Changed structure and prepared HSF1 mutants could specifically active or block HSF1 activation.
通过改变HSF1的结构构建其突变体，能特异地引起或阻碍HSF1的活化。
The condition of HSF1 gene silence, the survival rate of cells which was in RNAi was much lower than control group by cloning.
在HSF1基因沉默条件下，克隆法观察到转染后的细胞其细胞存活率比未转染的空白对照组明显降低。
As a transcription factor, heat shock transcription factor 1 (HSF1) is activated during stress and subsequently trans-activate its downstream factors.
热休克因子1 (HSF1)是一种转录因子，在正常时不活化，应激时活化而具有反式激活能力。
While it enhances organismal survival and longevity under most circumstances, HSF1 has the opposite effect in supporting the lethal phenomenon of cancer.
尽管在大多数情况下HSF - 1可以增加生物体的存活和生存时间，它有支持癌的致命现象的反作用。
ResultsIschemia and reperfusion caused renal injury as indicated by the increase of BUN and serum creatinine levels, which was exacerbated by HSF1 knock out.
结果肾缺血-再灌注导致BUN及血清肌酐浓度明显升高，HSF1基因敲除导致二者上升更加明显。
While heat shock promoted the phosphorylation and nuclear translocation of HSF1, the ability of this nucleus-localized HSF1 to form the DNA-binding trimer was reduced.
HSF1的亚细胞定位分析显示，HSF1主要存在于年轻细胞胞质中，热刺激促使三体形成和核转移；
The expression of HSF1 mRNA and FACL4 mRNA were not associated with the patient's gender, age, tumor size, pathologic grade, pathologic type, as well as level of serum AFP(P>0.05).
但FACL4表达水平与患者的性别，年龄，肿瘤大小，包膜的完整与否，分级，癌栓形成及血清AFP水平未见明显相关性（均P＞0.05）。
The expression of HSF1 mRNA and FACL4 mRNA were not associated with the patient's gender, age, tumor size, pathologic grade, pathologic type, as well as level of serum AFP(P>0.05).
但FACL4表达水平与患者的性别，年龄，肿瘤大小，包膜的完整与否，分级，癌栓形成及血清AFP水平未见明显相关性（均P＞0.05）。
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