Hypersensitivity to Cisplatin in Mouse Leukemia L1210/0 Cells: An XPG DNA Repair Defect

1996 ◽  
pp. 317-326
Author(s):  
Richard D. Wood ◽  
Juhani A. Vilpo ◽  
Leena M. Vilpo ◽  
David E. Szymkowski ◽  
Anne O’Donovan ◽  
...  
Keyword(s):  
Dna Repair ◽  
Mouse Leukemia ◽  
Repair Defect

Xeroderma pigmentosum A homolog from Hydra partially complements DNA repair defect in human XPA-deficient cells

2021 ◽  
Vol 46 (2) ◽  
Author(s):  
Alisha A Galande ◽  
Masafumi Saijo ◽  
Saroj S Ghaskadbi ◽  
Surendra Ghaskadbi
Keyword(s):  
Dna Repair ◽  
Xeroderma Pigmentosum ◽  
Repair Defect

Rapidly Progressive Familial Pulmonary Fibrosis In 4 Children With An Unknown DNA Repair Defect

2010 ◽  
Author(s):  
Timothy J. Vece ◽  
Marc G. Schecter ◽  
Claire Langston ◽  
Christine K. Garcia ◽  
Megan K. Dishop ◽  
...  
Keyword(s):  
Dna Repair ◽  
Pulmonary Fibrosis ◽  
Repair Defect ◽  
Familial Pulmonary Fibrosis

A DNA Repair Defect in a Patient With Ataxia, Mental Retardation, and Short Stature

1998 ◽  
Vol 18 (4) ◽  
pp. 358-361 ◽  
Author(s):  
Takanori Yamagata ◽  
Mariko Y. Momoi ◽  
Shigeko Saitoh ◽  
Kumiko Takadaya ◽  
Kenji Sato
Keyword(s):  
Dna Repair ◽  
Mental Retardation ◽  
Short Stature ◽  
Repair Defect

scholarly journals Genetic Recombination in Bacillus subtilis 168: Contribution of Holliday Junction Processing Functions in Chromosome Segregation

2004 ◽  
Vol 186 (17) ◽  
pp. 5557-5566 ◽  
Author(s):  
Begoña Carrasco ◽  
M. Castillo Cozar ◽  
Rudi Lurz ◽  
Juan C. Alonso ◽  
Silvia Ayora
Keyword(s):  
Dna Repair ◽  
Bacillus Subtilis ◽  
Genetic Recombination ◽  
Holliday Junction ◽  
Dna Helicases ◽  
Chromosomal Segregation ◽  
Dna Damaging Agents ◽  
Bacillus Subtilis 168 ◽  
Repair Deficiency ◽  
Repair Defect

ABSTRACT Bacillus subtilis mutants classified within the ε (ruvA, ΔruvB, ΔrecU, and recD) and η (ΔrecG) epistatic groups, in an otherwise rec+ background, render cells impaired in chromosomal segregation. A less-pronounced segregation defect in ΔrecA and Δsms (ΔradA) cells was observed. The repair deficiency of addAB, ΔrecO, ΔrecR, recH, ΔrecS, and ΔsubA cells did not correlate with a chromosomal segregation defect. The sensitivity of ε epistatic group mutants to DNA-damaging agents correlates with ongoing DNA replication at the time of exposure to the agents. The Δsms (ΔradA) and ΔsubA mutations partially suppress the DNA repair defect in ruvA and recD cells and the segregation defect in ruvA and ΔrecG cells. The Δsms (ΔradA) and ΔsubA mutations partially suppress the DNA repair defect of ΔrecU cells but do not suppress the segregation defect in these cells. The ΔrecA mutation suppresses the segregation defect but does not suppress the DNA repair defect in ΔrecU cells. These results result suggest that (i) the RuvAB and RecG branch migrating DNA helicases, the RecU Holliday junction (HJ) resolvase, and RecD bias HJ resolution towards noncrossovers and that (ii) Sms (RadA) and SubA proteins might play a role in the stabilization and or processing of HJ intermediates.

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