【求助】一个比较新的名词，因本人急用，敬请高人指教。急啊！诚恳的谢谢相助。
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A negative feedback loop exists
whereby NF-κB drives re-synthesis of IκBα
which promotes export of NF-κB from the
nucleus to the cytoplasm. This process
relies on Cezanne, a deubiquitinating
cysteine protease that stabilizes resynthesised
IκBα by removing
polyubiquitin from modified
intermediaries.这是2008年5月12日jbc上的一篇文章，文中出现Cezanne一词，我遍地搜索查询未果，应该是一个比较新的名词，因本人急用，敬请高人指教。急啊！诚恳的谢谢相助。
whereby NF-κB drives re-synthesis of IκBα
which promotes export of NF-κB from the
nucleus to the cytoplasm. This process
relies on Cezanne, a deubiquitinating
cysteine protease that stabilizes resynthesised
IκBα by removing
polyubiquitin from modified
intermediaries.这是2008年5月12日jbc上的一篇文章，文中出现Cezanne一词，我遍地搜索查询未果，应该是一个比较新的名词，因本人急用，敬请高人指教。急啊！诚恳的谢谢相助。
以 Cezanne为题搜索Pubmed，搜到一篇题为：NF-kappaB suppression by the deubiquitinating enzyme Cezanne: A NOVEL NEGATIVE FEEDBACK LOOP IN PRO-INFLAMMATORY SIGNALING.
PMID: 18178551
同样也是发表在JBC 2008 Mar 14
附摘要如下：
Transcription factors belonging to the NF-kappaB family regulate inflammation by inducing pro-inflammatory molecules (e.g. interleukin (IL)-8) in response to cytokines (e.g. tumor necrosis factor (TNF) alpha, IL-1) or other stimuli. Several negative regulators of NF-kappaB, including the ubiquitin-editing enzyme A20, participate in the resolution of inflammatory responses. We report that Cezanne, a member of the A20 family of the deubiquitinating cysteine proteases, can be induced by TNFalpha in cultured cells. Silencing of endogenous Cezanne using small interfering RNA led to elevated NF-kappaB luciferase reporter gene activity and enhanced expression of IL-8 transcripts in TNFalpha-treated cells. Thus we conclude that endogenous Cezanne can attenuate NF-kappaB activation and the induction of pro-inflammatory transcripts in response to TNF receptor (TNFR) signaling. Overexpression studies revealed that Cezanne suppressed NF-kappaB nuclear translocation and transcriptional activity by targeting the TNFR signaling pathway at the level of the IkappaB kinase complex or upstream from it. These effects were not observed in a form of Cezanne that was mutated at the catalytic cysteine residue (Cys209), indicating that the deubiquitinating activity of Cezanne is essential for NF-kappaB regulation. Finally, we demonstrate that Cezanne can be recruited to activated TNFRs where it suppresses the build-up of polyubiquitinated RIP1 signal adapter proteins. Thus we conclude that Cezanne forms a novel negative feedback loop in pro-inflammatory signaling and that it suppresses NF-kappaB activation by targeting RIP1 signaling intermediaries for deubiquitination.
注意红色字体，具体信号通路不是很清楚，对于专业的您或许有帮助！
附全文链接：
http://www.jbc.org/cgi/content/full/283/11/7036
PMID: 18178551
同样也是发表在JBC 2008 Mar 14
附摘要如下：
Transcription factors belonging to the NF-kappaB family regulate inflammation by inducing pro-inflammatory molecules (e.g. interleukin (IL)-8) in response to cytokines (e.g. tumor necrosis factor (TNF) alpha, IL-1) or other stimuli. Several negative regulators of NF-kappaB, including the ubiquitin-editing enzyme A20, participate in the resolution of inflammatory responses. We report that Cezanne, a member of the A20 family of the deubiquitinating cysteine proteases, can be induced by TNFalpha in cultured cells. Silencing of endogenous Cezanne using small interfering RNA led to elevated NF-kappaB luciferase reporter gene activity and enhanced expression of IL-8 transcripts in TNFalpha-treated cells. Thus we conclude that endogenous Cezanne can attenuate NF-kappaB activation and the induction of pro-inflammatory transcripts in response to TNF receptor (TNFR) signaling. Overexpression studies revealed that Cezanne suppressed NF-kappaB nuclear translocation and transcriptional activity by targeting the TNFR signaling pathway at the level of the IkappaB kinase complex or upstream from it. These effects were not observed in a form of Cezanne that was mutated at the catalytic cysteine residue (Cys209), indicating that the deubiquitinating activity of Cezanne is essential for NF-kappaB regulation. Finally, we demonstrate that Cezanne can be recruited to activated TNFRs where it suppresses the build-up of polyubiquitinated RIP1 signal adapter proteins. Thus we conclude that Cezanne forms a novel negative feedback loop in pro-inflammatory signaling and that it suppresses NF-kappaB activation by targeting RIP1 signaling intermediaries for deubiquitination.
注意红色字体，具体信号通路不是很清楚，对于专业的您或许有帮助！
附全文链接：
http://www.jbc.org/cgi/content/full/283/11/7036
由衷感谢，您是做学问的人。致敬！
您好，这个问题现在也困扰着我，请问您解决了吗？能不能给我解释一下啊？谢谢谢谢……
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