肿瘤相关抗原CT45的HLA-A2/A3限制性CTL表位的预测

目的:预测肿瘤相关抗原CT45的HLA-A2/A3限制性CTL表位,为CTL表位肽的合成和活性筛选提供依据。方法:基于新近发现的CT45抗原的氨基酸序列,用NetCTL 1.2 Server人工神经网络法远程预测系统进行HLA-A2/A3限制性CTL表位预测打分,挑选出分值较高的作为候选表位。结果:共预测出了5个潜在的HLA-A2限制性CTL表位九肽,15个潜在的HLA-A3限制性CTL表位九肽,所有这些表位均为首次报道。结论:NetCTL 1.2 Server人工神经网络法能高效的预测CTL表位肽,基于新近发现的CT45抗原,我们通过该系统成功预测出了5个潜在的HLA-A2限制性CTL表位,15个潜在的HLA-A3限制性CTL表位,可以对其进行进一步的研究。     

肝癌相关肿瘤抗原AFP新的HLA-A2/A24 限制性CTL表位的预测及分析

目的:预测肝癌肿瘤抗原AFP新的HLA-A2/A24限制性CTL表位,为肝癌CTL表位肽的筛选及鉴定提供依据.方法:选择与肝癌密切相关的肿瘤抗原AFP为研究目标,采用NetCTL 1.2 Server远程预测系统进行HLA-A2/A24限制性CTL表位预测.结果:共预测出与肝癌相关的肿瘤相关抗原AFP的8个HLA-A2 限制性CTL表位,13个HLA-A24限制性CTL 表位.结论:应用NetCTL 1.2 Server法预测CTL表位是一种高效准确的预测方法.所预测的肿瘤抗原AFP的HLA-A2/24 限制性CTL表位经实验筛选、鉴定后,可为肝癌治疗性疫苗的制备选择合适的CTL表位提供依据.     

肝癌相关肿瘤抗原AFP新的HLA—A2／A24限制性CTL表位的预测及分析

目的：预测肝癌肿瘤抗原AFP新的HLA—A2／A24限制性CTL表位,为肝癌CTL表位肽的筛选及鉴定提供依据。方法：选择与肝癌密切相关的肿瘤抗原AFP为研究目标,采用NetCTL1．2Server远程预测系统进行HLA—A2／A24限制性CTL表位预测。结果：共预测出与肝癌相关的肿瘤相关抗原AFP的8个HLA—A2限制性CTL表位,13个HLA—A24限制性CTL表位。结论：应用NetCTL1．2Server法预测CTL表位是一种高效准确的预测方法。所预测的肿瘤抗原AFP的HLA—A2／24限制性CTL表位经实验筛选、鉴定后,可为肝癌治疗性疫苗的制备选择合适的CTL表位提供依据。     

苦瓜蛋白MAP30的HLA-A2/A3限制性CTL表位预测

目的:预测苦瓜蛋白MAP30的HLA - A2/A3限制性CTL表位.方法:应用lasergene 7.0和NetCTL-1.2 Server对MAP30进行HLA - A2 /A3限制性CTL表位预测.结果:MAP30的二级结构含有8个α-螺旋和9个β-折叠股;柔韧性良好氨基酸区域为19-40、99-146、166-273;亲水性指数较高区域为22-45、97-114、117-148、180-198、224-257、265-275;抗原性指数较高区域为19-28、63-71、98-114、118-123、224-246、248-260、262-274;有30个可能CTL表位,综合分析后获得2个HLA - A2和5个HLA - A3限制性CTL表位.结论:MAP30具有潜在的7个HLA-A2/A3限制性CTL表位.     

