FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2094133050> ?p ?o ?g. }

• W2094133050 endingPage "178" @default.
• W2094133050 startingPage "167" @default.
• W2094133050 abstract "O6-Methylguanine (O6MeG) is important in induction of chromosome aberrations (abs), with the unusual property that new abs are produced in the second cycle after treatment; cells lacking repair by O6-alkylguanine DNA-alkyltransferase (AGT) have more abs at the second division (M2) than at the first (M1). These second-cycle abs are likely caused by attempted correction by mismatch repair (MMR) of O6MeG:T mispairs, since we previously showed that MMR-deficient human cells (MT1 lymphoblasts) treated with SN-1 methylating agents do not produce new abs at M2 and are resistant to killing. Here we used MMR-deficient rodent cells to examine ab induction by alkylators and by incorporated 6-thioguanine (6-tG) which produces mispairs. BrdUrd labeling was used to identify cells at first, second and third metaphase after treatment (M1, M2 and M3). MMR-deficient Chinese hamster Clone B cells were 10-fold more resistant to ab induction by methyl nitrosourea and 1-methyl-3-nitro-1-nitrosoguanidine compared to their MMR-proficient parent cells, CHO MT+. Both cell lines express AGT and can remove the methyl group from O6MeG. Clone B has twice the AGT activity of CHO MT+, but inhibition of AGT with O6-benzylguanine did not change ab induction, indicating that methylation tolerance of Clone B cells was due to defective MMR and not to increased repair of O6MeG. Confirming the importance of O6MeG in inducing abs, even when it is a minor component of the adducts induced, Clone B cells were 2-fold more resistant to ab induction by methyl methanesulfonate and dimethylsulfate, whereas they had normal sensitivity to ethyl nitrosourea and 1-ethyl-3-nitro-1-nitrosoguanidine. Clone B cells are also resistant to killing by 6-tG, and 6-tG induced few abs in MMR-deficient Clone B (6-fold lower than CHO MT+ cells). Since mispairs do not occur until the cell cycle following incorporation of 6-tG, new abs in MMR-proficient cells are expected one cell cycle later than with the methylators, i.e., at M3. As expected, in normal CHO MT+, high ab levels were seen at M3, but there was also ab induction at M2. Similarly, with methylating agents we saw higher levels of abs at M1 in the MMR-proficient CHO MT+ cells than in Clone B cells, suggesting that in the rodent cells, MMR is involved in ab formation from mispairs or modified base pairs induced in the first S-phase, such as O6MeG:C. These rodent cells thus differ from human MT1 lymphoblasts which had similar ab levels to their normal parent cells at the first metaphase after treatment with methylators." @default.
• W2094133050 created "2016-06-24" @default.
• W2094133050 creator A5011500193 @default.
• W2094133050 creator A5049860439 @default.
• W2094133050 date "1997-02-01" @default.
• W2094133050 modified "2023-10-17" @default.
• W2094133050 title "Mismatch repair provokes chromosome aberrations in hamster cells treated with methylating agents or 6-thioguanine, but not with ethylating agents" @default.
• W2094133050 cites W1651950734 @default.
• W2094133050 cites W1963581476 @default.
• W2094133050 cites W1966427133 @default.
• W2094133050 cites W1969204536 @default.
• W2094133050 cites W1972221070 @default.
• W2094133050 cites W1974292630 @default.
• W2094133050 cites W1974585387 @default.
• W2094133050 cites W1977492313 @default.
• W2094133050 cites W1981112371 @default.
• W2094133050 cites W1987580232 @default.
• W2094133050 cites W1990928895 @default.
• W2094133050 cites W1992541932 @default.
• W2094133050 cites W1999193867 @default.
• W2094133050 cites W2006984368 @default.
• W2094133050 cites W2008211855 @default.
• W2094133050 cites W2011793431 @default.
• W2094133050 cites W2012867725 @default.
• W2094133050 cites W2014242714 @default.
• W2094133050 cites W2017709322 @default.
• W2094133050 cites W2019514569 @default.
• W2094133050 cites W2035087138 @default.
