Stimulation of DNA repair synthesis of rat thymocytes by novobiocin and nalidixic acid in vitro without detectable DNA damage

1987 ◽  
Vol 60 (4) ◽  
pp. 287-292 ◽  
Author(s):  
Karlheinz Tempel ◽  
Alfred Spath
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Nalidixic Acid ◽  
Repair Synthesis ◽  
Dna Repair Synthesis ◽  
Stimulation Of

DNA repair synthesis following exposure of guinea-pig pancreatic slices to methyl-N-nitrosourethane in vitro

1975 ◽  
Vol 31 (4) ◽  
pp. 467-467 ◽  
Author(s):  
K. Hasumi ◽  
Z. M. Iqbal ◽  
A. Alarif ◽  
S. S. Epstein
Keyword(s):  
Dna Repair ◽  
Guinea Pig ◽  
Repair Synthesis ◽  
Dna Repair Synthesis

scholarly journals Small molecule inhibitors of a human recombination-associated ATPase, RAD54

2019 ◽  
Author(s):  
Kirk T. Ehmsen ◽  
Kenny K.H. Ang ◽  
William D. Wright ◽  
Julia L. Davies ◽  
Yassir Younis ◽  
...  
Keyword(s):  
Dna Repair ◽  
Small Molecule ◽  
Small Molecule Inhibitors ◽  
Homology Search ◽  
Dna Breaks ◽  
Repair Synthesis ◽  
Molecular Events ◽  
Dna Strand Exchange ◽  
Dna Repair Synthesis

ABSTRACTHomologous recombination (HR) is a principal support pathway for DNA replication and for recovery from DNA breaks and interstrand crosslinks, making it a rational target for inhibition in cancer therapy. The ATPase RAD54 functions in molecular events that promote DNA sequence-preservation during HR-mediated damage repair, including homology search, DNA strand exchange, and transition to DNA repair synthesis within a displacement loop intermediate. We developed a high-throughput biochemical screen to identify small-molecule inhibitors of human RAD54, using a phosphate detection assay to monitor RAD54 ATPase activity in the presence of double-stranded DNA (dsDNA). After filtering potential DNA intercalators and ‘frequent hitters,’ we identified two chemotypes that reproducibly inhibited RAD54 ATPase in vitro. We evaluated these chemotypes for inhibition of RAD54-dsDNA binding and cancer cell survival. A halogenated carbazole/dihydroacridine scaffold inhibited a panel of SWI2/SNF2-related ATPases but not VCP/p97, an unrelated ATPase. Small molecules that interfere with key steps in HR— such as inhibitors of RAD54—may expose DNA repair-dependent vulnerabilities in cancer cells.

2-Nitropropane induces DNA repair synthesis in rat hepatocytes in vitro and in vivo

1988 ◽  
Vol 9 (5) ◽  
pp. 811-815 ◽  
Author(s):  
U. Andrae ◽  
L. Vogl ◽  
J. Lichtmannegger ◽  
K.H. Summer
Keyword(s):  
Dna Repair ◽  
Rat Hepatocytes ◽  
Repair Synthesis ◽  
Dna Repair Synthesis

scholarly journals Sequestration of Mammalian Rad51-Recombination Protein into Micronuclei

1999 ◽  
Vol 144 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Thomas Haaf ◽  
Elke Raderschall ◽  
Gurucharan Reddy ◽  
David C. Ward ◽  
Charles M. Radding ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Dna Repair ◽  
Apoptotic Cell ◽  
Protein A ◽  
Dna Double Strand Breaks ◽  
Γ Irradiation ◽  
Repair Synthesis ◽  
Rad51 Protein ◽  
Dna Repair Synthesis

The mammalian Rad51 protein is involved in homologous recombination and in DNA damage repair. Its nuclear distribution after DNA damage is highly dynamic, and distinct foci of Rad51 protein, distributed throughout the nuclear volume, are induced within a few hours after γ irradiation; these foci then coalesce into larger clusters. Rad51-positive cells do not undergo DNA replication. Rad51 foci colocalize with both replication protein A and sites of unscheduled DNA repair synthesis and may represent a nuclear domain for recombinational DNA repair. By 24 h postirradiation, most foci are sequestered into micronuclei or assembled into Rad51-coated DNA fibers. These micronuclei and DNA fibers display genome fragmentation typical of apoptotic cell death. Other repair proteins, such as Rad52 and Gadd45, are not eliminated from the nucleus. DNA double strand breaks in repair-deficient cells or induced by the clastogen etoposide are also accompanied by the sequestering of Rad51 protein before cell death. The spindle poison colcemid causes cell cycle arrest and Rad51-foci formation without directly damaging DNA. Collectively, these observations suggest that mammalian Rad51 protein associates with damaged DNA and/or with DNA that is temporarily or irreversibly unable to replicate and these foci may subsequently be eliminated from the nucleus.

scholarly journals Recruitment of DNA repair synthesis machinery to sites of DNA damage/repair in living human cells

2007 ◽  
Vol 35 (9) ◽  
pp. 2913-2923 ◽  
Author(s):  
Kazunari Hashiguchi ◽  
Yoshihiro Matsumoto ◽  
Akira Yasui
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Dna Damage Repair ◽  
Human Cells ◽  
Repair Synthesis ◽  
Damage Repair ◽  
Dna Repair Synthesis
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