Single-Strand Break End Resection in Genome Integrity: Mechanism and Regulation by APE2
نویسندگان
چکیده
منابع مشابه
End resection at double-strand breaks: mechanism and regulation.
RecA/Rad51 catalyzed pairing of homologous DNA strands, initiated by polymerization of the recombinase on single-stranded DNA (ssDNA), is a universal feature of homologous recombination (HR). Generation of ssDNA from a double-strand break (DSB) requires nucleolytic degradation of the 5'-terminated strands to generate 3'-ssDNA tails, a process referred to as 5'-3' end resection. The RecBCD helic...
متن کاملA global view of meiotic double-strand break end resection.
DNA double-strand breaks that initiate meiotic recombination are exonucleolytically processed. This 5'→3' resection is a central, conserved feature of recombination but remains poorly understood. To address this lack, we mapped resection endpoints genome-wide at high resolution in Saccharomyces cerevisiae Full-length resection requires Exo1 exonuclease and the DSB-responsive kinase Tel1, but no...
متن کاملAPE2 promotes DNA damage response pathway from a single-strand break
As the most common type of DNA damage, DNA single-strand breaks (SSBs) are primarily repaired by the SSB repair mechanism. If not repaired properly or promptly, unrepaired SSBs lead to genome stability and have been implicated in cancer and neurodegenerative diseases. However, it remains unknown how unrepaired SSBs are recognized by DNA damage response (DDR) pathway, largely because of the lack...
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Introduction: Passage of ionizing radiation through the organs of living creatures develops clusters of damaged nucleotides inside the DNA rounds. 192Ir Gamma source is one of the most widely used sources in brachytherapy of cervical and prostate cancer. Thus, in this research, we investigated the flux of photons and its resulting secondary electrons, the single-strand break (S...
متن کاملTbf1 and Vid22 promote resection and non-homologous end joining of DNA double-strand break ends.
The repair of DNA double-strand breaks (DSBs) is crucial for maintaining genome stability. The Saccharomyces cerevisiae protein Tbf1, which is characterized by a Myb domain and is related to mammalian TRF1 and TRF2, has been proposed to act as a transcriptional activator. Here, we show that Tbf1 and its interacting protein Vid22 are new players in the response to DSBs. Inactivation of either TB...
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ژورنال
عنوان ژورنال: International Journal of Molecular Sciences
سال: 2018
ISSN: 1422-0067
DOI: 10.3390/ijms19082389