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Gene Review

MMS  -  Malignant mesothelioma, susceptibility to

Homo sapiens

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Disease relevance of MMS

  • A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5alpha strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent [1].
  • We delineated the clinical and laboratory features that help distinguish acute myelopathic MS (MMS) from acute transverse myelitis (ATM), specifically testing the hypothesis that the symmetry of motor and sensory impairments at presentation can reliably distinguish between ATM and MMS [2].
  • The AtRecQsim gene suppressed the MMS hypersensitivity phenotype of the sgs1 cells [3].
  • This method was used to quantify the levels of dTp(Me)dT in enzymatic hydrolysates of DNA obtained from a series of incubations of salmon testis DNA or mouse lymphoma cells with either MNU or MMS [4].
  • These strains were slightly more resistant to the toxic effect of MMS and showed a reduced frequency of MMS-induced chromosomal aberrations [5].

Psychiatry related information on MMS

  • In a double-blind, placebo-controlled study on the therapeutic efficacy and central effects of nicergoline, an ergot alkaloid with metabolic, antithrombotic and vasoactive action, 112 patients with mild to moderate dementia, diagnosed according to DSM III-R criteria (MMS 13-25), living in pensioners' homes, were included [6].
  • If the MMS score is 23 or less, a set of criteria will be used to establish the diagnosis of vascular dementia [7].
  • In this study we investigated the effects of the oral administration of citicoline alone (C1000:1000 mg/day; C500:500 mg/day) or in combination with nimodipine (C +NI:300 + 90 mg/day) during 4 weeks on memory performance in elderly subjects with memory deficits and without dementia (N = 24; age = 66.12 +/- 10.78 years; MMS score = 31.69 +/- 2.76) [8].
  • The usefulness, inter-rater reliability, and validity of six mental tests, the MMS, the GMS, the MSQ, the VRT, the OLT, and the DCT were studied in 81 patients over the age of 75 years [9].

High impact information on MMS

  • The GADD45-like genes are induced by environmental stresses, including MMS, UV, and gamma irradiation [10].
  • Methyl methanesulfonate (MMS; 0.5 mM, 1 h) induced the same frequency of single strand breaks (SSBs) (2.1-2.3 X 10(-8) SSBs per dalton) in NHSF6 normal human and C3H 10T1/2 mouse cells [11].
  • The effects of MMS on the expression of both gadd genes were inhibited by actinomycin D, suggesting that transcription is necessary for acute gadd induction.(ABSTRACT TRUNCATED AT 250 WORDS)[12]
  • For the MMS, the cranial nerves concerned are V2, V3 and VII [13].
  • Three systems play a role in the vascularization of cranial nerves: the inferolateral trunk (ILT), most often arising from the internal carotid artery, the middle meningeal system (MMS), and the ascending pharyngeal system (APS); the latter two are both derived from the external carotid artery [13].

Chemical compound and disease context of MMS


Biological context of MMS

  • ScaANBS1 also participates in G2-M checkpoint control upon DNA damage caused by MMS [19].
  • However, the accumulation of breaks in MMS-treated cellular DNA in the presence of novobiocin suggests that some "short-patch" alkylation repair may be inhibited by the antibiotic [20].
  • 3-Aminobenzamide (3-AB) interferes with DNA repair and enhances lethality in growing MMS (methyl methane sulfonate)-treated human fibroblasts [21].
  • Our results also show that, in contrast to C. elegans chk2, Drosophila chk2 is not essential for normal meiosis and recombination, and it also appears to be dispensable for the MMS-induced DNA damage checkpoint and the HU-induced DNA replication checkpoint during larval development [22].
  • No effect of treatment with MMS, QM, and Q on the distribution of SCEs in chromosomes was found compared with controls [23].

