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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >COMPLEXES OF P21(RAS) WITH JUN N-TERMINAL KINASE AND JUN PROTEINS
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COMPLEXES OF P21(RAS) WITH JUN N-TERMINAL KINASE AND JUN PROTEINS

机译：P21（RAS）与JUN N终端激酶和JUN蛋白的复合物

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摘要

RAS gene-encoded p21 protein has been found to increase in vitro phosphorylation of JUN via its kinase, JUN N-terminal kinase (JNK), This effect is mediated by increased phosphorylation of JNK in the presence of wild-type and oncogenic (Val-12) p21 protein in a dose-dependent manner, Oncogenic p21 protein is more potent in mediating this effect than its normal counterpart, Both normal and oncogenic p21 proteins bind to purified JNK and to JNK that is present in cell extracts from transformed fibroblasts and melanoma cells, Oncogenic and normal p21 proteins have also been found to bind to bacterially expressed JUN protein, This binding is dose dependent, enhanced by the presence of GTP, and depends on the presence of the first 89 amino acids of JUN (the delta domain), as it does not occur with v-jun, While the ability of both normal and oncogenic p21 proteins to bind JNK is strongly inhibited by a p21 peptide corresponding to aa 96-110, and more weakly inhibited by the p21 peptide corresponding to aa 115-126, p21-JUN interaction is inhibited by peptides corresponding to aa 96-110 and, to a lesser degree, by peptides corresponding to aa 35-47, The results suggest that the p21 protein interacts specifically with both JNK and JUN proteins. [References: 19]
机译：已发现RAS基因编码的p21蛋白可通过其激酶JUN N端激酶（JNK）增加JUN的体外磷酸化。这种作用是在野生型和致癌性（Val- 12）p21蛋白呈剂量依赖性，致癌的p21蛋白在介导此作用方面比其正常对应物更有效。正常的和致癌的p21蛋白都与纯化的JNK和转化成纤维细胞和黑色素瘤细胞提取物中存在的JNK结合。还发现，致癌和正常的p21蛋白与细菌表达的JUN蛋白结合，这种结合是剂量依赖性的，通过GTP的存在得以增强，并且取决于JUN的前89个氨基酸（δ域）的存在，因为v-jun不会发生，而正常和致癌的p21蛋白结合JNK的能力都受到对应于aa 96-110的p21肽的强烈抑制，而受到p21肽corre的抑制则较弱对应于氨基酸115-126，p21-JUN相互作用被对应于氨基酸96-110的肽抑制，并在较小程度上被对应于氨基酸35-47的肽抑制。结果表明，p21蛋白与JNK和JUN蛋白。 [参考：19]

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