N2-DMF-5'-phenylthio-2',5'-dideoxyguanosine | 1350751-83-5

• 分子结构分类: 有机化合物 - 核苷、核苷酸和类似物 - 嘌呤核苷
• 英文名称: N2-DMF-5'-phenylthio-2',5'-dideoxyguanosine
• CAS: 1350751-83-5
• 化学式: C₁₉H₂₂N₆O₃S
• 分子量: 414.488
• InChiKey: SIHPIWSIOWIUCS-RRFJBIMHSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.78
• 重原子数：
  29.0
• 可旋转键数：
  6.0
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.37
• 拓扑面积：
  108.63
• 氢给体数：
  2.0
• 氢受体数：
  8.0

反应信息

• 作为反应物：
  描述：

  N2-DMF-5'-phenylthio-2',5'-dideoxyguanosine 在 亚磷酸三乙酯 作用下， 以 乙腈 为溶剂， 反应 20.0h， 以52%的产率得到N2-DMF-5',8-cyclo-2',5'-dideoxyguanosine
  参考文献：
  名称：

  Structure of (5′S)-8,5′-Cyclo-2′-deoxyguanosine in DNA

  摘要：

  Diastereomeric 8,5'-cyclopurine 2'-deoxynucleosides, containing a covalent bond between the deoxyribose and the purine base, represent an important class of DNA damage induced by ionizing radiation. The 8,5'-cyclo-2'-deoxyguanosine lesion (cdG) has been recently reported to be a strong block of replication and highly mutagenic in Escherichia coli. The 8,5'-cyclopurine-2'-deoxyriboses are suspected to play a role in the etiology of neurodegeneration in xeroderma pigmentosum patients. These lesions cannot be repaired by base excision repair, but they are substrates for nucleotide excision repair. The structure of an oligodeoxynucleotide duplex containing a site-specific S-cdG lesion placed opposite dC in the complementary strand was obtained by molecular dynamics calculations restrained by distance and dihedral angle restraints obtained from NMR spectroscopy. The S-cdG deoxyribose exhibited the O4'-exo (west) pseudorotation. Significant perturbations were observed for the beta, gamma, and chi torsion angles of the S-cdG nucleoside. Watson Crick base pairing was conserved at the S-cdG center dot dC pair. However, the O4'-exo pseudorotation of the S-cdG deoxyribose perturbed the helical twist and base pair stacking at the lesion site and the 5'-neighbor dC center dot dG base pair. Thermodynamic destabilization of the duplex measured by UV melting experiments correlated with base stacking and structural perturbations involving the modified S-cdG center dot dC and neighbor dT center dot dA base pairs. These perturbations may be responsible for both the genotoxicity of this lesion and its ability to be recognized by nucleotide excision repair.

  DOI：

  10.1021/ja207407n
• 作为产物：
  描述：

  2'-脱氧鸟苷 在 三丁基膦 作用下， 以 甲醇 、 N,N-二甲基甲酰胺 为溶剂， 反应 78.0h， 生成 N2-DMF-5'-phenylthio-2',5'-dideoxyguanosine
  参考文献：
  名称：

  Structure of (5′S)-8,5′-Cyclo-2′-deoxyguanosine in DNA

  摘要：

  Diastereomeric 8,5'-cyclopurine 2'-deoxynucleosides, containing a covalent bond between the deoxyribose and the purine base, represent an important class of DNA damage induced by ionizing radiation. The 8,5'-cyclo-2'-deoxyguanosine lesion (cdG) has been recently reported to be a strong block of replication and highly mutagenic in Escherichia coli. The 8,5'-cyclopurine-2'-deoxyriboses are suspected to play a role in the etiology of neurodegeneration in xeroderma pigmentosum patients. These lesions cannot be repaired by base excision repair, but they are substrates for nucleotide excision repair. The structure of an oligodeoxynucleotide duplex containing a site-specific S-cdG lesion placed opposite dC in the complementary strand was obtained by molecular dynamics calculations restrained by distance and dihedral angle restraints obtained from NMR spectroscopy. The S-cdG deoxyribose exhibited the O4'-exo (west) pseudorotation. Significant perturbations were observed for the beta, gamma, and chi torsion angles of the S-cdG nucleoside. Watson Crick base pairing was conserved at the S-cdG center dot dC pair. However, the O4'-exo pseudorotation of the S-cdG deoxyribose perturbed the helical twist and base pair stacking at the lesion site and the 5'-neighbor dC center dot dG base pair. Thermodynamic destabilization of the duplex measured by UV melting experiments correlated with base stacking and structural perturbations involving the modified S-cdG center dot dC and neighbor dT center dot dA base pairs. These perturbations may be responsible for both the genotoxicity of this lesion and its ability to be recognized by nucleotide excision repair.

  DOI：

  10.1021/ja207407n