Overexpression of the E1B 55-kilodalton (482R) protein of human adenovirus type 12 appears to permit efficient transformation of primary baby rat kidney cells in the absence of the E1B 19-kilodalton protein.

摘要: To analyze the structure and function of E1B 19,000-molecular-weight protein (19K protein) (163R) human adenovirus type 12, mutants were produced at various positions across 163R-coding sequence. Viruses bearing mutations within first 100 or so amino acids yielded unstable 163R-related products, induced DNA degradation enhanced cytopathic effect (cyt/deg phenotype) in KB cells, transformed primary rodent cells much lower efficiencies than wild-type (wt) virus. Deletion final 16 residues carboxy terminus had no phenotypic effect. Alteration residue 105 reduced transforming efficiency significantly, suggesting that this region 163R is functionally important. Disruption AUG initiation codon nucleotide 1542 blocked production completely but resulted higher levels 55K-482R synthesis a similar to wt These data suggested while some importance, normal can be obtained its absence if 482R overexpressed.