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    Runt-related transcription factor RUNX3 is a target of MDM2-mediated ubiquitination

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    Authors
    Chi, Xin-Zi
    Kim, Jiyeon
    Lee, Yong-Hee
    Lee, Jung-Won
    Lee, Kyeong-Sook
    Wee, Hee-Jun
    Kim, Wun-Jae
    Park, Woo-Yoon
    Oh, Byung-Chul
    Stein, Gary S.
    Ito, Yoshiaki
    Van Wijnen, Andre J.
    Bae, Suk-Chul
    Show allShow less
    UMass Chan Affiliations
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2009-10-08
    Keywords
    Apoptosis
    Blotting, Western
    Cell Transformation, Neoplastic
    Cells, Cultured
    Core Binding Factor Alpha 3 Subunit
    inhibitors
    Gene Expression Regulation, Neoplastic
    Humans
    Immunoprecipitation
    Kidney
    Mutation
    Proto-Oncogene Proteins c-mdm2
    RNA, Small Interfering
    Transcription, Genetic
    Transcriptional Activation
    Transfection
    Tumor Suppressor Protein p14ARF
    Tumor Suppressor Protein p53
    Ubiquitination
    Ubiquitins
    ras Proteins
    Cell Biology
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    Link to Full Text
    http://dx.doi.org/10.1158/0008-5472.CAN-09-1057
    Abstract
    The p14(ARF)-MDM2-p53 pathway constitutes an effective mechanism for protecting cells from oncogenic stimuli such as activated Ras and Myc. Importantly, Ras activation induces p14(ARF) and often occurs earlier than p53 inactivation during cancer development. Here, we show that RUNX3, a tumor suppressor in various tumors including stomach, bladder, colon, and lung, is stabilized by Ras activation through the p14(ARF)-MDM2 signaling pathway. RUNX3 directly binds MDM2 through its Runt-related DNA-binding domain. MDM2 blocks RUNX3 transcriptional activity by interacting with RUNX3 through an acidic domain adjacent to the p53-binding domain of MDM2 and ubiquitinates RUNX3 on key lysine residues to mediate nuclear export and proteasomal degradation. Our data indicate that the lineage-specific tumor suppressor RUNX3 and the ubiquitous p53 protein are both principal responders of the p14(ARF)-MDM2 cell surveillance pathway that prevents pathologic consequences of abnormal oncogene activation.
    Source
    Cancer Res. 2009 Oct 15;69(20):8111-9. Epub 2009 Oct 6. Link to article on publisher's site
    DOI
    10.1158/0008-5472.CAN-09-1057
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/49590
    PubMed ID
    19808967
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1158/0008-5472.CAN-09-1057
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