Anatomical context of MMS


Associations of MMS with chemical compounds

  • Expression of the N169A and N169S AAG variants in S. cerevisiae during methyl methanesulfonate exposure resulted in greater sensitivity, greater mutation induction following MMS exposure, and more strand breaks in vivo [28].
  • The presence of adenine, an inhibitor of AP endonucleases, in the repair incubation of MMS-treated cells induced moderate accumulation of AP sites, suggesting inhibition of the activities of MPG as well as AP endonucleases by adenine metabolites [24].
  • Denbufylline induced a statistically significant and clinically relevant improvement in both SDAT and MID patients, whereas after placebo this was not the case in CGI, the TMT, and the DS, with interdrug differences being significant in all primary target variables such as the CGI, MMS, SCAG, and DSST [29].
  • 3-Aminobenzamide is lethal to MMS-damaged human fibroblasts primarily during S phase [21].
  • This effect was also seen when MNU pretreatment was used, but not with MMS or streptozotocin [30].

Regulatory relationships of MMS

  • In the cells with the highest basal ADPRT activity 12 h after block release, the MMS-induced ADPRT stimulation could not be observed [31].

Other interactions of MMS

  • This correlation was even better between PTH levels and MMS fr [32].
  • Expression of hRAD50 partially rescued the MMS (methyl methanesulfonate)-sensitive phenotype in rad50 mutant yeast, whereas hRAD50-3 did not show complementation [33].
  • Our data suggest a protective role for GM-CSF, IL-3 or other MMS cytokines in preventing SFI in patients receiving HDC [34].
  • The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS [35].
  • The lethality of 3-AB to a population of asynchronously cycling cells treated with MMS is thus the summation of effects on the cells as they traverse S phase [21].

