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您的检索式：作者名="Anna Maria Brunati"
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| 1 | Regulation of membrane band 3 Tyr-phosphorylation by proteolysis of p72^syk and possible involvement in senescence process显示文摘红血球老朽被房间表面 epitopes 的暴露在导致红血房间的有免疫力的调停的移动的房间膜蛋白质上描绘。为抗原形成的一机制是 transmembrane 蛋白质的酷氨酸 phosphorylation (Tyr-P ) 由 Syk kinase 的乐队 3。我们的目的是测试假设由到 isoform 提高的 36 kDa (p36Syk ) 的从 72 kDa (p72Syk ) 的变换的 Syk kinase 的那解朊的激活它的 phosphorylating 活动独立于有细胞骨架的 Syk kinase 的协会。Tyr-P 试金用 32P 举起的 quantification 被进行进在 p72Syk 或 p36Syk 的增加以后的乐队 3 的细胞质的领域。由调停 p72Syk 的 phosphorylation 上的 p36Syk 的红血球膜乐队 3 蛋白质的 pre-phosphorylation 的效果和调停 p72Syk 的 phosphorylation 上的一个朊酶禁止者(leupeptin ) 的增加的效果被 32P 举起的 autoradiographic 可视化学习。由骨胳的膜和乐队 3 的可溶的部分的 Syk isoforms 的 Tyr-P 被 immunoblotting 设想。p36Syk 有一个更高级的乐队,这被发现 3 酷氨酸 phosphorylating 活动与 p72Syk 相比。有 p36Syk 或 p72Syk 的 Pre-phosphorylation 增加了乐队 3 phosphorylating 活动。朊酶抑制处理显著地减少了 p72Syk 然而并非 p36Syk 乐队 3 酷氨酸 phosphorylating 活动。可溶并且乐队 3 蛋白质的骨胳的部分是的膜同等地由每 Syk isoform 的酷氨酸 phosphorylated。在结论,我们证实了 p72Syk 的解朊的劈开是为乐队 3 Tyr-P 和它与细胞骨架的乐队 3 的协会的独立的重要的规章的步的假设。 | Luciana Bordin Cristina Fiore Marcantonio Bragadin Anna Maria Brunati Giulio Clari | 2009 | Acta Biochimica et Biophysica Sinica2009，41，10： | 3 |
| 2 | Viral proteins and Src family kinases: Mechanisms of pathogenicity from a “liaison dangereuse”显示文摘To complete their life cycle and spread, viruses interfere with and gain control of diverse cellular processes, this most often occurring through interaction between viral proteins(VPs) and resident protein partners. Among the latter, Src family kinases(SFKs), a class of non-receptor tyrosine kinases that contributes to the conversion of extracellular signals into intracellular signaling cascades and is involved in virtually all cellular processes, have recently emerged as critical mediators between the cell's infrastructure and the viral demands. In this scenario, structural or ex novo synthesized VPs are able to bind to the different domains of these enzymes through specific short linear motifs present along their sequences. Proline-rich motifs displaying the conserved minimal consensus PxxP and recognizing the SFK Src homology(SH)3 domain constitute a cardinal signature for the formation of multiprotein complexes and this interaction may promote phosphorylation of VPs by SFKs, thus creating phosphotyrosine motifs that become a docking site for the SH2 domains of SFKs or other SH2 domain-bearing signaling molecules. Importantly, the formation of these assemblies also results in a change in the activity and/or location of SFKs, and these events are critical in perturbing key signalingpathways so that viruses can utilize the cell's machinery to their own benefit. In the light of these observations, although VPs as such, especially those with enzyme activity, are still regarded as valuable targets for therapeutic strategies, multiprotein complexes composed of viral and host cell proteins are increasingly becoming objects of investigation with a view to deeply characterize the structural aspects that favor their formation and to develop new compounds able to contrast viral diseases in an alternative manner. | Mario Angelo Pagano Elena Tibaldi Giorgio Palù Anna Maria Brunati | 2013 | World Journal of Virology2013，2，2： | 3 |
| 3 | The SH3 domain of HS1 protein recognizes lysine-rich polyproline motifs显示文摘 | Giuliano Siligardi Paolo Ruzza Rohanah Hussain Luca Cesaro Anna Maria Brunati Lorenzo A. Pinna Arianna Donella-Deana | 2012 | Amino Acids2012，，4： | 1 |
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