STAT2是信号转导和转录激活因子(signal transducers and activators of transcription,STAT)家族中的一员,它被激活后转入细胞核内与特异性DNA结合,影响基因转录,参与细胞的生长、分化、生存和凋亡。重要的是,目前研究表明,STAT2基因...STAT2是信号转导和转录激活因子(signal transducers and activators of transcription,STAT)家族中的一员,它被激活后转入细胞核内与特异性DNA结合,影响基因转录,参与细胞的生长、分化、生存和凋亡。重要的是,目前研究表明,STAT2基因缺失或过表达对肿瘤发生发展有着重要影响,与肿瘤血管生成、肿瘤增殖及肿瘤凋亡密切相关,并且在肿瘤的干扰素治疗中扮演着重要角色。本文就STAT2与肿瘤研究进展做一综述。展开更多
Objective:To measure the expression pattern of STAT2 in cenical cancer initiation and progression in tissue sections from patients with cervicitis,dysplasia,and cenical cancer. Methods:Antibody against human STAT2 was...Objective:To measure the expression pattern of STAT2 in cenical cancer initiation and progression in tissue sections from patients with cervicitis,dysplasia,and cenical cancer. Methods:Antibody against human STAT2 was confirmed by plasmids transient transfection and Western blot Immunohistochemistry was used to delect STAT2 expression in the cervical biopsies by using the confirmed antibody against STAT2 as the primary antibody.Results:It was found that the overall rate of positive STAT2 expression in the cervicitis,dysplasia and cenical cancer groups were 38.5%,69.49%and 76.991,respectively.The STAT2 levels are significantly increased in premalignant dysplasia and cervical cancer,as compared lo cervicitis(P【 0.05). Noticeably,STAT2 signals were mainly found in the cytoplasm,implying that STAT2 was not biologically active.Conclusions:These findings reveal an association between cenical cancer progression and augmented STAT2 expression.In conclusion.STAT2 increase appears to be an early detectable cellular event in cenical cancer development.展开更多
目的研究慢性丙型病毒性肝炎患者外周血单核细胞(PBMC)中2’,5’寡腺苷酸合成酶(2’,5’-Oligoadenylate synthetase,2-5AS)的表达及其传导与转录激活因子(Signal transducer and activator of transcription,Stat)Stat1和Stat2等的水...目的研究慢性丙型病毒性肝炎患者外周血单核细胞(PBMC)中2’,5’寡腺苷酸合成酶(2’,5’-Oligoadenylate synthetase,2-5AS)的表达及其传导与转录激活因子(Signal transducer and activator of transcription,Stat)Stat1和Stat2等的水平相关性分析。方法选择60例慢性丙肝患者,抽取外周血分离PBMC。首先测定每份标本的2-5AS活性。然后将所有丙肝患者的PBMC标本按按编号单双数分为对照组和实验组,进行体外培养。其中,对照组PBMC不添加干扰素α(interferon alpha,IFN-α),而实验组PBMC添加1000IU/ml IFN-α。体外培养大约24小时后,测定PBMC中2-5AS活性、Stat1和Stat2等的表达量。结果和对照组相比,实验组PBMC的2-5AS活性明显升高(P<0.05)。实验组PBMC中,在2-5AS活性增高的同时,Stat1和Stat2等表达量也呈现明显增多的趋势(P<0.05)。结论基础的2-5AS活性与加入IFNα刺激培养后Stat1的改变幅度呈负相关(P<0.05);2-5AS基础水平和IFNα刺激后的Stat2表达的变化没有相关性(P>0.05)。展开更多
Although much progress has been made in identifying the signaling pathways that mediate viral RNA-induced apoptosis and activation of interferon-stimulated genes, the role that bacterial RNA plays in regulating these ...Although much progress has been made in identifying the signaling pathways that mediate viral RNA-induced apoptosis and activation of interferon-stimulated genes, the role that bacterial RNA plays in regulating these responses has remained undetermined. Herein, we identified bacterial RNA as a novel inducer of the apoptotic cell death. Unlike the parental cells, STAT1 and STAT2 mutants display apoptotic defects which were reversed by restoring the expression of wild type proteins. While STAT1 mutants lacking tyrosine-701 or a functional SH2 domain were effective as the wild-type protein in restoring the apoptotic response, the mutant carrying a point mutation at serine-727 of STAT1 was resistant to bacterial RNA-induced apoptosis. We also determined that the lack of apoptosis in the STAT1 and STAT2 mutants was correlated with the constitutive and inducible activation of apoptosis regulating proteins. Furthermore, we show that bacterial RNA induces transcriptional activation of STAT1, STAT2, IRF1, and ISGF3, which was impaired in STAT1 or STAT2 mutants. These observations suggested that the participation of STATs in regulating the apoptotic response is independent of their downstream functions as cytokine-induced transcriptional activators. In addition to bacterial immunity, the results presented here may also have implications in cellular pathophysiology and RNA-based therapy.展开更多
