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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
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Hs-CUL-3 widely expressed in human tissues and its expression in cultured COLO205 colon cancer cells was increased when compared with that in normal colon cells [1].
Moreover, we show that a RhoBTB2 missense mutant identified in a lung cancercell line is neither able to bind Cul3 nor is it regulated by the ubiquitin/proteasome system, resulting in increased RhoBTB2 protein levels in vivo [2].
Neddylation of Cul3 on Lys 712 is required for Keap1-dependent ubiquitination of Nrf2 in vivo [3].
Oxidative stress sensor Keap1 functions as an adaptor for Cul3-based E3 ligase to regulate proteasomal degradation of Nrf2 [4].
We found that the resistant cells showed elevated expressions of Cul3, a member of the cullin family of E3 ubiquitin ligases [5].
Conversely, Cul3 overexpression by stable transfectionpromoted covalent complex degradation and reduced CPT-inducedcell death without affecting basal TOP1 expression levels [5].
KEL-8 is a substrate receptor for CUL3-dependent ubiquitin ligase that regulates synaptic glutamate receptor turnover [6].
Conclusion: Cul-3b is a novel transcript variant of CUL-3, which may be important not only for the development of human testis but also for that of other organs [7].
Northern blot analysis showed that phorbol 12-myristate 13-acetate increased the expression of Hs-CUL-3 mRNA in a concentration- and time-dependent manner, and this increase was inhibited by sodium salicylate[1].
