منابع مشابه
The 9-1-1 checkpoint clamp stimulates DNA resection by Dna2-Sgs1 and Exo1
Single-stranded DNA (ssDNA) at DNA ends is an important regulator of the DNA damage response. Resection, the generation of ssDNA, affects DNA damage checkpoint activation, DNA repair pathway choice, ssDNA-associated mutation and replication fork stability. In eukaryotes, extensive DNA resection requires the nuclease Exo1 and nuclease/helicase pair: Dna2 and Sgs1(BLM). How Exo1 and Dna2-Sgs1(BLM...
متن کاملExamining the roles of DNA2 during mammalian end resection
A healthy diet rich in fruits and vegetables is an important part of a healthy lifestyle. Whereas epidemiological data sometimes fail to provide proof of this concept, molecular evidence is accumulating that clearly shows both preventive as well as therapeutic effects of compounds from natural origins. in the paper of Guido Kroemer's group about pro-autophagic polyphenols and their inhibitory e...
متن کاملMolecular and Cellular Pathobiology Human Nuclease/Helicase DNA2 Alleviates Replication Stress by Promoting DNA End Resection
In precancerous and cancerous lesions, excessive growth signals resulting from activation of oncogenes or loss of tumor suppressor genes lead to intensive replication stress, which is recognized by a high level of replicationassociated DNA double-strand breaks (DSB). However, the molecular mechanism by which cells alleviate excessive replication stress remains unclear. In this study, we report ...
متن کاملSgs1 Helicase and Two Nucleases Dna2 and Exo1 Resect DNA Double-Strand Break Ends
Formation of single-strand DNA (ssDNA) tails at a double-strand break (DSB) is a key step in homologous recombination and DNA-damage signaling. The enzyme(s) producing ssDNA at DSBs in eukaryotes remain unknown. We monitored 5'-strand resection at inducible DSB ends in yeast and identified proteins required for two stages of resection: initiation and long-range 5'-strand resection. We show that...
متن کاملHuman nuclease/helicase DNA2 alleviates replication stress by promoting DNA end resection.
In precancerous and cancerous lesions, excessive growth signals resulting from activation of oncogenes or loss of tumor suppressor genes lead to intensive replication stress, which is recognized by a high level of replication-associated DNA double-strand breaks (DSB). However, the molecular mechanism by which cells alleviate excessive replication stress remains unclear. In this study, we report...
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ژورنال
عنوان ژورنال: Proceedings of the National Academy of Sciences
سال: 2019
ISSN: 0027-8424,1091-6490
DOI: 10.1073/pnas.1819276116