文摘STAT2是信号转导和转录激活因子(signal transducers and activators of transcription,STAT)家族中的一员,它被激活后转入细胞核内与特异性DNA结合,影响基因转录,参与细胞的生长、分化、生存和凋亡。重要的是,目前研究表明,STAT2基因缺失或过表达对肿瘤发生发展有着重要影响,与肿瘤血管生成、肿瘤增殖及肿瘤凋亡密切相关,并且在肿瘤的干扰素治疗中扮演着重要角色。本文就STAT2与肿瘤研究进展做一综述。
基金funded by 'Chinese National Nature Science Foundation(30771122)''Chinese Ministry of Education,Research Start-up Funding for Home Smdents' to Ming Li
文摘Objective:To measure the expression pattern of STAT2 in cenical cancer initiation and progression in tissue sections from patients with cervicitis,dysplasia,and cenical cancer. Methods:Antibody against human STAT2 was confirmed by plasmids transient transfection and Western blot Immunohistochemistry was used to delect STAT2 expression in the cervical biopsies by using the confirmed antibody against STAT2 as the primary antibody.Results:It was found that the overall rate of positive STAT2 expression in the cervicitis,dysplasia and cenical cancer groups were 38.5%,69.49%and 76.991,respectively.The STAT2 levels are significantly increased in premalignant dysplasia and cervical cancer,as compared lo cervicitis(P【 0.05). Noticeably,STAT2 signals were mainly found in the cytoplasm,implying that STAT2 was not biologically active.Conclusions:These findings reveal an association between cenical cancer progression and augmented STAT2 expression.In conclusion.STAT2 increase appears to be an early detectable cellular event in cenical cancer development.
文摘目的研究慢性丙型病毒性肝炎患者外周血单核细胞(PBMC)中2’,5’寡腺苷酸合成酶(2’,5’-Oligoadenylate synthetase,2-5AS)的表达及其传导与转录激活因子(Signal transducer and activator of transcription,Stat)Stat1和Stat2等的水平相关性分析。方法选择60例慢性丙肝患者,抽取外周血分离PBMC。首先测定每份标本的2-5AS活性。然后将所有丙肝患者的PBMC标本按按编号单双数分为对照组和实验组,进行体外培养。其中,对照组PBMC不添加干扰素α(interferon alpha,IFN-α),而实验组PBMC添加1000IU/ml IFN-α。体外培养大约24小时后,测定PBMC中2-5AS活性、Stat1和Stat2等的表达量。结果和对照组相比,实验组PBMC的2-5AS活性明显升高(P<0.05)。实验组PBMC中,在2-5AS活性增高的同时,Stat1和Stat2等表达量也呈现明显增多的趋势(P<0.05)。结论基础的2-5AS活性与加入IFNα刺激培养后Stat1的改变幅度呈负相关(P<0.05);2-5AS基础水平和IFNα刺激后的Stat2表达的变化没有相关性(P>0.05)。
文摘Although much progress has been made in identifying the signaling pathways that mediate viral RNA-induced apoptosis and activation of interferon-stimulated genes, the role that bacterial RNA plays in regulating these responses has remained undetermined. Herein, we identified bacterial RNA as a novel inducer of the apoptotic cell death. Unlike the parental cells, STAT1 and STAT2 mutants display apoptotic defects which were reversed by restoring the expression of wild type proteins. While STAT1 mutants lacking tyrosine-701 or a functional SH2 domain were effective as the wild-type protein in restoring the apoptotic response, the mutant carrying a point mutation at serine-727 of STAT1 was resistant to bacterial RNA-induced apoptosis. We also determined that the lack of apoptosis in the STAT1 and STAT2 mutants was correlated with the constitutive and inducible activation of apoptosis regulating proteins. Furthermore, we show that bacterial RNA induces transcriptional activation of STAT1, STAT2, IRF1, and ISGF3, which was impaired in STAT1 or STAT2 mutants. These observations suggested that the participation of STATs in regulating the apoptotic response is independent of their downstream functions as cytokine-induced transcriptional activators. In addition to bacterial immunity, the results presented here may also have implications in cellular pathophysiology and RNA-based therapy.
