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Kinesin家族是一类马达蛋白,它们能利用ATP水解所释放的能量驱动自身携带物质分子沿着微管运动,在细胞形成、细胞伸长等方面起着关键作用。本研究以拟南芥Atkinesin-13A蛋白序列作为探针序列,利用Blast比对从二倍体雷蒙德氏棉的基因组数据库中发现7个具有较高同源关系的基因。根据基因序列设计引物,利用RT-PCR技术从陆地棉纤维中分离出7个基因。依据7个基因与Atkinesin-13A和Atkinesin-13B的同源性高低,依次将其命名为Gh KIS13A1、Gh KIS13A2、Gh KIS13A3、Gh KIS13B1、Gh KIS13B2、Gh KIS13B3和Gh KIS13B4。生物信息学分析表明,7个Ghkinesin13均含有典型的KISC马达区域、ATP结合位点和微管结合位点,其马达区域属于中央马达。多重序列比对和进化树分析发现,这7个蛋白可被分为2个(Kinesin13A和Kinesin13B)亚类。实时荧光定量PCR结果表明,7个Ghkinesin13亚家族基因在棉花各组织中均有表达,但表达模式各不相同,其中Gh KIS13B4在纤维中优势表达,表明其在纤维发育过程中可能发挥着重要作用。 相似文献
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AIM: To investigated the effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on the expression of kinesin superfamily (KIF) genes in striatum and substantia nigra in C57BL mice. METHODS: The Parkinson's disease model was established by consecutive administration of MPTP to C57BL mice. The levels of mRNA for five kinesin superfamily genes, KIF1A, KIF2, KIF3A, KIF4, and KIF5A, in striatum and substantia nigra of mice, were estimated by RT-PCR. RESULTS: In substantia nigra, the expression of KIF genes were decreased after MPTP treatment except KIF2 that showed no significant change. However, the expression of KIF1A, KIF3A and KIF4 were increased in striatum after MPTP treatment, while the expression of KIF2 and KIF5A were similar to that in substantia nigra. CONCLUSION: The lose of dopaminergic neurons in nigrostriatal pathway after MPTP treatment may be related to the expression of KIF genes. 相似文献
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以黄瓜果实总RNA为模板,通过RT-PCR获得了动蛋白基因CsKF1和CsKF2的cDNA序列,进行测序,构建T-easy载体。SMART在线预测CsKF1和CsKF2均含有动蛋白（Kinesin）约340个氨基酸残基的马达区保守序列（moter domain）。体外表达蛋白的马达区和非马达区,将带有His标签的CsKF1-N、CsKF2-C、CsKF1-M、CsKF2-M融合蛋白通过E. coli BL21（DE3）表达,摸索不同诱导条件下目的蛋白的表达和纯化。其中His-CsKF1-N、His-CsKF2-C、His-CsKF1-M原核表达蛋白的分子量分别为25、30和40 kD,均以0.1 mmol · L-1 IPTG,22 ℃ 6 h诱导表达效果最好。His-CsKF2-M原核表达蛋白的分子量约38 kD,以18 ℃ 8 h诱导表达效果最好。融合蛋白His-CsKF1-N和His-CsKF2-C经过亲和纯化后作为抗原,通过5轮免疫注射兔子后,取心脏血作为抗血清,通过AminoLink Plus kit试剂盒亲和纯化得到多克隆抗体anti-CsKF1-N和anti-CsKF2-C。经过Western blot分析表明多克隆抗体具有特异性,可与抗原特异结合。 相似文献
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AIM:To study the effects of microRNA-105(miR-105) on the cell proliferation, migration and invasion abilities of non-small-cell lung cancer (NSCLC) H460 cells, and further to explore its mechanism. METHODS:The expression of miR-105 and kinesin family member C1 (KIFC1) mRNA in the NSCLC tissues and adjacent tissues and cells was detected by RT-qPCR. The protein expression of KIFC1 in the NSCLC tissues, adjacent normal tissues and cells was determined by Western blot. The H460 cells were divided into miR-105 group (transfection with miR-105 mimics), miR-negative control (NC) group (transfection with miR-NC), inhibitor-NC group (transfection with NC of inhibitor), inhibitor-miR-105 group (transfection with miR-105 inhibitor), si-NC group (transfection with NC siRNA), si-KIFC1 group (transfection with KIFC1 siRNA), miR-105+vector group (miR-105 mimics and pcDNA 3.1 co-transfection) and miR-105+KIFC1 group (miR-105 mimics and pcDNA 3.1-KIFC1 co-transfection). The cell proliferation was measured by MTT assay and colony formation assay. The migration and invasion abilities were detected by Transwell methods. The relative luciferase acitivity was evaluated by double luciferase reporter assay. RESULTS:Compared with the adjacent tissues, the expression of miR-105 was significantly decreased and the expression of KIFC1 was significantly increased in NSCLC tissues (P<0.05). Compared with human normal embryonic lung fibroblasts MRC-5, the expression of miR-105 in the H460 cells was significantly decreased, and the expression of KIFC1 was significantly increased (P<0.05). miR-105 inhibited the relative luciferase activity of H460 cells with wild-type KIFC1 and negatively regulated the protein expression of KIFC1. Over-expression of miR-105 and knockdown of KIFC1 expression significantly inhibited the proliferation, migration and invasion abilities of H460 cells. Over-expression of KIFC1 reversed the inhibitory effect of miR-105 on the cell proliferation, migration and invasion abilities of H460 cells. CONCLUSION:miR-105 inhibits the proliferation, migration and invasion abilities of NSCLC cells. The mechanism may be related to targeting and negatively regulating expression of KIFC1. 相似文献
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