Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 15, Issue 11, Pages 20321-20338Publisher
MDPI AG
DOI: 10.3390/ijms151120321
Keywords
DNA damage; DNA (6-4) photoproduct; ultraviolet light; nucleotide flipping; crystal structure; antigen-binding fragment; antibody; photolyase; nucleotide excision repair
Funding
- Ministry of Education, Culture, Sports, Science and Technology in Japan [21770122]
- Grants-in-Aid for Scientific Research [26440034] Funding Source: KAKEN
Ask authors/readers for more resources
Exposure to the ultraviolet component of sunlight causes DNA damage, which subsequently leads to mutations, cellular transformation, and cell death. DNA photoproducts with (6-4) pyrimidine-pyrimidone adducts are more mutagenic than cyclobutane pyrimidine dimers. These lesions must be repaired because of the high mutagenic potential of (6-4) photoproducts. We here reviewed the structures of (6-4) photoproducts, particularly the detailed structures of the (6-4) lesion and (6-4) lesion-containing double-stranded DNA. We also focused on interactions with their binding proteins such as antibody Fabs, (6-4) photolyase, and nucleotide excision repair protein. The (6-4) photoproducts that bound to these proteins had common structural features: The 5'-side thymine and 3'-side pyrimidone bases of the T(6-4) T segment were in half-chair and planar conformations, respectively, and both bases were positioned nearly perpendicularly to each other. Interactions with binding proteins showed that the DNA helices flanking the T(6-4) T segment were largely kinked, and the flipped-out T(6-4) T segment was recognized by these proteins. These proteins had distinctive binding-site structures that were appropriate for their functions.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available