منابع مشابه
Cells expressing murine RAD52 splice variants favor sister chromatid repair.
The RAD52 gene is essential for homologous recombination in the yeast Saccharomyces cerevisiae. RAD52 is the archetype in an epistasis group of genes essential for DNA damage repair. By catalyzing the replacement of replication protein A with Rad51 on single-stranded DNA, Rad52 likely promotes strand invasion of a double-stranded DNA molecule by single-stranded DNA. Although the sequence and in...
متن کاملInduction by alkylating agents of sister chromatid exchanges and chromatid breaks in Fanconi's anemia.
Sister chromatid exchanges, which may reflect chromosome repair in response to certain types of DNA damage, provide a means of investigating the increased chromosome fragility characteristic of Fanconi's anemia. By a recently developed technique using 33258 Hoechst and 5-bromodeoxyuridine, it was observed that the baseline frequency of sister chromatid exchanges in phytohemagglutinin-stimulated...
متن کاملMitomycin-induced Chromatid Breaks in HeLa Cells: A Consequence of Incomplete DNA Replication1
The formation of chromosome aberrations induced by alkylating agents such as mitomycin C has been shown to require the passage of the treated cell through S phase. However, the exact mechanisms by which mitomycin C-induced DNA lesions are translated into chromosome aberra tions during S phase are not known. The purpose of these studies was to better understand the molecular basis of chromosome ...
متن کاملMitomycin-induced chromatid breaks in HeLa cells: a consequence of incomplete DNA replication.
The formation of chromosome aberrations induced by alkylating agents such as mitomycin C has been shown to require the passage of the treated cell through S phase. However, the exact mechanisms by which mitomycin C-induced DNA lesions are translated into chromosome aberrations during S phase are not known. The purpose of these studies was to better understand the molecular basis of chromosome a...
متن کاملDNA double-strand breaks, p53, and apoptosis during lymphomagenesis in scid/scid mice.
The tumor-suppressing phenotype of p53 is thought to be due to its accumulation in response to DNA damage and resultant cell cycle arrest or apoptosis. scid/scid mice are defective in DNA double-strand break repair due to a mutation in DNA-dependent protein kinase (DNAPK). Treatment of scid/scid mice with gamma radiation or N-ethyl-N-nitrosourea resulted in approximately 86% incidence of T-cell...
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ژورنال
عنوان ژورنال: Mutagenesis
سال: 1998
ISSN: 0267-8357,1464-3804
DOI: 10.1093/mutage/13.5.481