Mutation/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-02-25
    Description: Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal human premature ageing disease, characterized by premature arteriosclerosis and degeneration of vascular smooth muscle cells (SMCs). HGPS is caused by a single point mutation in the lamin A (LMNA) gene, resulting in the generation of progerin, a truncated splicing mutant of lamin A. Accumulation of progerin leads to various ageing-associated nuclear defects including disorganization of nuclear lamina and loss of heterochromatin. Here we report the generation of induced pluripotent stem cells (iPSCs) from fibroblasts obtained from patients with HGPS. HGPS-iPSCs show absence of progerin, and more importantly, lack the nuclear envelope and epigenetic alterations normally associated with premature ageing. Upon differentiation of HGPS-iPSCs, progerin and its ageing-associated phenotypic consequences are restored. Specifically, directed differentiation of HGPS-iPSCs to SMCs leads to the appearance of premature senescence phenotypes associated with vascular ageing. Additionally, our studies identify DNA-dependent protein kinase catalytic subunit (DNAPKcs, also known as PRKDC) as a downstream target of progerin. The absence of nuclear DNAPK holoenzyme correlates with premature as well as physiological ageing. Because progerin also accumulates during physiological ageing, our results provide an in vitro iPSC-based model to study the pathogenesis of human premature and physiological vascular ageing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088088/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088088/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Guang-Hui -- Barkho, Basam Z -- Ruiz, Sergio -- Diep, Dinh -- Qu, Jing -- Yang, Sheng-Lian -- Panopoulos, Athanasia D -- Suzuki, Keiichiro -- Kurian, Leo -- Walsh, Christopher -- Thompson, James -- Boue, Stephanie -- Fung, Ho Lim -- Sancho-Martinez, Ignacio -- Zhang, Kun -- Yates, John 3rd -- Izpisua Belmonte, Juan Carlos -- P41 RR011823/RR/NCRR NIH HHS/ -- R01 DA025779/DA/NIDA NIH HHS/ -- R01 DA025779-01/DA/NIDA NIH HHS/ -- R01-DA025779/DA/NIDA NIH HHS/ -- T32 CA009370/CA/NCI NIH HHS/ -- T32 CA009370-25A1/CA/NCI NIH HHS/ -- England -- Nature. 2011 Apr 14;472(7342):221-5. doi: 10.1038/nature09879. Epub 2011 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21346760" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/metabolism/pathology/physiology ; Aging, Premature/genetics/pathology/physiopathology ; Calcium-Binding Proteins/analysis ; Cell Aging ; Cell Differentiation ; Cell Line ; Cellular Reprogramming ; DNA-Activated Protein Kinase/metabolism ; Epigenesis, Genetic ; Fibroblasts/pathology ; Holoenzymes/metabolism ; Humans ; Induced Pluripotent Stem Cells/metabolism/*pathology ; Lamin Type A ; Microfilament Proteins/analysis ; Models, Biological ; Muscle, Smooth, Vascular/pathology ; Nuclear Envelope/pathology ; Nuclear Proteins/analysis/genetics/metabolism ; Phenotype ; Progeria/genetics/pathology/physiopathology ; Protein Precursors/analysis/genetics/metabolism ; Substrate Specificity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Progressive degeneration of human neural stem cells caused by pathogenic LRRK2 (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-19
    Description: Nuclear-architecture defects have been shown to correlate with the manifestation of a number of human diseases as well as ageing. It is therefore plausible that diseases whose manifestations correlate with ageing might be connected to the appearance of nuclear aberrations over time. We decided to evaluate nuclear organization in the context of ageing-associated disorders by focusing on a leucine-rich repeat kinase 2 (LRRK2) dominant mutation (G2019S; glycine-to-serine substitution at amino acid 2019), which is associated with familial and sporadic Parkinson's disease as well as impairment of adult neurogenesis in mice. Here we report on the generation of induced pluripotent stem cells (iPSCs) derived from Parkinson's disease patients and the implications of LRRK2(G2019S) mutation in human neural-stem-cell (NSC) populations. Mutant NSCs showed increased susceptibility to proteasomal stress as well as passage-dependent deficiencies in nuclear-envelope organization, clonal expansion and neuronal differentiation. Disease phenotypes were rescued by targeted correction of the LRRK2(G2019S) mutation with its wild-type counterpart in Parkinson's disease iPSCs and were recapitulated after targeted knock-in of the LRRK2(G2019S) mutation in human embryonic stem cells. Analysis of human brain tissue showed nuclear-envelope impairment in clinically diagnosed Parkinson's disease patients. Together, our results identify the nucleus as a previously unknown cellular organelle in Parkinson's disease pathology and may help to open new avenues for Parkinson's disease diagnoses as well as for the potential development of therapeutics targeting this fundamental cell structure.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504651/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504651/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Guang-Hui -- Qu, Jing -- Suzuki, Keiichiro -- Nivet, Emmanuel -- Li, Mo -- Montserrat, Nuria -- Yi, Fei -- Xu, Xiuling -- Ruiz, Sergio -- Zhang, Weiqi -- Wagner, Ulrich -- Kim, Audrey -- Ren, Bing -- Li, Ying -- Goebl, April -- Kim, Jessica -- Soligalla, Rupa Devi -- Dubova, Ilir -- Thompson, James -- Yates, John 3rd -- Esteban, Concepcion Rodriguez -- Sancho-Martinez, Ignacio -- Izpisua Belmonte, Juan Carlos -- ES017166/ES/NIEHS NIH HHS/ -- GTB07001/Telethon/Italy -- P41 RR011823/RR/NCRR NIH HHS/ -- U01 ES017166/ES/NIEHS NIH HHS/ -- England -- Nature. 2012 Nov 22;491(7425):603-7. doi: 10.1038/nature11557. Epub 2012 Oct 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. ghliu@ibp.ac.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23075850" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Cell Differentiation ; Cell Division ; Cell Line ; Clone Cells/metabolism/pathology ; Embryonic Stem Cells/metabolism/pathology ; Gene Knock-In Techniques ; Humans ; Induced Pluripotent Stem Cells/metabolism/pathology ; Mutant Proteins/genetics/*metabolism ; Mutation ; Neural Stem Cells/metabolism/*pathology ; Nuclear Envelope/genetics/pathology ; Parkinson Disease/*pathology ; Proteasome Endopeptidase Complex/metabolism ; Protein-Serine-Threonine Kinases/*genetics/*metabolism ; Stress, Physiological
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Stem cells: Surf the waves of reprogramming (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sancho-Martinez, Ignacio -- Izpisua Belmonte, Juan Carlos -- England -- Nature. 2013 Jan 17;493(7432):310-1. doi: 10.1038/493310b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23325209" target="_blank"〉PubMed〈/a〉
    Keywords: *Cellular Reprogramming ; Humans ; Single-Cell Analysis ; Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Stem cells: A designer's guide to pluripotency (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Jun -- Izpisua Belmonte, Juan Carlos -- England -- Nature. 2014 Dec 11;516(7530):172-3. doi: 10.1038/516172a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25503227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming/*genetics/*physiology ; *Epigenesis, Genetic ; Female ; Genome/*genetics ; Induced Pluripotent Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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