Analytical, diagnostic and therapeutic context of MMS


  1. Sequence-specific p53 gene damage by chloroacetaldehyde and its repair kinetics in Escherichia coli. Kowalczyk, P., Cieśla, J.M., Saparbaev, M., Laval, J., Tudek, B. Acta Biochim. Pol. (2006) [Pubmed]
  2. Transverse myelitis. Comparison with spinal cord presentations of multiple sclerosis. Scott, T.F., Bhagavatula, K., Snyder, P.J., Chieffe, C. Neurology (1998) [Pubmed]
  3. Arabidopsis RecQsim, a plant-specific member of the RecQ helicase family, can suppress the MMS hypersensitivity of the yeast sgs1 mutant. Bagherieh-Najjar, M.B., de Vries, O.M., Kroon, J.T., Wright, E.L., Elborough, K.M., Hille, J., Dijkwel, P.P. Plant Mol. Biol. (2003) [Pubmed]
  4. Quantitation of DNA adduct of thymidylyl(3'-5')thymidine methyl phosphotriester by liquid chromatography/negative electrospray tandem mass spectrometry. Zhang, F., Bartels, M.J., Pottenger, L.H., Gollapudi, B.B., Schisler, M.R. Rapid Commun. Mass Spectrom. (2005) [Pubmed]
  5. Effect of transfection of human poly(ADP-ribose)polymerase in Chinese hamster cells on mutagen resistance. Fritz, G., Auer, B., Kaina, B. Mutat. Res. (1994) [Pubmed]
  6. Nicergoline in senile dementia of Alzheimer type and multi-infarct dementia: a double-blind, placebo-controlled, clinical and EEG/ERP mapping study. Saletu, B., Paulus, E., Linzmayer, L., Anderer, P., Semlitsch, H.V., Grünberger, J., Wicke, L., Neuhold, A., Podreka, I. Psychopharmacology (Berl.) (1995) [Pubmed]
  7. Is prevention of vascular dementia possible? The Syst-Eur Vascular Dementia Project. Forette, F., Amery, A., Staessen, J., Strasser, T., Thijs, L., Beevers, D.G., Bert, P., Clement, D., Cox, J., De Leeuw, P.W. Aging (Milan, Italy) (1991) [Pubmed]
  8. Citicoline improves memory performance in elderly subjects. Alvarez, X.A., Laredo, M., Corzo, D., Fernández-Novoa, L., Mouzo, R., Perea, J.E., Daniele, D., Cacabelos, R. Methods and findings in experimental and clinical pharmacology. (1997) [Pubmed]
  9. Efficacy of short mental tests in the detection of mental impairment in old age. Engedal, K., Haugen, P., Gilje, K., Laake, P. Comprehensive gerontology. Section A, Clinical and laboratory sciences. (1988) [Pubmed]
  10. A family of stress-inducible GADD45-like proteins mediate activation of the stress-responsive MTK1/MEKK4 MAPKKK. Takekawa, M., Saito, H. Cell (1998) [Pubmed]
  11. Differential induction of indirect DNA breaks but no inhibition of strand-break ligation of alkylated DNA by 3-aminobenzamide in human and C3H 10T1/2 cells. Fujiwara, Y. Cancer Res. (1987) [Pubmed]
  12. Genotoxic agents increase expression of growth arrest and DNA damage--inducible genes gadd 153 and gadd 45 in rat pancreatic islets. Eizirik, D.L., Björklund, A., Cagliero, E. Diabetes (1993) [Pubmed]
  13. Cranial nerve ischaemic arterial syndromes. A review. Lapresle, J., Lasjaunias, P. Brain (1986) [Pubmed]
  14. Radiation equivalence of genotoxic chemicals. Validation in cultured mammalian cell lines. MUrthy, M.S. Mutat. Res. (1982) [Pubmed]
  15. Double-blind cross-over study of phosphatidylserine vs. placebo in patients with early dementia of the Alzheimer type. Engel, R.R., Satzger, W., Günther, W., Kathmann, N., Bove, D., Gerke, S., Münch, U., Hippius, H. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. (1992) [Pubmed]
  16. hOGG1 recognizes oxidative damage using the comet assay with greater specificity than FPG or ENDOIII. Smith, C.C., O'Donovan, M.R., Martin, E.A. Mutagenesis (2006) [Pubmed]
  17. Accuracy of three-dimensional simulation in the sizing of aortic endoluminal devices. Aziz, I., Lee, J., Lee, J.T., Donayre, C.E., Walot, I., Kopchok, G., Mirahashemi, S., Esmailzadeh, H., White, R.A. Annals of vascular surgery. (2003) [Pubmed]
  18. In vivo detection of a novel macrophage-derived protein involved in the regulation of mucus-like glycoconjugate secretion. Sperber, K., Gollub, E., Goswami, S., Kalb, T.H., Mayer, L., Marom, Z. Am. Rev. Respir. Dis. (1992) [Pubmed]
  19. Different roles of the Mre11 complex in the DNA damage response in Aspergillus nidulans. Semighini, C.P., von Zeska Kress Fagundes, M.R., Ferreira, J.C., Pascon, R.C., de Souza Goldman, M.H., Goldman, G.H. Mol. Microbiol. (2003) [Pubmed]