食管癌高表达抗原HLA-A2/A3 限制性细胞毒性T 淋巴细胞表位预测

 目的 预测食管癌普遍高表达蛋白COX-2和MAGE-4的HLA-A2/A3限制性CTL表位。方法运用生物信息学的方法,SYFPEITHI初步预测,结合三维构效定量关系和蛋白酶体酶切位点分析。结果 对SYFPEITHI预测〉20的九肽用MHCPred和NetChop3.0作进一步分析,并与已报道抗原肽进行比对,初步筛选出了42个潜在的CTL表位。结论 这42个九肽均未见文献报道,进一步鉴定将为CTL表位疫苗的研究提供更多的线索。其中,MAGE-422-30、202-210、286-294及COX-2479-4874个九肽具有与HLA-A2和HLA-A3超型潜在的交叉免疫活性,将为研制简约的高效广谱食管癌疫苗提供候选肽。     

肿瘤抗原MAGE-12新的HLA-A2限制性细胞毒性T细胞表位的预测

目的预测黑色素瘤抗原MAGE-12的HLA—A2限制性CTL表位。方法采用SYFPEITHI超基序远程预测系统与量化基序多项式法、延展基序联合应用，筛选MAGE-12抗原HLA—A0201限制性CTL表位。结果共预测出5个MAGE-12抗原HLA—A2限制性CTL表位。结论超基序法与量化基序，延展基序联合应用可以提高预测效率，为实验方法探索MAGE-12的表位提供有用线索。     

乙型脑炎病毒E蛋白HLA—A＊0201限制性细胞毒性T细胞表位的预测

目的:预测乙型脑炎病毒E蛋白(Japanese encephalitis virus envelope protein,JEV E 蛋白)的HLA-A2限制性CTL表位.方法:采用SYFPEITHI超基序法、量化基序多项式方案分析及延展基序方案联合应用,筛选JEV E 蛋白HLA-A2限制性的九肽细胞毒性T淋巴细胞(cytotoxic lymphocyte,CTL)表位.结果:通过预测获得了9个JEV E 蛋白HLA-A0201限制性的九肽CTL表位.结论:超基序法与量化基序多项式方案分析及延展基序方案的联合应用所产生的JEV E 蛋白CTL表位,为进一步研制新型乙脑肽疫苗奠定了重要的基础.     

原癌基因Bmi-1 B细胞抗原表位及 HLA I类限制性CTL表位的生物信息学分析

目的:预测原癌基因Bmi-1(B-cell-specific Moloney murine leukemia virus insertion site 1)的B细胞抗原表位及HLA I类限制性细胞毒性T细胞（cytotoxic T cell）表位。方法:采用Ellipro(http://tools.immuneepitope.org/ellipro/)预测Bmi-1蛋白中可能存在的线性B细胞表位和构象B细胞表位;采用ProtParam、NetCTL等软件和方法预测Bmi-1中可能存在的HLA I类限制性CTL表位。结果:Bmi-1蛋白中含有6个线性B细胞表位和8个构象B细胞表位;结合HLA结合力、蛋白酶体切割效率和TAP转运效率,经过NetCTL程序预测表明:针对不同的HLA I类分子,原癌基因Bmi-1中都存在多个HLA I类分子的限制性CTL表位。结论:综合运用多个程序预测了原癌基因Bmi-1中的B细胞抗原表位及HLA I类分子的限制性CTL表位,为下一步开展针对Bmi-1的免疫靶向治疗等研究打下了基础。     

联合表位肽诱导HLA-A2+人PBMC产生抗原特异性CTL及杀伤活性研究

目的:探讨MAGE-3,MAGE-n抗原表位体外联合诱导的CTL,并研究其特异性杀伤活性。方法:候选抗原表位以固相多肽合成技术合成,并用HPLC进行纯化,质谱法(MS)鉴定,以流式细胞仪筛选HLA-A2 人外周血PBMC,T2细胞负载抗原肽反复刺激活化诱导抗原特异性CTL,LDH检测其杀伤活性。结果:联合表位肽体外刺激人PBMC,能够较强地诱导抗原特异性CTL并产生特异性杀伤。结论:MAGE-3与MAGE-n的HLA-A2限制性CTL表位肽的联合应用能够产生较强的体外抗肿瘤免疫反应。     

