
@article {3555,
	title = {The N(2)-Furfuryl-deoxyguanosine Adduct Does Not Alter the Structure of B-DNA.},
	journal = {J Org Chem},
	volume = {81},
	year = {2016},
	month = {2016 Jan 15},
	pages = {502-11},
	abstract = {<p>N(2)-Furfuryl-deoxyguanosine (fdG) is carcinogenic DNA adduct that originates from furfuryl alcohol. It is also a stable structural mimic of the damage induced by the nitrofurazone family of antibiotics. For the structural and functional studies of this model N(2)-dG adduct, reliable and rapid access to fdG-modified DNAs are warranted. Toward this end, here we report the synthesis of fdG-modified DNAs using phosphoramidite chemistry involving only three steps. The functional integrity of the modified DNA has been verified by primer extension studies with DNA polymerases I and IV from E. coli. Introduction of fdG into a DNA duplex decreases the Tm by \~{}1.6 {\textdegree}C/modification. Molecular dynamics simulations of a DNA duplex bearing the fdG adduct revealed that though the overall B-DNA structure is maintained, this lesion can disrupt W-C H-bonding, stacking interactions, and minor groove hydrations to some extent at the modified site, and these effects lead to slight variations in the local base pair parameters. Overall, our studies show that fdG is tolerated at the minor groove of the DNA to a better extent compared with other bulky DNA damages, and this property will make it difficult for the DNA repair pathways to detect this adduct.</p>
},
	issn = {1520-6904},
	doi = {10.1021/acs.joc.5b02341},
	author = {Ghodke, Pratibha P and Gore, Kiran R and Harikrishna, S and Samanta, Biswajit and Kottur, Jithesh and Nair, Deepak T and Pradeepkumar, P I}
}
@article {856,
	title = {Unique structural features in DNA polymerase IV enable efficient bypass of the N2 adduct induced by the nitrofurazone antibiotic.},
	journal = {Structure},
	volume = {23},
	year = {2015},
	month = {2015 Jan 6},
	pages = {56-67},
	abstract = {<p>The reduction in the efficacy of therapeutic antibiotics represents a global problem of increasing intensity and concern. Nitrofuran antibiotics act primarily through the formation of covalent adducts at the N(2) atom of the deoxyguanosine nucleotide in genomic DNA. These adducts inhibit replicative DNA polymerases (dPols), leading to the death of the prokaryote. N(2)-furfuryl-deoxyguanosine (fdG) represents a stable structural analog of the nitrofuran-induced adducts. Unlike other known dPols, DNA polymerase IV (PolIV) from E.\&nbsp;coli can bypass the fdG adduct accurately with high catalytic efficiency. This property of PolIV is central to its role in reducing the sensitivity of E.\&nbsp;coli toward nitrofuran antibiotics such as nitrofurazone (NFZ). We present the mechanism used by PolIV to bypass NFZ-induced adducts and thus improve viability of E.\&nbsp;coli in the presence of NFZ. Our results can be used to develop specific inhibitors of PolIV that may potentiate the activity of nitrofuran antibiotics.</p>
},
	keywords = {Anti-Bacterial Agents, Crystallography, X-Ray, DNA Adducts, DNA Polymerase beta, Drug Resistance, Bacterial, Escherichia coli, Escherichia coli Proteins, Models, Molecular, Nitrofurazone, Nitrogen Compounds, Protein Structure, Tertiary, Reactive Nitrogen Species},
	issn = {1878-4186},
	doi = {10.1016/j.str.2014.10.019},
	author = {Kottur, Jithesh and Sharma, Amit and Gore, Kiran R and Narayanan, Naveen and Samanta, Biswajit and Pradeepkumar, Pushpangadan I and Nair, Deepak T}
}
