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首页> 外文期刊>Cell Research >The effect of C-terminal fragment of JNK2 on the stability of p53 and cell proliferation.
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The effect of C-terminal fragment of JNK2 on the stability of p53 and cell proliferation.

机译:JNK2 C端片段对p53稳定性和细胞增殖的影响。

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摘要

The basal activity of JNK is low in normal growing cells and inactivated JNK targets p53 for ubiquitination. To elucidate if the C-terminal part of JNK is responsible for its binding to p53, the low background tet-off inducible NIH3T3 cell line was selected by luciferase reporter gene and a double stable C-JNK Aa (203-424) cell line was established. After withdrawing tetracycline, the C-JNK fragment expression was induced and cell growth was dramatically inhibited 24 h later. However, the expresion of p53 was found to be increased after the induction of C-JNK fragment, evaluated by transfecting p21waf-luciferase reporter genes. Our further studies showed that C-JNK fragment could form complex with p53 both in vivo and in vitro. Induction of C-JNK fragment in vivo can increase p53 stability by inhibiting p53 ubiquitination.
机译:在正常生长的细胞中,JNK的基础活性低,失活的JNK靶向p53进行泛素化。为了阐明JNK的C末端部分是否负责其与p53的结合,通过荧光素酶报道基因选择了低背景tet-off诱导型NIH3T3细胞系,并使用了双重稳定的C-JNK Aa(203-424)细胞系。成立。退出四环素后,诱导C-JNK片段表达,并在24小时后显着抑制细胞生长。然而,通过转染p21waf-萤光素荧光素酶报告基因评估了诱导C-JNK片段后p53的表达增加。我们的进一步研究表明,C-JNK片段在体内和体外均可与p53形成复合物。体内诱导C-JNK片段可通过抑制p53泛素化来增加p53稳定性。

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