Figure: Superposition of excision-enhancing mutation or TAM (
M41L,
D67N,
K70R,
T215Y, and
K219Q)
RT dsDNA AZTppppA structure4 on
K65R RT dsDNA dATP structure at their dNTP-binding sites; AZTppppA is the product of AZT monophosphate by ATP-mediated excision.
Discussion: 4) has shown that
T215Y significantly contributes to the binding of ATP to the mutant
RT for excision by stacking with its adenine base and
K70R forms a network of hydrogen-bonding interactions with the alpha'-phosphate and 3'-OH of ATP.4 The
K65R mutation has the opposite effect of decreasing the rate of ex