title: [DNA homologous recombination repair in mammalian cells].
abstract: DNA double-strand breaks (DSBs) are the most serious DNA damage. Due to a great variety of factors causing DSBs, the efficacy of their repair is crucial for the cell's functioning and prevents DNA fragmentation, chromosomal translocation and deletion. In mammalian cells DSBs can be repaired by non-homologous end joining (NHEJ), homologous recombination (HRR) and single strand annealing (SSA). HRR can be divided into the first and second phase. The first phase is initiated by sensor proteins belonging to the MRN complex, that activate the ATM protein which target HRR proteins to obtain the second response phase--repair. HRR is precise because it utilizes a non-damaged homologous DNA fragment as a template. The key players of HRR in mammalian cells are MRN, RPA, Rad51 and its paralogs, Rad52 and Rad54.
authors.affiliation: Katedra Genetyki Molekularnej, Uniwersytet Lódzki, Lódź.
authors.forename: Tomasz
authors.initials: T
authors.lastname: Popławski
authors.forename: Janusz
authors.initials: J
authors.lastname: Błasiak
mesh_terms: D000818:Animals; D004249:DNA Damage; D053938:DNA Fragmentation; D004260:DNA Repair / Q000502:physiology*; D051747:DNA-Activated Protein Kinase / Q000378:metabolism; D005785:Gene Conversion; D006801:Humans; D051135:Rad51 Recombinase / Q000378:metabolism*; D051721:Rad52 DNA Repair and Recombination Protein / Q000378:metabolism*; D011995:Recombination, Genetic / Q000502:physiology*
chemical_list: D051721:Rad52 DNA Repair and Recombination Protein; D051747:DNA-Activated Protein Kinase; D051135:Rad51 Recombinase