简介:无
简介:摘要目的研究CaMKⅡ激酶在KIF5B-RET阳性肺癌细胞中的作用。方法通过生长曲线、westernblot、抑制剂实验等探索KIF5B-RET蛋白与CaMKⅡ激酶的相互作用。结果CaMKII激酶在KIF5B-RET阳性细胞中存在持续活化,下调CaMKII活性明显抑制阳性细胞增殖能力。结论CaMKII激酶是KIF5B-RET基因促增殖过程中的关键调控点。
简介:摘要目的探讨胰腺癌双特异性抗体诱导特异性T淋巴细胞的效应及其对KIF20A阳性表达的胰腺癌PANC1细胞系的杀伤作用。方法采用化学交联的方法,经凝胶分子排阻Sephrose-G25层析纯化,制备CD3/KIF20A双特异性抗体(双抗)并浓缩。采集健康志愿者外周血,采用淋巴细胞分离液分离出单核细胞,再分别培养为树突样细胞(DC)及T细胞,并联合培养为DC-T细胞,同时应用维生素C干预DC-T细胞(vcDC-T细胞)。采用流式细胞仪检测各组T细胞亚群及培养上清中IFN-γ、IL-2、IL-4、IL-12水平。将10、50、100、300 ng双抗装载的1×105个T细胞、DC-T细胞、vcDC-T细胞与PANC1细胞(20∶1)共培养2、6、10 h后,明确杀伤率最高的双抗装载剂量;将DC-T细胞及装载杀伤率最高的双抗剂量的DC-T细胞、vcDC-T细胞与PANC1细胞(20∶1)共培养2、4、6、8、10、12 h,倒置显微镜下观察效应细胞对靶细胞的聚集效应,乳酸脱氢酶(LDH)法检测肿瘤细胞杀伤率。结果CD3/KIF20A双抗经SDS凝胶电泳鉴定,其分子质量为130 000。与DC-T细胞比较,vcDC-T细胞的CD8+CD28+及CD40L亚群比例增加[(47.6±15.8)%比(38.2±7.6)%,(52.1±4.9)%比(44.7±3.2)%],负性调节细胞Treg比例降低[(4.3±0.8)%比(8.3±1.1)%],分泌的IL-2、IFN-γ、IL-12增加[(201.2±17.3)ng/L比(163.4±13.1)ng/L,(303.3±22.6)ng/L比(221.8±17.6)ng/L,(190.4±11.7)ng/L比(80.3±8.6)ng/L],差异均有统计学意义(P值均<0.05);显微镜下可观察到100 ng CD3/KIF20A双抗装载T细胞对KIF20A+胰腺癌PANC1细胞有明显的靶向性,有最强的杀伤力。效靶细胞比20∶1、共培养4 h时,双抗vcDC-T细胞对PANC1细胞的杀伤率为(88.6±2.6)%,显著高于双抗DC-T组的(68.4±3.4)%及DC-T组的(39.2±2.1)%,杀伤率分别提高20%及45%以上。结论CD3/KIF20A双特异性抗体装载的DC-T细胞能显著提高对KIF20A阳性表达的胰腺癌PANC1细胞的杀伤率,维生素C干预后更进一步增强对双抗装载T细胞的细胞杀伤能力。
简介:摘要KIF3复合体是一种依赖于微管的驱动蛋白,参与细胞内物质运输、有丝分裂等重要生物学过程。本文总结KIF3复合体的结构和生理功能(介导初级纤毛的发生、调控神经元发育等),及其与各种疾病发生的关系,以期为今后更进一步了解KIF3复合体与研究疾病发生发展机制提供新的思路。
简介:AbstractBackground:Gastric cancer (GC) is one of the most globally prevalent cancers in the world. The pathogenesis of GC has not been fully elucidated, and there still lacks effective targeted therapeutics. The influence of altered kinesin superfamily protein 22 (KIF22) expression in GC progression is still unclearly. The aim of this study was to investigate the KIF22 effects on GC and related mechanisms.Methods:Gastric carcinoma tissues and matching non-cancerous tissues were collected from patients with GC who have accepted a radical gastrectomy in Lanzhou University Second Hospital from May 2013 to December 2014. The expression of KIF22 was examined in GC of 67 patients and 20 para-carcinoma tissues by immunochemical staining. The relationship between the expression of KIF22 and clinicopathologic characteristics was next investigated in the remaining 52 patients except for 15 patients who did not complete follow-up for 5 years. Cell viability was performed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) test and colony formation assay in the MGC-803 and BGC-823 GC cells. Cell scratch and trans-well invasion assay was performed to assess migration ability in the MGC-803 and BGC-823 GC cells. Gene set enrichment analysis (GSEA) pathway enrichment analysis was performed to explore the potential functions. Cell cycle was detected by flow cytometry. In addition, the two GC cell lines were used to elucidate the underlying mechanism of KIF22 in GC in vitro via assessing the effects on mitogenactivated protein kinase and extracellular regulated protein kinases (MAPK/ERK) signal transduction pathway-related expressions by Western blotting assays. The differences were compared by t tests, one-way analysis of variance, and Chi-squared tests.Results:The study showed that KIF22 was up-regulated in GC, and KIF22 high expression was significantly related to differentiation degree (χ2 = 12.842, P = 0.002) and poorly overall survivals. GSEA pathway enrichment analysis showed that KIF22 was correlated with the cell cycle. Silence of KIF22 decreased the ability of the proliferation and migration in gastric cells, induced G1/S phase cell cycle arrest via regulating the MAPK-ERK pathways.Conclusions:KIF22 protein level was negatively correlated with prognosis. KIF22 knockdown might inhibit proliferation and metastasis of GC cells via the MAPK-ERK signaling pathway.
