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Chemical Compound Review

CPD-3746     methanesulfonate

Synonyms: CHEBI:25224, CHEBI:62081, AC1L393I, 16053-58-0, 24319-06-0, ...
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Disease relevance of methanesulfonic acid

 

Psychiatry related information on methanesulfonic acid

 

High impact information on methanesulfonic acid

  • Here we quantitatively examine genetic interactions among 26 Saccharomyces cerevisiae genes conferring resistance to the DNA-damaging agent methyl methanesulfonate (MMS), as determined by chemogenomic fitness profiling of pooled deletion strains [9].
  • The ros1 mutant shows enhanced sensitivity to genotoxic agents methyl methanesulfonate and hydrogen peroxide [10].
  • Mre11 repairs methyl methanesulfonate-induced DSBs by reactions that require the nuclease activities and those that do not [11].
  • PC12 cells mutagenized with ethyl methanesulfonate were cultured in the presence of NGF, causing normal cells to cease proliferation and allowing the isolation of cell clones which do not show growth inhibition by NGF [12].
  • Ectopic expression of wild-type, but not mutated, BRCA1 in these cells rendered them less sensitive to the DNA damage agent, methyl methanesulfonate [13].
 

Chemical compound and disease context of methanesulfonic acid

 

Biological context of methanesulfonic acid

 

Anatomical context of methanesulfonic acid

 

Associations of methanesulfonic acid with other chemical compounds

 

Gene context of methanesulfonic acid

 

Analytical, diagnostic and therapeutic context of methanesulfonic acid

  • These associations were prominent in unstimulated cells, decreasing dramatically after treatment with the genotoxin methyl methanesulfonate (MMS) [37].
  • BACKGROUND: Experiments were carried out using the new Na(+)-H+ exchange inhibitor (3-methylsulfonyl-4-piperidinobenzoyl)guanidine methanesulfonate (HOE 694) to assess the role of Na(+)-H+ exchange in myocardial ischemic and reperfusion injury [38].
  • Use of ethyl methanesulfonate and site-directed mutagenesis has identified 18 residues that are critical for in vivo excision of a target mariner element [39].
  • Rabbit antisera directed against a mixture of proteins solubilized from the wild-type adult Caenorhabditis elegans cuticle were used to isolate mutants, induced by ethyl methanesulfonate treatment, that exhibit alterations in surface antigenicity by immunofluorescence [40].
  • Approximately 60% (21 of 35) of ethyl methanesulfonate-induced Hphr clones showed rearrangements detectable by Southern blot analysis within a 40-kb region surrounding the integrated construct, including a nonhomologous recombination event and, possibly, a large insertion [41].

References

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  37. Posttranscriptional derepression of GADD45alpha by genotoxic stress. Lal, A., Abdelmohsen, K., Pullmann, R., Kawai, T., Galban, S., Yang, X., Brewer, G., Gorospe, M. Mol. Cell (2006) [Pubmed]
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