  20. Studies on the inhibition of repair of ultraviolet- and methyl methanesulfonate-induced damage in the DNA of human fibroblasts by novobiocin. Snyder, R.D., Van Houten, B., Regan, J.D. Nucleic Acids Res. (1982) [Pubmed]
  21. 3-Aminobenzamide is lethal to MMS-damaged human fibroblasts primarily during S phase. Boorstein, R.J., Pardee, A.B. J. Cell. Physiol. (1984) [Pubmed]
  22. The Drosophila chk2 gene loki is essential for embryonic DNA double-strand-break checkpoints induced in S phase or G2. Masrouha, N., Yang, L., Hijal, S., Larochelle, S., Suter, B. Genetics (2003) [Pubmed]
  23. Simultaneous staining of sister chromatid exchanges and Q-bands in human chromosomes after treatment with methyl methane sulphonate, quinacrine mustard, and quinacrine. Haglund, U., Zech, L. Hum. Genet. (1979) [Pubmed]
  24. Repair kinetics of abasic sites in mammalian cells selectively monitored by the aldehyde reactive probe (ARP). Asaeda, A., Ide, H., Tano, K., Takamori, Y., Kubo, K. Nucleosides Nucleotides (1998) [Pubmed]
  25. Differential effects on cell killing in metallothionein overexpressing CHO mutant cell lines. Lohrer, H., Robson, T., Grindley, H., Foster, S., Hall, A. Carcinogenesis (1990) [Pubmed]
  26. Microtus oeconomus (Rodentia), a useful mammal for studying the induction of sex-chromosome nondisjunction and diploid gametes in male germ cells. Tates, A.D. Environ. Health Perspect. (1979) [Pubmed]
  27. Indications for a threshold of chemically-induced aneuploidy in vitro in human lymphocytes. Elhajouji, A., Van Hummelen, P., Kirsch-Volders, M. Environ. Mol. Mutagen. (1995) [Pubmed]
  28. Effects of substrate specificity on initiating the base excision repair of N-methylpurines by variant human 3-methyladenine DNA glycosylases. Connor, E.E., Wilson, J.J., Wyatt, M.D. Chem. Res. Toxicol. (2005) [Pubmed]
  29. EEG mapping and psychopharmacological studies with denbufylline in SDAT and MID. Saletu, B., Anderer, P., Fischhof, P.K., Lorenz, H., Barousch, R., Böhmer, F. Biol. Psychiatry (1992) [Pubmed]
  30. Pretreatment of human colon tumor cells with DNA methylating agents inhibits their ability to repair chloroethyl monoadducts. Zlotogorski, C., Erickson, L.C. Carcinogenesis (1984) [Pubmed]
  31. Cell cycle effects on the basal and DNA-damaging-agent-stimulated ADPRT activity in cultured mammalian cells. Yu, Y.N., Ding, C., Cai, Z.N., Chen, X.R. Mutat. Res. (1986) [Pubmed]
  32. Relation between middle molecules and parathyroid hormone in patients with chronic renal failure. Fröhling, P.T., Kokot, F., Cernacek, P., Vetter, K., Kuska, J., Spustova, V., Kaschube, I., Dzurik, R. Mineral and electrolyte metabolism. (1982) [Pubmed]
  33. Molecular cloning and characterization of splice variants of human RAD50 gene. Kim, K.K., Shin, B.A., Seo, K.H., Kim, P.N., Koh, J.T., Kim, J.H., Park, B.R. Gene (1999) [Pubmed]
  34. Antifungal effects of yeast-derived rhu-GM-CSF in patients receiving high-dose chemotherapy given with or without autologous stem cell transplantation: a retrospective analysis. Peters, B.G., Adkins, D.R., Harrison, B.R., Velasquez, W.S., Dunphy, F.R., Petruska, P.J., Bowers, C.E., Niemeyer, R., McIntyre, W., Vrahnos, D., Auberry, S.E., Spitzer, G. Bone Marrow Transplant. (1996) [Pubmed]
  35. Inhibition of p53 by lentiviral mediated shRNA abrogates G1 arrest and apoptosis in retinal pigmented epithelial cell line. Nair, A.R., Schliekelman, M., Thomas, M.B., Wakefield, J., Jurgensen, S., Ramabhadran, R. Cell Cycle (2005) [Pubmed]
  36. Lung cell fiber evanescent wave spectroscopic biosensing of inhalation health hazards. Riley, M.R., Lucas, P., Le Coq, D., Juncker, C., Boesewetter, D.E., Collier, J.L., Derosa, D.M., Katterman, M.E., Boussard-Pl??del, C., Bureau, B. Biotechnol. Bioeng. (2006) [Pubmed]
  37. Multiplicity reactivation of alkylating agent damaged herpes simplex virus (type I) in human cells. Das, S.K. Mutat. Res. (1982) [Pubmed]
  38. Indications and limitations of Mohs micrographic surgery. Lang, P.G., Osguthorpe, J.D. Dermatologic clinics. (1989) [Pubmed]
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