作者: Zhe Cheng , Shan Zhu , Liang Wang , Fan Liu , Huimin Tian
DOI: 10.1016/J.IJPARA.2015.02.010
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摘要: Larvae of the fox tapeworm, Echinococcus multilocularis, cause alveolar echinococcosis, which is considered to be most lethal helminthic infection in humans. Since it develops host organs, parasite must have evolved a stress defense system cope with various genotoxic and cellular stresses that may DNA damage genomic instability. Tumor suppressor p53, well known as "guardian genome", plays vital role response many types damage. In present study, we describe characterisation Emp53 from E. multilocularis demonstrate structural functional homologue mammalian tumor p53. We show binds specifically oligonucleotides containing conventional p53 binding sites, indicating exhibits function transcription factor. Inhibition can suppress UV irradiation-induced apoptosis metacestode, an important induction following also reveal roles resistance oxidative regulation stress-induced apoptosis. Our results suggest that, similar its human counterpart, central network responses multilocularis. These help exploring mechanisms parasitic helminths provide useful information for development new interventions therapeutic drugs control echinococcosis.