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    Kinome-wide functional analysis highlights the role of cytoskeletal remodeling in somatic cell reprogramming

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    Authors
    Sakurai, Kumi
    Talukdar, Indrani
    Patil, Veena S.
    Dang, Jason
    Li, Zhonghan
    Chang, Kung-Yen
    Lu, Chih-Chung
    Delorme-Walker, Violaine
    Dermardirossian, Celine
    Anderson, Karen
    Hanein, Dorit
    Yang, Chao-Shun
    Wu, Dongmei
    Liu, Yang
    Rana, Tariq M.
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    Student Authors
    Chao-Shun Yang
    UMass Chan Affiliations
    Department of Biochemistry and Molecular Pharmacology
    Document Type
    Journal Article
    Publication Date
    2014-04-03
    Keywords
    Actin Depolymerizing Factors; Animals; *Cell Differentiation; Cells, Cultured; Cellular Reprogramming; Cytoskeleton; Embryo, Mammalian; Embryonic Stem Cells; Fibroblasts; Gene Regulatory Networks; Humans; Induced Pluripotent Stem Cells; Lim Kinases; Mice; Microscopy, Confocal; Phosphorylation; Protein-Serine-Threonine Kinases; RNA Interference; RNA, Small Interfering; Teratoma
    Cell and Developmental Biology
    Cell Biology
    Genetics and Genomics
    Genomics
    
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    Link to Full Text
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071169/
    Abstract
    The creation of induced pluripotent stem cells (iPSCs) from somatic cells by ectopic expression of transcription factors has galvanized the fields of regenerative medicine and developmental biology. Here, we report a kinome-wide RNAi-based analysis to identify kinases that regulate somatic cell reprogramming to iPSCs. We prepared 3,686 small hairpin RNA (shRNA) lentiviruses targeting 734 kinase genes covering the entire mouse kinome and individually examined their effects on iPSC generation. We identified 59 kinases as barriers to iPSC generation and characterized seven of them further. We found that shRNA-mediated knockdown of the serine/threonine kinases TESK1 or LIMK2 promoted mesenchymal-to-epithelial transition, decreased COFILIN phosphorylation, and disrupted Actin filament structures during reprogramming of mouse embryonic fibroblasts. Similarly, knockdown of TESK1 in human fibroblasts also promoted reprogramming to iPSCs. Our study reveals the breadth of kinase networks regulating pluripotency and identifies a role for cytoskeletal remodeling in modulating the somatic cell reprogramming process.
    Source
    Cell Stem Cell. 2014 Apr 3;14(4):523-34. doi: 10.1016/j.stem.2014.03.001. Link to article on publisher's site
    DOI
    10.1016/j.stem.2014.03.001
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/33402
    PubMed ID
    24702998
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.stem.2014.03.001
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