共查询到20条相似文献,搜索用时 46 毫秒
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Adipogenesis is governed by a plethora of regulatory proteins which are most commonly controlled by the ubiquitin proteasome system. Here, we show that the differentiation of LiSa-2 preadipocytes is associated with an increase of cullin-associated and neddylation-dissociated 1 (CAND1), COP9 signalosome (CSN), neddylated cullin 3 (Cul3) and the BTB protein Keap1. Silencing of CAND1 leads to a decrease and reduced integration of Keap1 into Cul3-RING ubiquitin ligases (CRL3) and to a retardation of adipogenesis. Transient transfection of LiSa-2 cells with CAND1 targeting miRNA148a also reduces Keap1 and slowed down adipogenesis of LiSa-2 cells. These results demonstrate for the first time that CAND1 acts as a BTB-protein exchange factor for CRL3 complexes. The specific increase of neddylated Cul3 might be explained by the recruitment of Cul3 or CRL3 in a membrane-bound location during adipogenesis. Together, the results show that during adipogenesis in LiSa-2 cells a CAND1-dependent remodeling and activation/neddylation of CRL3 complexes take place. 相似文献
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McMahon M Thomas N Itoh K Yamamoto M Hayes JD 《The Journal of biological chemistry》2006,281(34):24756-24768
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Substrate-mediated regulation of cullin neddylation 总被引:1,自引:0,他引:1
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Specific patterns of electrophile adduction trigger Keap1 ubiquitination and Nrf2 activation 总被引:10,自引:0,他引:10
Hong F Sekhar KR Freeman ML Liebler DC 《The Journal of biological chemistry》2005,280(36):31768-31775
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