Abasic Site
Abasic Site - Related Videos
02:10
Translesion DNA Polymerases
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2020
Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication. TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
06:13
Solid Plate-based Dietary Restriction in Caenorhabditis elegans
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Cited by 19 •
2011
Here we present a protocol for performing solid plate-based dietary restriction in C. elegans with killed bacteria.
09:24
O-Ring Aortic Banding Versus Traditional Transverse Aortic Constriction for Modeling Pressure Overload-Induced Cardiac Hypertrophy
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Cited by 1 •
2022
The present protocol describes a new technique of aortic banding in mice to induce pressure overload cardiac hypertrophy. For banding, a rubber ring with a fixed inner diameter is used. This new technique promises less variance and more reproducible data for future experiments.
10:46
Rapid in vivo Drug Response Prediction Using Leukemia Cell Grafts in Zebrafish Embryos
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2025
This protocol provides step-by-step instructions for generating and troubleshooting human acute lymphoblastic leukemia (ALL) xenografts from cell lines and fresh patient material in transiently immunosuppressed zebrafish embryos, along with guidelines for drug response assessment using flow cytometry. The experimental pipeline can also be adapted for solid tumors.
07:05
Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy
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Cited by 1 •
2024
This protocol presents a method for inducing mesenteric ischemia-reperfusion injury and visualizing neutrophil extracellular traps (NETs) in mesenteric venules using intravital microscopy. Blood flow in the superior mesenteric artery was restricted for 1 h, followed by reperfusion, allowing direct quantification of leukocyte adhesion and NETosis.
FAQs
AP endonuclease initiates repair by cleaving the DNA backbone near the damaged position. This incision creates an entry point for removal of the abnormal sugar residue. DNA polymerase can then fill the resulting gap, while DNA ligase seals the remaining break. This ordered division of labor converts lesion recognition into restoration of an intact DNA region.
An unrepaired abasic site can interfere with the progress of replication, so the copying machinery may be unable to proceed normally. Alternatively, replication can place an incorrect nucleotide opposite the lesion. That error converts temporary DNA damage into a potential mutation, and repeated or unresolved lesions can contribute to broader genomic instability.
They may form when a DNA base is lost spontaneously, but they can also appear as intermediates generated during DNA repair. This distinction matters because the same lesion can represent either intrinsic chemical damage to DNA or a transient product of an active repair pathway. In both cases, subsequent processing is needed to prevent harmful persistence.
A repair sequence can be followed from recognition of the damaged position through AP endonuclease incision, removal of the sugar residue, gap filling, and final ligation. Tracking these stages helps distinguish lesion detection from restoration of the DNA strand. It also clarifies whether an apparent repair defect affects cleavage, synthesis, or sealing.
Studying these lesions connects molecular DNA damage with larger biological outcomes. Their persistence or incorrect copying can be examined in relation to mutagenesis and genomic instability, while repair processing provides a way to investigate DNA damage responses. This makes abasic sites relevant to questions about how genome integrity is maintained.
Abasic sites provide a mechanistic context for investigating how DNA damage may participate in aging and disease mechanisms. They also help researchers examine the effects of chemicals that target DNA, especially by considering whether lesions are repaired or instead block replication or encourage incorrect nucleotide insertion. These outcomes connect molecular damage with altered genome stability.