國家衛生研究院 NHRI:Item 3990099045/7344
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    题名: Tylophorine induces c-Jun protein accumulation through two discrete prolonged pathways NF-kappaB/PKCdelta/JNK and PI3K/PDK1/PP2A/eEF2 to promote G1 arrest in carcinoma cells
    作者: Yang, CW;Lee, YZ;Hsu, HY;Wu, CM;Chang, HY;Chao, YS;Lee, SJ
    贡献者: Institute of Biotechnology and Pharmaceutical Research
    摘要: Herein, we report that c-Jun protein, a component of AP-1, was elevated in the carcinoma cells by tylophorine treatment and the c-Jun phosphorylation was mainly through activated JNK. Moreover, ectopically overexpressed c-Jun significantly facilitated G1 arrest in the presence of tylophorine analyzed by flow cytometry analysis. Ultimately, the participation of c-Jun in downregulated cyclin A2 by tylophorine in carcinoma cells was dissected by ChIP and element reporter assays. Upon increase in binding of c-Jun to the deregulation AP-1 site and decrease in binding to up-regulation ATF site in c-Jun promoter, the tylophorine elevated c-Jun downregulated cyclin A2 promoter activity and thus its expression thereby leading to G1 arrest. Further biochemical studies using pharmacological inhibitors and RNA silencing approaches demonstrated that tylophorine elevated the c-Jun protein level is mainly through two discrete prolonged signaling pathways: 1) a prolonged activation of NF-kB_PKC?_(MKK4)_JNK cascade to phosphorylate c-Jun and increase its stability; 2) a prolonged activated PI3K_PDK1_PP2A_eEF2 cascade to sustain eEF2 activity and thus the c-Jun protein translation.
    日期: 2013-04
    關聯: FASEB Journal. 2013 Apr;27:lb74.
    Link to: http://www.fasebj.org/cgi/content/meeting_abstract/27/1_MeetingAbstracts/lb74
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0892-6638&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000319883503330
    显示于类别:[李秀珠] 會議論文/會議摘要
    [趙宇生(2002-2013)] 會議論文/會議摘要

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