慢性粒细胞白血病相关抗原HLA-A2.1限制性CTL表位的生物信息学分析

目的:预测慢性粒细胞白血病BCR/ABL融合基因HLA-A2.1限制性细胞毒性T细胞表位.方法:运用BIMAS、SYFPEITHI、Predep、Immune Epitope Database和Analysis Resource(IEDB)软件预测BCR/ABL融合基因可能的HLA-A2.1限制性CTL表位.结果:结合BIMAS、SYFPEITHI、Predep和IEDB预测BCR/ABL融合基因的HLA-A2.1限制性CTL表位,共6条.结论:综合运用多个预测软件可提高预测效率获得目的表位肽,为下一步基础实验打下基础.     

Polyamine metabolism and interconversion in NIH 3T3 and ras-transfected NIH 3T3 cells

The effect of transfection of NIH 3T3 cells by the human ras (c-Ha-ras-1) oncogene on uptake, interconversion, and excretion of polyamines was studied. Uptake and interconversion of spermidine were higher in the ras-transfected cells. Acetylpolyamines were excreted into the medium by the ras-transfected cells, whereas they were retained by NIH 3T3 cells. In addition to acetylpolyamines, some unknown polyamine conjugates occurred in the ras-transfected cells.     

Prostaglandin production in cultures of BALB/3T3 and SV3T3 mouse fibroblasts.

The concentration of different prostaglandins (PG's) was determined in both cells and culture medium of growing BALB/3T3 and BALB/3T3 (3T3) cultures transformed by simian virus 40 (SV3T3). Most PG's were found in the culture medium rather than in the cells. Further, the larger PG measurements were PGE and a composite measurement of PGA and PGB. PGF was detected at lower levels. The sum of PGE and the composite measurement (PGA+PGB) was the best indication of PG production in culture. When 2-day medium collections from 3T3 and SV3T3 cells were measured by radioimmunoassay for PGs, higher concentrations of PG were detected in the media of SV3T3 cultures. This difference in PG production was not due merely to differences in cell density, since SV3T3 cells produced higher PG concentrations, even at equal cell densities. PG production for a 2-day interval was more a function of cell type than cell density.     

PIK3R3 promotes chemotherapeutic sensitivity of colorectal cancer through PIK3R3/NF-kB/TP pathway

Phosphoinositide-3-kinase regulatory subunit 3(PIK3R3) is overexpressed in different types of human cancer. We previously reported the important role of PIK3R3 in colorectal cancer (CRC). However, the prognosis effect of PIK3R3 in CRC is still remaining unclear. In this study, we explored online clinical databases to analyze the prognosis differences between higher and lower expression of PIK3R3 in CRC patients. Interestingly, we found that better disease-free survival (DFS) were occurred in patients with higher expression of PIK3R3, but there is no significant difference in overall survival (OS). For further, we showed that PIK3R3 could enhance 5-FU induced apoptosis by regulating the expression of thymmidine phosphorylase (TP). In conclusion, PIK3R3 could be considered as a predictor of 5-FU sensitivity for personalized treatment, and a therapeutic target for colorectal cancer.     

1 alpha,25-Dihydroxyvitamin D3 induces anchorage-independent growth and c-Ki-ras expression of BALB/3T3 and NIH/3T3 cells

1 alpha,25-Dihydroxyvitamin D3, a hormonally active form of vitamin D, induces anchorage-independent growth of BALB/3T3 A31-1-1 and NIH/3T3 cells with concomitant increase of their mRNA level of c-Ki-ras but not of c-Ha-ras or c-myc, through a receptor-mediated mechanism. Under the same conditions, 12-O-tetradecanoylphorbol-13-acetate did not induce anchorage-independent growth in these cell lines.