Differential regulation of myelin gene expression in SV40 T antigen-transfected rat glioma C6 cells.

Differential regulation of myelin gene expression in SV40 T antigen-transfected rat glioma C6 cells.
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SV40 T 抗原转染的大鼠神经胶质瘤 C6 细胞中髓磷脂基因表达的差异调节。

DOI:
10.1007/bf01000381
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发表时间:
1991
影响因子:
3.6
通讯作者:
Konat,G
Konat,G
中科院分区:
医学3区
文献类型:
--
作者:
Bong,M;Chakrabarti,A;Banik,N;Hogan,EL;Kanoh,M;Wiggins,RC;Konat,G

文献摘要

相似文献

用含有SV 40 T抗原基因的pSV 3-neo质粒稳定转染大鼠胶质瘤C6细胞,并克隆了京尼霉素抗性转染子(命名为C6 T细胞)。C6 T细胞生长为边界清楚的细胞灶,显示鳞状或不规则形态。与对照C6细胞相比,转染细胞的倍增时间减少约40%。T抗原的转染还影响编码结构髓鞘蛋白和髓鞘相关酶的基因的表达。C6 T细胞中蛋白脂质蛋白(PLP)特异性mRNA的稳态水平比亲代C6细胞低44%。另一方面,转染使髓鞘相关糖蛋白(MAG)的表达上调了153%。与未转染的对照细胞相比,C6 T细胞中2′∶3′环AMP磷酸二酯酶(CNP)的活性增加约80%。钙激活中性蛋白酶(CANP)的活性也显着提高了约50%和220%的转染分别为毫摩尔和微摩尔形式。结果表明,T抗原影响髓鞘基因的表达,虽然,个别基因似乎是不同的调节暗示存在几个独立的调节机制。
Rat glioma C6 cells were stably transfected with a pSV3-neo plasmid containing SV40 T antigen gene, and geniticin-resistant transfectants (designated C6T cells) were cloned. The C6T cells grew as well-defined foci of cells showing squamous or irregular morphology. The doubling time for transfected cells was reduced by approximately 40% as compared to control C6 cells. The transfection with T-antigen also affected the expression of genes coding for structural myelin proteins and for myelin-associated enzymes. The steady-state level of proteolipid protein (PLP)-specific mRNA in C6T cells was 44% lower than in parental C6 cells. On the other hand, the transfection upregulated the expression of myelin-associated glycoprotein (MAG) by 153%. The activity of 2′∶3′cyclic AMP phosphodiesterase (CNP) was increased by approximately 80 % in the C6T cells as compared to untransfected, control cells. The activity of calcium-activated neutral proteinase (CANP) was also significantly elevated in the transfectants by approximately 50% and 220% for millimolar and micromolar form respectively. The results indicate that T antigen affects the expression of myelin genes, although, individual genes appear to be differently regulated implying the existence of several independent regulatory mechanisms.