DNA is considered to be a promising biomolecule as a template and scaffold for arranging and organizing functional molecules on the nanoscale. The construction and evaluation of DNAs containing multiple functional molecules that are useful for optoelectronic devices and sensors has been studied. In this paper we report the efficient incorporation of perylenediimide (PDI) units into DNA by using abasic sites both as binding sites and as reactive sites and the construction of PDI stacks within the DNA structure, accomplished through the preorganization of the PDI units in the hydrophobic pocket within the DNA. Our approach could become a valuable method for construction of DNA/chromophore hybrid structures potentially useful for the design of DNA-based devices and biosensors.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/cbic.201600454 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Bypass of Methoxyamine-Adducted Abasic Sites by Eukaryotic Translesion DNA Polymerases.
Int J Mol Sci
January 2025
Siberian Branch of the Russian Academy of Sciences Institute of Chemical Biology and Fundamental Medicine, 8 Lavrentieva Ave., 630090 Novosibirsk, Russia.
The apurinic/apyrimidinic site (AP site) is a highly mutagenic and cytotoxic DNA lesion. Normally, AP sites are removed from DNA by base excision repair (BER). Methoxyamine (MOX), a BER inhibitor currently under clinical trials as a tumor sensitizer, forms adducts with AP sites (AP-MOX) resistant to the key BER enzyme, AP endonuclease.
View Article and Find Full Text PDFAbasic sites are one of the most frequent forms of DNA damage that interfere with DNA replication. However, abasic sites exhibit complex effects because they can be processed into other types of DNA damage. Thus, it remains poorly understood how abasic sites affect replisome progression, which replication-coupled repair pathways they elicit, and whether this is affected by the template strand that is damaged.
View Article and Find Full Text PDFSingle-molecule studies of repair proteins in base excision repair.
BMB Rep
January 2025
Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Korea.
Base excision repair (BER) is an essential cellular mechanism that repairs small, non-helix-distorting base lesions in DNA, resulting from oxidative damage, alkylation, deamination, or hydrolysis. This review highlights recent advances in understanding the molecular mechanisms of BER enzymes through single-molecule studies. We discuss the roles of DNA glycosylases in lesion recognition and excision, with a focus on facilitated diffusion mechanisms such as sliding and hopping that enable efficient genome scanning.
View Article and Find Full Text PDFOctahedral Iron in Catalytic Sites of Endonuclease IV from and .
Biochemistry
January 2025
Department of Microbiology and Molecular Genetics, Institute for Medical Research Israel-Canada, The Hebrew University of Jerusalem, Jerusalem 9112102, Israel.
Article Synopsis
- - During infections, reactive oxygen species can cause DNA damage, necessitating a repair process that involves the enzyme endonuclease IV (Nfo), which removes defective DNA bases through hydrolysis.
- - The crystal structure of Nfo from a Gram-positive organism shows that it contains two iron ions and one zinc ion, with unique water molecule coordination that may play a role in how the enzyme distinguishes between these metals.
- - Nfo exhibits slow product release and optimal activity at high salt concentrations, which ties into its function and potentially significant role in organisms that thrive in salty environments.
ATR safeguards replication forks against APOBEC3B-induced toxic PARP1 trapping.
bioRxiv
November 2024
Department of Biological Chemistry, School of Medicine, University of California Irvine, Irvine, CA, USA.
ATR is the master safeguard of genomic integrity during DNA replication. Acute inhibition of ATR with ATR inhibitor (ATRi) triggers a surge in origin firing, leading to increased levels of single-stranded DNA (ssDNA) that rapidly deplete all available RPA. This leaves ssDNA unprotected and susceptible to breakage, a phenomenon known as replication catastrophe.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!