The interstrand crosslinks that appear in stored depurinated DNA interfere with the counting of apurinic sites and strand breaks by sucrose gradient analysis. They could not be cleaved at acid or alkaline pH, or by treatment with methoxyamine.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0167-4781(84)90071-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
USP1 in regulation of DNA repair pathways.
DNA Repair (Amst)
January 2025
School of Molecular Biosciences, University of Glasgow, Glasgow G12 8QQ, Scotland. Electronic address:
Ubiquitin-specific protease 1 (USP1) is the founding member of the family of cysteine proteases that catalyse hydrolysis of the isopeptide bond between ubiquitin and targets. USP1 is often overexpressed in various cancers, and expression levels correlate with poor prognosis. USP1 and its partner USP1-associated Factor 1 (UAF1) are required for deubiquitinating monoubiquitin signals in DNA interstrand crosslink repair, and in Translesion synthesis, among others, and both proteins are subject to multiple regulations themselves.
View Article and Find Full Text PDFDesign of Cell-Penetrating Domain Antibodies via a Genetically Encoded β-Lactam Amino Acid.
Angew Chem Int Ed Engl
January 2025
Department of Chemistry, State University of New York at Buffalo, Buffalo, New York, 14260-3000, United States.
Domain antibodies such as monobodies provide an attractive immunoglobin fold for evolving high-affinity protein binders targeting the intracellular proteins implicated in cell signalling. However, it remains a challenge to endow cell permeability to these small and versatile protein binders. Here, we report a streamlined approach combining orthogonal crosslinking afforded by a genetically encoded β-lactam-lysine (BeLaK) and genetic supercharging to generate cell-penetrating monobodies.
View Article and Find Full Text PDFHROB Is Implicated in DNA Replication.
Genes (Basel)
December 2024
Project Group Biochemistry, Leibniz Institute on Aging-Fritz Lipmann Institute, D-07745 Jena, Germany.
DNA replication represents a series of precisely regulated events performed by a complex protein machinery that guarantees accurate duplication of the genetic information. Since DNA replication is permanently faced by a variety of exogenous and endogenous stressors, DNA damage response, repair and replication must be closely coordinated to maintain genomic integrity. HROB has been identified recently as a binding partner and activator of the Mcm8/9 helicase involved in DNA interstrand crosslink (ICL) repair.
View Article and Find Full Text PDFDNA Damage Response Network and Intracellular Redox Status in the Clinical Outcome of Patients with Lung Cancer.
Cancers (Basel)
December 2024
Institute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.
: DNA damage response (DDR) is a network of molecular pathways associated with the pathogenesis and progression of several diseases, as well as the outcome of chemotherapy. Moreover, the intracellular redox status is essential for maintaining cell viability and controlling cellular signaling. Herein, we analyzed DDR signals and redox status in peripheral blood mononuclear cells (PBMCs) from patients with lung cancer with different response rates to platinum-based chemotherapy.
View Article and Find Full Text PDFBroad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.
Nucleic Acids Res
January 2025
The David and Inez Myers Laboratory for Cancer Research, Tel Aviv University, Tel Aviv 6997801, Israel.
Cellular senescence plays a significant role in tissue aging. Senescent cells, which resist apoptosis while remaining metabolically active, generate endogenous DNA-damaging agents, primarily reactive oxygen species. Efficient DNA repair is therefore crucial in these cells, especially when they undergo senescence escape, resuming DNA replication and cellular proliferation.
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!