Role of Transient Anions in Chemoradiation Therapy: Base Modifications, Cross-Links, and Cluster Damages Induced to Cisplatin-DNA Complexes by 1–20 eV Electrons

2020 ◽  
Vol 124 (16) ◽  
pp. 3315-3325 ◽  
Author(s):  
Yanfang Dong ◽  
Yaxiao Wang ◽  
Puxiang Zhuang ◽  
Xianzhi Fu ◽  
Yi Zheng ◽  
...  
Keyword(s):  
Chemoradiation Therapy ◽  
Dna Complexes ◽  
Cross Links ◽  
Base Modifications

scholarly journals Role of Copper in Biosynthesis of Intramolecular Cross-links in Chick Tendon Collagen

1969 ◽  
Vol 244 (21) ◽  
pp. 5785-5789
Author(s):  
W.S. Chou ◽  
J.E. Savage ◽  
B.L. O'Dell
Keyword(s):  
Cross Links ◽  
Tendon Collagen

Role of Multivalent Cations in the Self-Assembly of Phospholipid−DNA Complexes

2007 ◽  
Vol 111 (51) ◽  
pp. 14233-14238 ◽  
Author(s):  
Guillaume Tresset ◽  
Wun Chet Davy Cheong ◽  
Yeng Ming Lam
Keyword(s):  
Self Assembly ◽  
The Self ◽  
Dna Complexes

The role of hydrophobic alkyl chains in the physicochemical properties of poly(β-amino ester)/DNA complexes

2015 ◽  
Vol 126 ◽  
pp. 374-380 ◽  
Author(s):  
Azahara Rata-Aguilar ◽  
Nathaly Segovia-Ramos ◽  
Ana Belén Jódar-Reyes ◽  
Víctor Ramos-Pérez ◽  
Salvador Borrós ◽  
...  
Keyword(s):  
Physicochemical Properties ◽  
Amino Ester ◽  
Dna Complexes ◽  
Alkyl Chains

scholarly journals Repair Kinetics of Genomic Interstrand DNA Cross-Links: Evidence for DNA Double-Strand Break-Dependent Activation of the Fanconi Anemia/BRCA Pathway

2004 ◽  
Vol 24 (1) ◽  
pp. 123-134 ◽  
Author(s):  
Andreas Rothfuss ◽  
Markus Grompe
Keyword(s):  
Fanconi Anemia ◽  
Strand Break ◽  
S Phase ◽  
Dna Double Strand Breaks ◽  
Subsequent Formation ◽  
Strand Breaks ◽  
Dna Double Strand Break ◽  
Cross Links ◽  
Kinetics Of

ABSTRACT The detailed mechanisms of DNA interstrand cross-link (ICL) repair and the involvement of the Fanconi anemia (FA)/BRCA pathway in this process are not known. Present models suggest that recognition and repair of ICL in human cells occur primarily during the S phase. Here we provide evidence for a refined model in which ICLs are recognized and are rapidly incised by ERCC1/XPF independent of DNA replication. However, the incised ICLs are then processed further and DNA double-strand breaks (DSB) form exclusively in the S phase. FA cells are fully proficient in the sensing and incision of ICL as well as in the subsequent formation of DSB, suggesting a role of the FA/BRCA pathway downstream in ICL repair. In fact, activation of FANCD2 occurs slowly after ICL treatment and correlates with the appearance of DSB in the S phase. In contrast, activation is rapid after ionizing radiation, indicating that the FA/BRCA pathway is specifically activated upon DSB formation. Furthermore, the formation of FANCD2 foci is restricted to a subpopulation of cells, which can be labeled by bromodeoxyuridine incorporation. We therefore conclude that the FA/BRCA pathway, while being dispensable for the early events in ICL repair, is activated in S-phase cells after DSB have formed.

Role of the FAD-dependent polyamine oxidase in the selective formation of N1,N8-bis(γ- glutamyl)spermidine protein cross-links1

2007 ◽  
Vol 35 (2) ◽  
pp. 396-400 ◽  
Author(s):  
A. Lentini ◽  
P. Mattioli ◽  
B. Provenzano ◽  
A. Abbruzzese ◽  
M. Caraglia ◽  
...  
Keyword(s):  
Stratum Corneum ◽  
Polyamine Oxidase ◽  
Polyamine Metabolism ◽  
Suitable Model ◽  
Cross Link ◽  
Cellular Mechanisms ◽  
Preferential Formation ◽  
Cross Links ◽  
Selective Formation

Protein-bound γ-glutamylpolyamines have highlighted a new pathway in polyamine metabolism. Human foreskin keratinocytes offer a suitable model for this study. Indeed, they develop polymerized envelopes, as they differentiate, rich in ϵ-(γ-glutamyl)lysine and N1,N8-bis(γ-glutamyl)spermidine cross-links. We have found that the selective oxidation of N1-(γ-glutamyl)spermidine and N-(γ-glutamyl)spermine by FAD-dependent polyamine oxidase (PAO) may be one of the cellular mechanisms regulating the preferential formation of a sterically defined bis(γ-glutamyl)spermidine cross-link. The significance of this finding is unknown, but it suggests that the target of this PAO-modulation is to achieve the biochemical prerequisite for production of a normal epidermal stratum corneum.

scholarly journals Oxidative DNA base modifications as factors in carcinogenesis.

1998 ◽  
Vol 45 (2) ◽  
pp. 561-572 ◽  
Author(s):  
R Olinski ◽  
P Jaruga ◽  
T H Zastawny
Keyword(s):  
Metastatic Potential ◽  
Base Damage ◽  
Normal Tissues ◽  
Dna Base ◽  
Dna Modifications ◽  
Cancer Initiation ◽  
Base Modifications ◽  
Therapeutic Doses ◽  
Oxidative Base Damage

Reactive oxygen species can cause extensive DNA modifications including modified bases. Some of the DNA base damage has been found to possess premutagenic properties. Therefore, if not repaired, it can contribute to carcinogenesis. We have found elevated amounts of modified bases in cancerous and precancerous tissues as compared with normal tissues. Most of the agents used in anticancer therapy are paradoxically responsible for induction of secondary malignancies and some of them may generate free radicals. The results of our experiments provide evidence that exposure of cancer patients to therapeutic doses of ionizing radiation and anticancer drugs causes base modifications in genomic DNA of lymphocytes. Some of these base damages could lead to mutagenesis in critical genes and ultimately to secondary cancers such as leukemias. This may point to an important role of oxidative base damage in cancer initiation. Alternatively, the increased level of the modified base products may contribute to genetic instability and metastatic potential of tumor cells.

On the Possible Role of tRNA Base Modifications in the Evolution of Codon Usage: Queuosine and Drosophila

2010 ◽  
Vol 70 (4) ◽  
pp. 339-345 ◽  
Author(s):  
Ylenia Chiari ◽  
Kirstin Dion ◽  
James Colborn ◽  
Aristeidis Parmakelis ◽  
Jeffrey R. Powell
Keyword(s):  
Codon Usage ◽  
Base Modifications
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