简介:摘要将KIF5B-RET序列连接到Lenti6.3-eGFP上,重组获得慢病毒载体,包装生产慢病毒并测定其滴度,再将此慢病毒转染肺癌细胞系并筛选验证。本实验成功构建了KIF5B-RET慢病毒载体,并建立稳定表达KIF5B-RET的肺癌细胞系。
简介:[1]BASFUSP4479906[2]BASFBP1443541[3]BASFDE3618265[4]WangL.,WuZ.,ChinaLeather,26(8),11,(1997)[5]YuanL.,DinY.,ChineseChemistryBulletin,(2),19(1988)[6]KurokiH.,ChemistryofDyeingTheory(ChineseTranslation),TextileIndustryPress,Beijing,89(1982)[7]WangS.,LiP.,WuZ.DyestuffIndustry(Chinese),34(4),1,(1997)[8]Tian,Y.,Wu,Z.,Wang,G.,Zhang,S.J.ChineseChem.Eng.,46,156(1995)[9]Tian,Y.,Wang,G.,Wu,Z.,J.ChineseChem.Eng.,47,75(1996)[10]Lycka,A.,DyesandPigment,32,11(1996)[11]Griffith,J.,ColourandConstitutionofOrganicMolecules,AcademicPress,London,191(1976)
简介:摘要目的探讨驱动蛋白家族成员20A(KIF20A)在人表皮生长因子受体2(HER2)过表达型乳腺癌中的表达和临床意义。方法回顾性分析82例HER2过表达型乳腺癌病例的临床病理特征资料。用免疫组织化学的方法检测组织中KIF20A的表达,分析HER2过表达型乳腺癌中KIF20A的表达及与临床病理特征的关系。通过生物信息学的方法分析KIF20A在HER2过表达型乳腺癌组织及癌旁正常组织中的mRNA水平,并分析其表达与患者的生存率间的关系。结果KIF20A的阳性表达在胞核,成棕黄色颗粒。在HER2过表达型乳腺癌组织中,KIF20A阳性高表达率为57.3%,而在癌旁组织中主要是低表达或无表达。KIF20A高表达与肿瘤大小和pTNM分期显著相关,而与年龄和肿瘤分级的相关性无统计学意义。生物信息学分析结果提示侵袭性乳腺癌中KIF20A高表达与不良的无疾病生存期显著相关。结论KIF20A在HER2过表达型乳腺癌中存在异常表达,与HER2过表达型乳腺癌肿瘤分级和pTNM分期相关,并且KIF20A高表达提示预后不良。
简介:РоссийскийспортвгодыВеликойОтечественнойвойныИзвестныйнамкомплексГТО1нетолькопомогалкрепитьобороннуюмощьСССР,ноиоткрывалфеноменальныеспортивныеталанты.
简介:Dibromobiphenylreactedwithcynomethylanioninammoniaunderirradiationtoformnucleophilicbis-substitutedproductinhighyieldwithoutsubstantialmonosubstitutedproduct.Quantumyieldsfortheformationsofbis-andmonosubstitutedproductswerefoundtobe85.6and2.3×10-6respectively,whilethecorrespondingpseudo-first-orderrateswere6.9×10-3and5.2×10-10mol.L-1.S-1.Blockupthepossibleelectrontransferof4-brome-4’-cyanomethylbiphenylylradicalanionto4-cyanometbyl-biphenylylradicalandbromineion.