记者从厦门大学生命科学学院获悉，因研究一种被称为karyopherin beta的家族蛋白质取得突破，该院一篇论文3月19日在线发表于蛋白质组学领域的国际顶级刊物《分子与细胞蛋白质组学》（Molecular & Cellular Proteomics）上，该杂志的审稿人认为此项研究成果是一项非常优秀的工作，将对大分子在细胞核质间运输研究领域的发展有极大的帮助。
这项研究成果是厦门大学生科院陶涛教授实验室和纪志梁副教授实验室三年合作的结晶。陶涛介绍说，蛋白质和核酸等大分子负责调控基因的转录、蛋白质的翻译和信号转导，它们在真核细胞中核质间的运输和定位是细胞最重要的生理功能之一。在哺乳动物细胞中已发现有20个蛋白质来承担大分子运输和定位生理功能，这类蛋白质被称为karyopherin beta家族蛋白质。
在此前没有人大规模系统研究该家族蛋白质的进化和转录调控方式。陶涛和纪志梁应用生物信息学等研究手段，系统研究了从原核生物基因组到人类基因组所有可能编码的karyopherin beta家族蛋白质和其前体蛋白质的分子进化的过程、方式和分子机理，并揭示了这些基因在不同发育时期、不同组织器官和不同细胞周期中的调控方式。此项成果对研究细胞的生理功能和机体发育有重要的意义。
《分子与细胞蛋白质组学》（Molecular & Cellular Proteomics）是国际蛋白质组学领域的顶级刊物，其影响因子为9.9，具有权威的学术影响力。
生物谷推荐原始出处：
Mol. Cell. Proteomics, Mar 2008; 7: 612 - 625.
Proteomics Analysis of Host Cells Infected with Infectious Bursal Disease Virus*,S
Xiaojuan Zheng, Lianlian Hong, Lixue Shi, Junqing Guo, Zhen Sun and Jiyong Zhou,,¶,||
From the Institute of Preventive Veterinary Medicine, Zhejiang University, Hangzhou 310029, China, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University, Hangzhou 310003, China, and ¶ Key Laboratory of conservation genetics and reproductive biology for endangered wild animals of the Ministry of Education, Zhejiang University, Hangzhou 310058, China
The effect of infectious bursal disease virus (IBDV) infection on cellular protein expression is essential for viral pathogenesis. To characterize the cellular response to IBDV infection, the differential proteomes of chicken embryo fibroblasts, with and without IBDV infection, were analyzed at different time points with two-dimensional gel electrophoresis (2-DE) followed by MALDI-TOF/TOF identification. Comparative analysis of multiple 2-DE gels revealed that the majority of protein expression changes appeared at 48 and 96 h after IBDV infection. Mass spectrometry identified 51 altered cellular proteins, including 13 up-regulated proteins and 38 down-regulated proteins 12–96 h after infection. Notably 2-DE analysis revealed that IBDV infection induced the increased expression of polyubiquitin, apolipoprotein A-I, heat shock 27-kDa protein 1, actins, tubulins, eukaryotic translation initiation factor 4A isoform 2, acidic ribosomal phosphoprotein, and ribosomal protein SA isoform 2. In addition, IBDV infection considerably suppressed those cellular proteins involved in ubiquitin-mediated protein degradation, energy metabolism, intermediate filaments, host translational apparatus, and signal transduction. Moreover 38 corresponding genes of the differentially expressed proteins were quantitated by real time RT-PCR to examine the transcriptional profiles between infected and uninfected chicken embryo fibroblasts. Western blot further confirmed the inhibition of Rho protein GDP dissociation inhibitor expression and the induction of polyubiquitin during IBDV infection. Subcellular distribution analysis of the cytoskeletal proteins vimentin and β-tubulin clearly demonstrated that IBDV infection induced the disruption of the vimentin network and microtubules late in IBDV infection. Thus, this work effectively provides useful dynamic protein-related information to facilitate further investigation of the underlying mechanism of IBDV infection and pathogenesis.
