Abstract:
:The pivotal role of LYRIC/AEG-1 in malignant transformation, tumourigenesis and chemo-resistance has previously been demonstrated in different cell types and sub-cellular compartments. The localisation of LYRIC/AEG-1 appears crucial to its function and is regulated by three lysine-rich nuclear localisation signal regions, one of which was previously demonstrated to be modified by ubiquitin. Here we show that mutation of LYRIC/AEG-1 at K486 and K491 results in a loss of ubiquitination. A K486/491R double mutant that is incapable of ubiquitination shows reduced binding to the NFκB subunit p65 or importin-β resulting in a distinctive peri-nuclear localisation of LYRIC/AEG-1. We also provide evidence to suggest that TOPORS, an E3 ligase that also regulates p53 modification may be responsible for LYRIC/AEG-1 ubiquitin modification. Overall we demonstrate that specific sites of LYRIC/AEG-1 ubiquitination are essential for regulating LYRIC/AEG-1 localisation and functionally interacting proteins.
journal_name
Mol Oncoljournal_title
Molecular oncologyauthors
Luxton HJ,Barnouin K,Kelly G,Hanrahan S,Totty N,Neal DE,Whitaker HCdoi
10.1016/j.molonc.2014.01.009subject
Has Abstractpub_date
2014-05-01 00:00:00pages
633-41issue
3eissn
1574-7891issn
1878-0261pii
S1574-7891(14)00021-0journal_volume
8pub_type
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journal_title:Molecular oncology
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更新日期:2017-07-01 00:00:00
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pub_type: 临床试验,杂志文章,多中心研究
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pub_type: 杂志文章
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journal_title:Molecular oncology
pub_type: 杂志文章
doi:10.1016/j.molonc.2015.03.009
更新日期:2015-08-01 00:00:00
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pub_type: 杂志文章
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doi:10.1016/j.molonc.2015.09.006
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pub_type: 杂志文章,评审
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