We also investigated a possible interconversion of guanine-based purines during incubation time.

Simultaneous exposure with these guanine-based purines did not show an additive effect.

Following metabolic activation, PhIP causes bulky DNA lesions at the C8-position of guanine.

Most of the M. bovis isolates had a guanine at the cited position.

The synthesis of a novel series of guanine analogues is reported.

These clusters represent potential alternate nucleobase pairs, geometrically equivalent to guanine-cytosine.

This interaction does not depend on the presence of guanine nucleotides.

This lesion contains an exocyclic ring obstructing the Watson-Crick hydrogen-bonding edge of guanine.

The best-understood of these events are those which involve guanine nucleotide binding regulatory proteins.

The initial difference Fourier maps clearly indicated the presence of inosine instead of guanine.

The other three amino acids facilitate, but are not essential for, guanine N-7 methylation.

Taken together, these results suggest that GUO is the guanine-based purines responsible for glutamate uptake activation.

Here we report that TG2 on the cell surface and in guanine nucleotide-bound form promotes phagocytosis.

The mutation also conferred resistance to oligomer disassembly by guanine nucleotides and high ionic strength solutions.

Homology is particularly high in the seven putative membrane-spanning domains of these guanine nucleotide-binding protein-coupled receptors.

The guanine nucleotide selectivity sequence and the divalent cation requirements were also similar for both responses.