• W2094133050 cites W2037685690 @default.
• W2094133050 cites W2040512937 @default.
• W2094133050 cites W2054046690 @default.
• W2094133050 cites W2064700784 @default.
• W2094133050 cites W2068285061 @default.
• W2094133050 cites W2077162937 @default.
• W2094133050 cites W2080028600 @default.
• W2094133050 cites W2085060564 @default.
• W2094133050 cites W2086475611 @default.
• W2094133050 cites W2166382251 @default.
• W2094133050 cites W2174274173 @default.
• W2094133050 cites W2327876243 @default.
• W2094133050 doi "https://doi.org/10.1016/s0027-5107(96)00234-5" @default.
• W2094133050 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9042397" @default.
• W2094133050 hasPublicationYear "1997" @default.
• W2094133050 type Work @default.
• W2094133050 sameAs 2094133050 @default.
• W2094133050 citedByCount "53" @default.
• W2094133050 countsByYear W20941330502013 @default.
• W2094133050 countsByYear W20941330502014 @default.
• W2094133050 countsByYear W20941330502015 @default.
• W2094133050 countsByYear W20941330502016 @default.
• W2094133050 countsByYear W20941330502017 @default.
• W2094133050 countsByYear W20941330502019 @default.
• W2094133050 crossrefType "journal-article" @default.
• W2094133050 hasAuthorship W2094133050A5011500193 @default.
• W2094133050 hasAuthorship W2094133050A5049860439 @default.
• W2094133050 hasConcept C113842279 @default.
• W2094133050 hasConcept C134935766 @default.
• W2094133050 hasConcept C153911025 @default.
• W2094133050 hasConcept C175656101 @default.
• W2094133050 hasConcept C185592680 @default.
• W2094133050 hasConcept C2777755551 @default.
• W2094133050 hasConcept C54355233 @default.
• W2094133050 hasConcept C552990157 @default.
• W2094133050 hasConcept C60748783 @default.
• W2094133050 hasConcept C81089528 @default.
• W2094133050 hasConcept C81885089 @default.
• W2094133050 hasConcept C86803240 @default.
• W2094133050 hasConceptScore W2094133050C113842279 @default.
• W2094133050 hasConceptScore W2094133050C134935766 @default.
• W2094133050 hasConceptScore W2094133050C153911025 @default.
• W2094133050 hasConceptScore W2094133050C175656101 @default.
• W2094133050 hasConceptScore W2094133050C185592680 @default.
• W2094133050 hasConceptScore W2094133050C2777755551 @default.
• W2094133050 hasConceptScore W2094133050C54355233 @default.
• W2094133050 hasConceptScore W2094133050C552990157 @default.
• W2094133050 hasConceptScore W2094133050C60748783 @default.
• W2094133050 hasConceptScore W2094133050C81089528 @default.
• W2094133050 hasConceptScore W2094133050C81885089 @default.
• W2094133050 hasConceptScore W2094133050C86803240 @default.
• W2094133050 hasIssue "2" @default.
• W2094133050 hasLocation W20941330501 @default.
• W2094133050 hasLocation W20941330502 @default.
• W2094133050 hasOpenAccess W2094133050 @default.
• W2094133050 hasPrimaryLocation W20941330501 @default.
• W2094133050 hasRelatedWork W119418178 @default.
• W2094133050 hasRelatedWork W1779172654 @default.
• W2094133050 hasRelatedWork W2019099201 @default.
• W2094133050 hasRelatedWork W2083274803 @default.
• W2094133050 hasRelatedWork W2313181124 @default.
• W2094133050 hasRelatedWork W2364175713 @default.
• W2094133050 hasRelatedWork W2368733723 @default.
• W2094133050 hasRelatedWork W3138321581 @default.
• W2094133050 hasRelatedWork W4250091031 @default.
• W2094133050 hasRelatedWork W4283802959 @default.
• W2094133050 hasVolume "373" @default.
• W2094133050 isParatext "false" @default.
• W2094133050 isRetracted "false" @default.
• W2094133050 magId "2094133050" @default.

• next