scholarly journals NF-κB-dependent DNA damage-signaling differentially regulates DNA double-strand break repair mechanisms in immature and mature human hematopoietic cells

Leukemia ◽  
2015 ◽  
Vol 29 (7) ◽  
pp. 1543-1554 ◽  
Author(s):  
D Kraft ◽  
M Rall ◽  
M Volcic ◽  
E Metzler ◽  
A Groo ◽  
...  
Keyword(s):  
Dna Damage ◽  
Hematopoietic Cells ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dna Damage Signaling ◽  
Dna Double Strand Break ◽  
Repair Mechanisms ◽  
Break Repair

scholarly journals The Caenorhabditis elegans Homolog of Gen1/Yen1 Resolvases Links DNA Damage Signaling to DNA Double-Strand Break Repair

PLoS Genetics ◽  
2010 ◽  
Vol 6 (7) ◽  
pp. e1001025 ◽  
Author(s):  
Aymeric P. Bailly ◽  
Alasdair Freeman ◽  
Julie Hall ◽  
Anne-Cécile Déclais ◽  
Arno Alpi ◽  
...  
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dna Damage Signaling ◽  
Dna Double Strand Break ◽  
Break Repair

scholarly journals Modulation of Saccharomyces cerevisiae DNA double-strand break repair by SRS2 and RAD51.

Genetics ◽  
1995 ◽  
Vol 139 (3) ◽  
pp. 1189-1199
Author(s):  
G T Milne ◽  
T Ho ◽  
D T Weaver
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Recombinational Repair ◽  
Multiple Alleles ◽  
Dna Double Strand Break ◽  
Repair Mechanisms ◽  
Break Repair ◽  
Insight Into

Abstract RAD52 function is required for virtually all DNA double-strand break repair and recombination events in Saccharomyces cerevisiae. To gain greater insight into the mechanism of RAD52-mediated repair, we screened for genes that suppress partially active alleles of RAD52 when mutant or overexpressed. Described here is the isolation of a phenotypic null allele of SRS2 that suppressed multiple alleles of RAD52 (rad52B, rad52D, rad52-1 and KlRAD52) and RAD51 (KlRAD51) but failed to suppress either a rad52 delta or a rad51 delta. These results indicate that SRS2 antagonizes RAD51 and RAD52 function in recombinational repair. The mechanism of suppression of RAD52 alleles by srs2 is distinct from that which has been previously described for RAD51 overexpression, as both conditions were shown to act additively with respect to the rad52B allele. Furthermore, overexpression of either RAD52 or RAD51 enhanced the recombination-dependent sensitivity of an srs2 delta RAD52 strain, suggesting that RAD52 and RAD51 positively influence recombinational repair mechanisms. Thus, RAD52-dependent recombinational repair is controlled both negatively and positively.

scholarly journals Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review

2021 ◽  
Vol 8 ◽  
Author(s):  
Alejandra Fernandez ◽  
Connor O’Leary ◽  
Kenneth J O’Byrne ◽  
Joshua Burgess ◽  
Derek J Richard ◽  
...  
Keyword(s):  
Dna Damage ◽  
Chromatin Structure ◽  
Dna Methyltransferase ◽  
Strand Break ◽  
Dna Methyltransferases ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Epigenetic Mechanisms ◽  
Dna Double Strand Break ◽  
Break Repair

Upon the induction of DNA damage, the chromatin structure unwinds to allow access to enzymes to catalyse the repair. The regulation of the winding and unwinding of chromatin occurs via epigenetic modifications, which can alter gene expression without changing the DNA sequence. Epigenetic mechanisms such as histone acetylation and DNA methylation are known to be reversible and have been indicated to play different roles in the repair of DNA. More importantly, the inhibition of such mechanisms has been reported to play a role in the repair of double strand breaks, the most detrimental type of DNA damage. This occurs by manipulating the chromatin structure and the expression of essential proteins that are critical for homologous recombination and non-homologous end joining repair pathways. Inhibitors of histone deacetylases and DNA methyltransferases have demonstrated efficacy in the clinic and represent a promising approach for cancer therapy. The aims of this review are to summarise the role of histone deacetylase and DNA methyltransferase inhibitors involved in DNA double strand break repair and explore their current and future independent use in combination with other DNA repair inhibitors or pre-existing therapies in the clinic.

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