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IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response.

IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response. Research Abstract Details 

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  • IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response. Abstract Text:

    lun songLun Song,jingxia liJingxia Li,dongyun zhangDongyun Zhang,zheng-gang liuZheng-Gang Liu,jianping yeJianping Ye,qimin zhanQimin Zhan,han-ming shenHan-Ming Shen,matt whitemanMatt Whiteman,chuanshu huangChuanshu Huang,

    Cross talk between NF-kappaB and c-Jun N-terminal kinases (JNKs) has been implicated in the cell life and death decision under various stresses. Functional suppression of JNK activation by NF-kappaB has recently been proposed as a key cellular survival mechanism and contributes to cancer cells escaping from apoptosis. We provide a novel scenario of the proapoptotic role of IkappaB kinase beta (IKKbeta)-NF-kappaB, which can act as the activator of the JNK pathway through the induction of GADD45alpha for triggering MKK4/JNK activation, in response to the stimulation of arsenite, a cancer therapeutic reagent. This effect of IKKbeta-NF-kappaB is dependent on p50 but not the p65/relA NF-kappaB subunit, which can increase the stability of GADD45alpha protein through suppressing its ubiquitination and proteasome-dependent degradation. IKKbeta-NF-kappaB can therefore either activate or suppress the JNK cascade and consequently mediate pro- or antiapoptotic effects, depending on the manner of its induction. Furthermore, the NF-kappaB p50 subunit can exert a novel regulatory function on protein modification independent of the classical NF-kappaB transcriptional activity.

    IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response. Publishing Authors By Initials

    l songL Song,j liJ Li,d zhangD Zhang,zg liuZG Liu,j yeJ Ye,q zhanQ Zhan,hm shenHM Shen,m whitemanM Whiteman,c huangC Huang,

    For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

    PUBMED ID PMID:

    MEDLINE DATE:

    IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: The Journal of cell biology

    VOLUME: 175

    Page Numbers: 607-17

    Journal Abbreviation: J. Cell Biol.

    ISSN: 0021-9525

    DAY: 20

    MONTH: Nov

    YEAR: 2006

    IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 375356

    IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response. Keywords Mesh Terms:

    KEYWORDS: Up-Regulation

    MESH TERMS: drug effects

    Chemical & Substance for Abstract: IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response. Information

    Substance Name: Proteasome Endopeptidase Complex

    Registry Number: EC 3.4.25.1

    Grant and Affiliation Information for IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response.

    AFFILIATION: Nelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIEHS

    GRANT: ES012451

    ACRONYM: ES

    MEDLINETA: J Cell Biol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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    IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response Related Publications

     

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