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作 者:易丽娴[1] 高兵[2] 高菲[2] 傅丰庆[2] 张学光[2] 孙静[1]
机构地区:[1]苏州卫生职业技术学院检验药学系,江苏苏州215009 [2]苏州大学生物技术研究所,江苏苏州215006
出 处:《细胞与分子免疫学杂志》2012年第8期815-817,共3页Chinese Journal of Cellular and Molecular Immunology
基 金:国家自然科学基金(31100626);江苏省自然科学基金(BK2011320)
摘 要:目的:利用生物信息学及分子生物学体外探讨剪切因子SC35对协同刺激分子B7-H3的表达调控机制。方法:通过生物信息方法筛选可能参与协同刺激分子B7-H3表达的调控蛋白,再通过定量PCR及RNA干扰实验验证剪切因子是否参与该分子的调控。结果:剪切因子SC35、SRP40、SF55可能参与B7-H3的表达调控,体外发现T细胞活化后B7-H3表达上调,SC35同时也表达上调;继而通过RNA干扰抑制SC35的表达,发现B7-H3的表达也同时降低。结论:剪切因子SC35可能参与了B7-H3的表达调控,对研究该分子的生物学功能奠定了基础。AIM: To explore the mechanisms by which splicing factor SC35 regulates the costimulatory molecule B7-H3 expression in vitro through bioinformatic and molecular biological methods.METHODS: We screened some regulatory proteins which might take part in regulating B7-H3 expression using bioinformatic methods.Then RNA interference(RNAi) and real-time PCR were performed to test if these proteins took part in the regulation.RESULTS: Splicing factor SC35,SRP40 and SF50 might play an important role in the regulation of B7-H3 expression.In PHA-activated T cells,B7-H3 was upregulated obviously and at the same time SC35 was also upregulated.When we suppressed SC35 expression using RNAi,we found B7-H3 was also downregulated.CONCLUSION: Splicing factor SC35 might take part in the regulation of B7-H3 expression,which could help understand B7-H3 biological function.
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