作者: Stanley Mak , Irene Mak
DOI: 10.1007/978-1-4613-2293-1_11
关键词: Transformation (genetics) 、 Cell biology 、 Mutagenesis (molecular biology technique) 、 Biology 、 Gene 、 Carcinogenesis 、 Lytic cycle 、 Cell morphology 、 Adenovirus genome 、 Oncovirus
摘要: Some adenoviruses such as Ad12 can induce tumors in newborn animals while others Ad2 and Ad5 cannot. However, all of them cause morphological transformation rodent cells vitro. Hamster rat transformed by the highly oncogenic viruses, for example Ad12, are tumorigenic syngeneic immunocompetent hosts. Although hamster non-oncogenic group (Ad2 Ad5) tumorigenic, this viruses not. This difference their biological properties affords an opportunity to dissect viral genes responsible cellular tumorigenesis vivo. The left 11% adenovirus genome (the E1 region) is sufficient transform tumor induction. region further subdivided into E1A (0–4.5%) E1B (4.5–11%). encodes several polypeptides some which have capacity regulate activity other during lytic infection, immortalization primary cells. E1B, three five polypeptides, confers cells, anchorage independent growth cell morphology cases. It appears that both required tumorigenicity Ad12-transformed animals. 58K polypeptide or its N-terminal portion “fully” phenotype. Available experimental data indicate 19K plays important role efficiency but not induction Much what known about functions various has come from studies using cloned DNA fragments virus containing mutations El region. anticipated increasing use recombinant technology construct genomes specific (site-directed mutagenesis) will our understanding transforming proteins.