Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture

Abstract

The polyoma virus middle-T and the T24 Harvey ras1 genes are individually unable to transform primary baby rat kidney cells. Adenovirus early region 1A provides functions required by these genes to transform primary cells following DNA-mediated gene transfer. These results suggest that separate establishment and transforming functions are required for oncogenic transformation of primary cells in culture.

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma

“…There are a number of similarities between the myc-and Ela genes, including a nuclear localization of their gene products and an ability of each to cooperate with ras oncogenes in the transformation of primary cells (Yee et al, 1983;Land et al, 1983;Ruley, 1983;Persson and Leder, 1984). Other evidence suggests that the c-myc protein, like Ela, can enhance the transcription of other genes (Kingston et al, 1984).…”

Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms

“…Using the Ras cooperation assay performed in primary rat embryo ®broblasts (REFs) (Land et al, 1983;Ruley, 1983), we previously showed that Bin1 inhibits malignant transformation by c-Myc in a MBDdependent manner . To de®ne other regions required, REFs were transfected with expression vectors for Myc, oncogenic Ras, and Bin1 or Bin1 deletion mutants, and transformed cell foci were scored 2 weeks later ( Figure 5).…”

The leukemia-associated cytoplasmic nucleophosmin mutant is an oncogene with paradoxical functions: Arf inactivation and induction of cellular senescence

“…E1A CR2 binds retinoblastoma (RB) family members, de-repressing E2F transcription factors and inducing cell cycle progression. However, E1A-expressing cells eventually degenerate in soft agar and do not form colonies (Ruley, 1983). This is largely due to E1A's ability to induce p53 stabilization through upregulation of Arf (de Stanchina et al, 1998), CBP/p300 binding (Grossman et al, 1998) and proteosome modification by E1A CR1 (Zhang et al, 2004).…”