近日，韓國(guó)建國(guó)大學(xué)微生物工程教授安成冠（音譯）引領(lǐng)的研究團(tuán)隊(duì)稱(chēng),，一種名為“木蘭E3”的連接酶可侵入絲氨酸蛋白激酶，而后者正是各種癌細(xì)胞生長(zhǎng)的關(guān)鍵“組件”,。學(xué)術(shù)論文發(fā)表在最新一期英國(guó)《自然》雜志的《細(xì)胞研究》（Cell Research）分刊,。
“我們發(fā)現(xiàn)木蘭酶可以侵入絲氨酸蛋白激酶細(xì)胞的線粒體，進(jìn)而分解絲氨酸蛋白激酶,，”韓聯(lián)社18日援引研究團(tuán)隊(duì)的結(jié)論說(shuō),。
線粒體是細(xì)胞的動(dòng)力工廠，控制細(xì)胞的分裂,、生長(zhǎng)和死亡,。
韓聯(lián)社說(shuō)，科學(xué)界上世紀(jì)90年代便發(fā)現(xiàn)絲氨酸蛋白激酶與癌細(xì)胞生長(zhǎng)之間的直接關(guān)聯(lián)性,，但迄今沒(méi)有特別有效的方法抑制特性活躍的絲氨酸蛋白激酶,。在傳統(tǒng)化學(xué)療法中，蛋白激酶表現(xiàn)出相當(dāng)強(qiáng)耐受度,，這也是化學(xué)療法在癌癥面前顯現(xiàn)弱點(diǎn)的主要原因,。
研究團(tuán)隊(duì)說(shuō)，木蘭E3連接酶可控制絲氨酸蛋白激酶的特性為癌癥治療打開(kāi)一條新的通道,。借助這一原理,，或可找到治療癌癥的“全能療法”，不僅可治療肺癌,、乳腺癌,、子宮癌等固體腫瘤類(lèi)癌癥，而且可醫(yī)治白血病,、骨髓癌,、淋巴癌等血液型癌癥。（生物谷Bioon.com）
doi: 10.1038/cr.2012.38
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Akt is negatively regulated by the MULAN E3 ligase
Bae S, Kim SY, Jung JH, Yoon Y, Cha HJ, Lee H, Kim K, Kim J, An IS, Kim J, Um HD, Park IC, Lee SJ, Nam SY, Jin YW, Lee JH, An S.
The serine/threonine kinase Akt functions in multiple cellular processes, including cell survival and tumor development. Studies of the mechanisms that negatively regulate Akt have focused on dephosphorylation-mediated inactivation. In this study, we identified a negative regulator of Akt, MULAN, which possesses both a RING finger domain and E3 ubiquitin ligase activity. Akt was found to directly interact with MULAN and to be ubiquitinated by MULAN in vitro and in vivo. Other molecular assays demonstrated that phosphorylated Akt is a substantive target for both interaction with MULAN and ubiquitination by MULAN. The results of the functional studies suggest that the degradation of Akt by MULAN suppresses cell proliferation and viability. These data provide insight into the Akt ubiquitination signaling network.
