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- 저자 : Farewell, V. (검색결과 2 건)
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Jansson, K.,Warringer, J.,Farewell, A.,Park, H.O.,Hoe, K.L.,Kim, D.U.,Hayles, J.,Sunnerhagen, P. Elsevier 2008 Mutation research Vol.644 No.1
The DNA glycosylase MutY is strongly conserved in evolution, and homologs are found in most eukaryotes and prokaryotes examined. This protein is implicated in repair of oxidative DNA damage, in particular adenine mispaired opposite 7,8-dihydro-8-oxoguanine. Previous investigations in Escherichia coli, fission yeast, and mammalian cells show an association of mutations in MutY homologs with a mutator phenotype and carcinogenesis. Eukaryotic MutY homologs physically associate with several proteins with a role in replication, DNA repair, and checkpoint signaling, specifically the trimeric 9-1-1 complex. In a genetic investigation of the fission yeast MutY homolog, myh1<SUP>+</SUP>, we show that the myh1 mutation confers a moderately increased UV sensitivity alone and in combination with mutations in several DNA repair genes. The myh1 rad1, and to a lesser degree myh1 rad9, double mutants display a synthetic interaction resulting in enhanced sensitivity to DNA damaging agents and hydroxyurea. UV irradiation of myh1 rad1 double mutants results in severe chromosome segregation defects and visible DNA fragmentation, and a failure to activate the checkpoint. Additionally, myh1 rad1 double mutants exhibit morphological defects in the absence of DNA damaging agents. We also found a moderate suppression of the slow growth and UV sensitivity of rhp51 mutants by the myh1 mutation. Our results implicate fission yeast Myh1 in repair of a wider range of DNA damage than previously thought, and functionally link it to the checkpoint pathway.
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Hanly, J. G.,Urowitz, M. B.,Siannis, F.,Farewell, V.,Gordon, C.,Bae, S. C.,Isenberg, D.,Dooley, M. A.,Clarke, A.,Bernatsky, S.,Gladman, D.,Fortin, P. R.,Manzi, S.,Steinsson, K.,Bruce, I. N.,Ginzler, E Wiley Subscription Services, Inc., A Wiley Company 2008 Vol.58 No.3
<B>Objective</B><P>To examine, in an inception cohort of systemic lupus erythematosus (SLE) patients, the association between neuropsychiatric (NP) events and anti–ribosomal P (anti-P), antiphospholipid (lupus anticoagulant [LAC], anticardiolipin), anti–β2-glycoprotein I, and anti–NR2 glutamate receptor antibodies.</P><B>Methods</B><P>NP events were identified using the American College of Rheumatology case definitions and clustered into central/peripheral and diffuse/focal events. Attribution of NP events to SLE was determined using decision rules of differing stringency. Autoantibodies were measured without knowledge of NP events or their attribution.</P><B>Results</B><P>Four hundred twelve patients were studied (87.4% female; mean ± SD age 34.9 ± 13.5 years, mean ± SD disease duration 5.0 ± 4.2 months). There were 214 NP events in 133 patients (32.3%). The proportion of NP events attributed to SLE varied from 15% to 36%. There was no association between autoantibodies and NP events overall. However, the frequency of anti-P antibodies in patients with central NP events attributed to SLE was 4 of 20 (20%), versus 3 of 107 (2.8%) in patients with other NP events and 24 of 279 (8.6%) in those with no NP events (P = 0.04). Among patients with diffuse NP events, 3 of 11 had anti-P antibodies (27%), compared with 4 of 111 patients with other NP events (3.6%) and 24 of 279 of those with no NP events (8.6%) (P = 0.02). Specific clinical–serologic associations were found between anti-P and psychosis attributed to SLE (P = 0.02) and between LAC and cerebrovascular disease attributed to SLE (P = 0.038). There was no significant association between other autoantibodies and NP events.</P><B>Conclusion</B><P>Clinically distinct NP events attributed to SLE and occurring around the time of diagnosis were found to be associated with anti-P antibodies and LAC. This suggests that there are different autoimmune pathogenetic mechanisms, although low sensitivity limits the clinical application of testing for these antibodies.</P>
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