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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >β-arrestin 2 oligomerization controls the Mdm2-dependent inhibition of p53
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β-arrestin 2 oligomerization controls the Mdm2-dependent inhibition of p53

机译：β-arrestin2寡聚控制Mdm2依赖的p53抑制

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摘要

β-arrestins (β-arrs), two ubiquitous proteins involved in serpentine heptahelical receptor regulation and signaling, form constitutive homo- and heterooligomers stabilized by inositol 1,2,3,4,5,6-hexakisphosphate (IP6). Monomeric β-arrs are believed to interact with receptors after agonist activation, and therefore, β-arr oli-gomers have been proposed to represent a resting biologically inactive state. In contrast to this, we report here that the interaction with and subsequent titration out of the nucleus of the protooncogene Mdm2 specifically require β-arr2 oligomers together with the previously characterized nucleocytoplasmic shuttling of β-arr2. Mutation of the IP6-binding sites impair oligomerization, reduce interaction with Mdm2, and inhibit p53-dependent antiproliferative effects of β-arr2, whereas the competence for receptor regulation and signaling is maintained. These observations suggest that the intracellular concentration of β-arr2 oligomers might control cell survival and proliferation.
机译：β-arrestins（β-arrs）是参与蛇形七螺旋受体调节和信号转导的两种普遍存在的蛋白，形成由肌醇1,2,3,4,5,6-六六磷酸（IP6）稳定的组成型均聚物和杂聚物。单体β-arr被认为在激动剂活化后与受体相互作用，因此，有人提出β-arr寡聚体代表静止的生物惰性状态。与此相反，我们在此报告，与原癌基因Mdm2的核相互作用和随后的滴定特别需要β-arr2低聚物以及先前表征的β-arr2核质穿梭。 IP6结合位点的突变会削弱寡聚，减少与Mdm2的相互作用，并抑制p53依赖性的β-arr2的抗增殖作用，而受体调节和信号传导的能力得以维持。这些观察结果表明，β-arr2寡聚物的细胞内浓度可能控制细胞存活和增殖。

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