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局灶性脑缺血后Krox-20表达的诱导

Induction of Krox-20 expression after focal cerebral ischemia.

作者信息

An G, Lin T N, Liu J S, Hsu C Y

机构信息

Division of Restorative Neurology, Baylor College of Medicine, Houston, TX 77030.

出版信息

Biochem Biophys Res Commun. 1992 Nov 16;188(3):1104-10. doi: 10.1016/0006-291x(92)91345-q.

Abstract

Krox-20 is one of the transcription factors of "zinc finger" family. The expression of Krox-20 was investigated in a rat focal cerebral ischemia model by Northern blot analysis and in situ hybridization. Northern blot analysis showed that ischemia for 30 min which caused little cortical infarction induced a 29-fold increase in Krox-20 mRNA signal exclusively in the ischemic cortex. Ischemia for 90 min which led to large cortical infarction induced Krox-20 mRNA not only in the ischemic cortex but also in the ipsilateral hippocampus. The induction of Krox-20 mRNA was rapid, transient and appeared to be controlled at the transcriptional level, as indicated by nuclear run-on assays. The regional induction of Krox-20 mRNA was further confirmed by in situ hybridization. These results suggest that the expression of transcription factor genes may play a role in the post-ischemic changes of the injured brain.

摘要

Krox-20是“锌指”家族的转录因子之一。通过Northern印迹分析和原位杂交技术,在大鼠局灶性脑缺血模型中研究了Krox-20的表达情况。Northern印迹分析显示,缺血30分钟仅在缺血皮层引起轻微皮质梗死,但导致Krox-20 mRNA信号增加了29倍。缺血90分钟导致大面积皮质梗死,不仅在缺血皮层诱导了Krox-20 mRNA表达,同侧海马也有表达。核转录分析表明,Krox-20 mRNA的诱导迅速、短暂,且似乎在转录水平受到调控。原位杂交进一步证实了Krox-20 mRNA的区域诱导现象。这些结果表明,转录因子基因的表达可能在损伤脑的缺血后变化中发挥作用。

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