國家衛生研究院 NHRI:Item 3990099045/7752
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 908091      Online Users : 914
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/7752


    Title: JMJD5 regulates PKM2 nuclear translocation and reprograms HIF-1alpha-mediated glucose metabolism
    Other Titles: JMJD5 regulates PKM2 nuclear translocation and reprograms HIF-1α-mediated glucose metabolism
    Authors: Wang, HJ;Hsieh, YJ;Cheng, WC;Lin, CP;Lin, YS;Yang, SF;Chen, CC;Izumiya, Y;Yu, JS;Kung, HJ;Wang, WC
    Contributors: Institute of Molecular and Genomic Medicine
    Abstract: JMJD5, a Jumonji C domain-containing dioxygenase, is important for embryonic development and cancer growth. Here, we show that JMJD5 is up-regulated by hypoxia and is crucial for hypoxiainduced cell proliferation. JMJD5 interacts directly with pyruvate kinase muscle isozyme (PKM)2 to modulate metabolic flux in cancer cells. The JMJD5-PKM2 interaction resides at the intersubunit interface region of PKM2, which hinders PKM2 tetramerization and blocks pyruvate kinase activity. This interaction also influences translocation of PKM2 into the nucleus and promotes hypoxiainducible factor (HIF)-1α-mediated transactivation. JMJD5 knockdown inhibits the transcription of the PKM2-HIF-1α target genes involved in glucose metabolism, resulting in a reduction of glucose uptake and lactate secretion in cancer cells. JMJD5, along with PKM2 and HIF-1α, is recruited to the hypoxia response element site in the lactate dehydrogenase A and PKM2 loci and mediates the recruitment of the latter two proteins. Our data uncover a mechanism whereby PKM2 can be regulated by factor-binding- induced homo/heterooligomeric restructuring, paving the way to cell metabolic reprogram.
    Date: 2014-01-07
    Relation: Proceedings of the National Academy of Sciences of the United States of America. 2014 Jan 7;111(1):279-284.
    Link to: http://dx.doi.org/10.1073/pnas.1311249111
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0027-8424&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000329350700076
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84891953688
    Appears in Collections:[Hsing-Jien Kung] Periodical Articles
    [Hung-Jung Wang] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    SCP84891953688.pdf1256KbAdobe PDF665View/Open


    All items in NHRI are protected by copyright, with all rights reserved.

    Related Items in TAIR

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback