Abstract: The 173A mutant was defective for the transcriptional activation function but retained wild-type DNA replication activity, whereas the
E39A mutant wild-type transcriptional activation function but was defective in transient DNA replication assays.
Abstract: The
E39A mutant was also defective for HPV16
E1 binding in vitro, suggesting that the ability of
E2 protein to form a complex with
E1 appears to be essential for its function as an auxiliary replication factor.