Chaussepied M, Lallemand D, Moreau M F, Adamson R, Hall R, Langsley G
URA 1960 du CNRS, Département d'Immunologie, Institut Pasteur, Paris, France.
Mol Biochem Parasitol. 1998 Aug 1;94(2):215-26. doi: 10.1016/s0166-6851(98)00070-x.
Theileria parasitises bovine leukocytes and transforms them into proliferating, metastatic tumours, where the infection resembles a leukaemia-like disease. We have studied the signal transduction pathways leading to activation of the transcription factor AP-1 in different transformed leukocytes. Parasite infection leads to an up-regulation of all members of the Jun/Fos family of proteins and surprisingly, this occurs in the absence of any detectable ERK, or p38 MAP kinase activity. In the parasitised B-sarcoma TBL3, AP-1 induction occurs in the absence of any JNK activity. In contrast, in infected macrophage and B-cell lines, AP-1 transcriptional activity is strictly associated with the parasite-induced constitutive activation of JNK and subsequent c-Jun N-terminal phosphorylation. Thus, constant AP-1 transcriptional activity involves both an upregulation in the levels of Jun and Fos proteins and constitutive JNK activation.
泰勒虫寄生于牛白细胞，并将其转化为增殖性转移性肿瘤，这种感染类似于白血病样疾病。我们研究了不同转化白细胞中转录因子AP-1激活的信号转导途径。寄生虫感染导致Jun/Fos蛋白家族所有成员的上调，令人惊讶的是，这发生在没有任何可检测到的ERK或p38丝裂原活化蛋白激酶活性的情况下。在被寄生的B肉瘤TBL3中，AP-1的诱导在没有任何JNK活性的情况下发生。相反，在受感染的巨噬细胞和B细胞系中，AP-1转录活性与寄生虫诱导的JNK组成性激活及随后的c-Jun N端磷酸化严格相关。因此，持续的AP-1转录活性涉及Jun和Fos蛋白水平的上调以及JNK的组成性激活。
