[4] In infected cells, the expression of E1A results in the degradation of MCL-1, which normally binds the propaptotic protein, BAK.
[4] BAK activation induces apoptosis by cooligomerizing with another proapoptotic protein, BAX.
[6] However, in adenovirus-infected cells, activated BAK and BAX are sequestered by E1B-19k, preventing the pathway.
Additionally, p53 bound to E1B-55k has an affinity for its binding site that is ten times higher than free p53.
[13] Structural and bioinformatics studies have shown that E1B-55k, which is specific to mammalian mastadenoviruses, has evolved by exaptation from an LH3-like minor capsid protein encoded by atadenoviruses.