61 research outputs found
Stereoview of C2′- and C1′- AAF-dG structures, superimposed on the base and AAF moiety
<p><b>Copyright information:</b></p><p>Taken from "A new conformation for -(deoxyguanosin-8-yl)-2-acetylaminofluorene (AAF-dG) allows Watson–Crick pairing in the P2 DNA polymerase IV (Dpo4)"</p><p>Nucleic Acids Research 2006;34(3):785-795.</p><p>Published online 1 Feb 2006</p><p>PMCID:PMC1360743.</p><p>© The Author 2006. Published by Oxford University Press. All rights reserved</p> The C1′- AAF-dG is taken from the last snapshot of the 1-AAF-dG:-dCTP trajectory ( = 120.4°). The C2′- AAF-dG ( = 162.0 °) differs from the C1′- AAF-dG only in the sugar pucker pseudorotation angle, (,). Other torsions are χ = 201.8°, α′ = 101.0°, β′ = 30.7° and γ′ = 33.6°. The nucleotides are colored by atom with the AAF moiety shown in red and the methyl of the acetyl group in cyan. For clarity hydrogen atoms are not shown. Collision is denoted by the red circle
<b>MD package of wtXPD-damaged-ssDNA</b>
MD simulation: wtXPD-damaged-ssDNAXPD-64PP.tgz and XPD-CPD.tgzThe 8 µs MD simulations of human XPD bound to damaged ssDNA, containing a 6−4PP (XPD-64PP) or a CPD (XPD-CPD) lesion right outside the entry pore of XPD, are provided.Descriptions of each simulations1. Simulation of XPD-64PP reveals that 6−4PP initially positioned outside the entry pore is translocated in the 3' to 5' direction as its bases flip into the unoccupied space within the pore.2. Simulation of XPD-CPD reveals that CPD initially positioned outside the DNA entry pore undergoes a backbone-translocation into the pore, but its bases are blocked from entering.Files includedFor each system, the trajectory files are presented in binary NETCDF format, *.nc, a corresponding topology PRMTOP files, *.top, and the coordinates of the initial structure in PDB files, *.pdb are also provided, where * = XPD-64PP, XPD-CPD.Note1. Water molecules and ions are not included in all files.2. The trajectories were saved every 1 ns.</h4
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
Nucleotide Excision Repair Efficiencies of Bulky Carcinogen–DNA Adducts Are Governed by a Balance between Stabilizing and Destabilizing Interactions
The nucleotide excision repair (NER) machinery, the primary
defense
against cancer-causing bulky DNA lesions, is surprisingly inefficient
in recognizing certain mutagenic DNA adducts and other forms of DNA
damage. However, the biochemical basis of resistance to repair remains
poorly understood. To address this problem, we have investigated a
series of intercalated DNA–adenine lesions derived from carcinogenic
polycyclic aromatic hydrocarbon (PAH) diol epoxide metabolites that
differ in their response to the mammalian NER apparatus. These stereoisomeric
PAH-derived adenine lesions represent ideal model systems for elucidating
the effects of structural, dynamic, and thermodynamic properties that
determine the recognition of these bulky DNA lesions by NER factors.
The objective of this work was to gain a systematic understanding
of the relation between aromatic ring topology and adduct stereochemistry
with existing experimental NER efficiencies and known thermodynamic
stabilities of the damaged DNA duplexes. For this purpose, we performed
100 ns molecular dynamics studies of the lesions embedded in identical
double-stranded 11-mer sequences. Our studies show that, depending
on topology and stereochemistry, stabilizing PAH–DNA base van
der Waals stacking interactions can compensate for destabilizing distortions
caused by these lesions that can, in turn, cause resistance to NER.
The results suggest that the balance between helix stabilizing and
destabilizing interactions between the adduct and nearby DNA residues
can account for the variability of NER efficiencies observed in this
class of PAH–DNA lesions
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