The ubiquitin-proteasome system and activation of NF-κB: involvement of the ubiquitin ligase KPC1 in p105 processing and tumor suppression
The ubiquitin-proteasome system and activation of NF-κB: involvement of the ubiquitin ligase KPC1 in p105 processing and tumor suppression
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DOI：
10.1080/23723556.2015.1054552
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发表时间：
2015-01-01
影响因子：
2.1
通讯作者：
Ciechanover, Aaron
中科院分区：
文献类型：
--
作者：
Kravtsova-Ivantsiv, Yelena;Ciechanover, Aaron
核因子-κ B（NF-κ B）的p50亚基由p105前体的加工产生。我们确定KIP 1泛素化促进复合物1（KPC 1）作为泛素（Ub）连接酶介导这一过程。KPC 1的过表达导致肿瘤抑制，可能是由于p50-p50同源二聚体的产生。高水平的KPC 1和核p50似乎对维持非恶性状态很重要。
The p50 subunit of nuclear factor-kappa B (NF-kappa B) is generated from processing of the p105 precursor. We identified KIP1 ubiquitination-promoting complex 1 (KPC1) as the ubiquitin (Ub) ligase mediating this process. Overexpression of KPC1 results in tumor suppression, probably due to the generation of p50-p50 homodimers. It appears that high levels of KPC1 and nuclear p50 are important for maintaining the non-malignant state.