|1.||Suzuki, Kayoko: 1 article (03/2009)|
|2.||Yagami, Akiko: 1 article (03/2009)|
|3.||Kosai, Nobuhiko: 1 article (03/2009)|
|4.||Matsunaga, Kayoko: 1 article (03/2009)|
|5.||Kawai, Nariumi: 1 article (03/2009)|
|6.||Inoue, Tomoko: 1 article (03/2009)|
|7.||Cook, Michael J: 1 article (01/2008)|
|8.||Ohno-Okumura, Eiko: 1 article (01/2008)|
|9.||Sakamoto, Keiichi: 1 article (01/2008)|
|10.||Watanabe, Masaki: 1 article (01/2008)|
11/01/1980 - "[Pathogenesis of acute dimethyl sulfate poisoning (an experimental study)]."
01/01/1977 - "Poisoning by dimethyl sulfate (clinical and bibliographic study)."
02/01/2007 - "[Clinical observation and treatment of acute severe dimethyl sulfate poisoning]."
02/01/2007 - "[Nasopharyngeal manifestations and outcomes of acute dimethyl sulfate poisoning]."
04/01/2006 - "[An accident of acute dimethyl sulfate poisoning]."
01/01/1966 - "I. Dimethylsulfate, carcinogenic action in rats and probable cause of occupational cancer]."
06/30/1978 - "II. Chemical methylation of normal, methyl-deficient and tumor tRNA with dimethylsulfate]."
10/10/2004 - "In vivo footprinting analysis revealed the presence of dimethylsulfate (DMS) hypersensitive site in the untranslated region around nucleotide--35 only in the cancer cells but not in cells derived from normal tissue, and analysis of KMnO4 reactive nucleotides showed that the stem loop structure could be formed in vivo of the cancer cells. "
01/01/2008 - "During the evaluation of zinc bis(1,4-didecylbenzo)-bis(2,3-pyrido) porphyrazine for its photodynamic therapy of cancer (PDT) efficacy by cancer cell culture, the light exposed dimethyl sulfate quaternized zinc bis(1,4-didecylbenzo)-bis(2,3-pyrido) porphyrazines in IU-002 cells produce cell disruption that can be detected as a decrease in fluorescence."
08/01/1985 - "Ten of the 17 carcinogens negative in the rat liver foci assay are believed to exhibit tumor-promoting activity; 3 are direct-acting alkylating agents (dimethylsulfate, epichlorohydrin, and beta-propiolactone); and the remaining 3 are azobenzene, 1,2-dibromoethane, and thioacetamide. "
10/10/2004 - "Gelsolin gene silencing involving unusual hypersensitivities to dimethylsulfate and KMnO4 in vivo footprinting on its promoter region."
05/01/2000 - "In vivo dimethyl sulfate footprinting of the cyclin E promoter revealed several regions of protection and hypersensitivity that were unique to infected cells. "
01/01/1992 - "However, the extent of protection and hypersensitivity to DNase I or dimethyl sulfate within the ISRE region was changed upon transcriptional induction, suggesting the binding of different factors in different transcriptional states. "
01/01/1982 - "Modification of CEA with dimethylsulfate or acetic anhydride resulted in derivatives which preferentially induced delayed-type hypersensitivity (DTH) against native CEA in mice. "
03/01/2000 - "In liver chromatin, however, DNase I hypersensitivity and partial protection of the regulatory motifs from DNase I digestion or reaction with dimethyl sulfate was observed and phenobarbital treatment increased the hypersensitivity but only modestly affected protection. "
04/24/1998 - "Finally, in vivo footprint analysis of the topoIIalpha gene promoter revealed that two G residues of ICE1 that were protected in control cells became sensitive to dimethyl sulfate modification after heat shock. "
11/01/1995 - "We observed that the second heat shock element (HSE-2; -201 to -178) was clearly protected from methylation by dimethyl sulfate in parallel with the increase in HSP70-1 mRNA. "
12/05/1990 - "In combination with two complementary techniques, DNase I footprinting and dimethyl sulfate methylation protection, we have obtained a high-resolution map of the promoter region of the yeast HSP82 heat shock gene, which resides within a constitutive nuclease hypersensitive site. "
12/15/1999 - "Strikingly, DNase I footprints mapping to the binding sites for heat shock factor (HSF) and TATA-binding protein (TBP) are strengthened and broadened, while groove-specific interactions, as detected by dimethyl sulfate, are diminished. "
|5.||Hepatocellular Carcinoma (Hepatoma)
06/10/1984 - "Nuclear mono- and poly(ADP-ribosyl) protein conjugates formed in living hepatoma AH 7974 cells in response to treatment with the alkylating agent dimethyl sulfate have been studied. "
06/01/1985 - "Treatment of hepatoma AH 7974 cells with dimethyl sulfate led to a marked accumulation in vivo of mono)ADP-ribosyl)-histone H1A, H1B, H1 and H2B, respectively. "
06/10/1984 - "Identification of histone H2B as a major acceptor for mono- and poly(ADP-ribose) in dimethyl sulfate-treated hepatoma AH 7974 cells."
12/01/1987 - "The endogenous poly(ADP-ribosyl)--nonhistone protein conjugates were isolated from dimethyl-sulfate-treated rat hepatoma AH 7974 cells using aminophenylboronic-acid--agarose chromatography. "
01/25/1984 - "ADP-ribosylation in vivo of histone H1 was studied in hepatoma cells (Yoshida AH 7974) after treatment with the alkylating agent dimethyl sulfate for 30 min and compared with that of other polypeptides. "
|1.||Deoxyribonuclease I (Nickase)
|2.||Adenosine Diphosphate (ADP)
|4.||DNA (Deoxyribonucleic Acid)
|8.||TATA-Box Binding Protein (TATA-Binding Protein)
|9.||Untranslated Regions (Untranslated Region)
|1.||Photochemotherapy (Photodynamic Therapy)