Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.37 (DNA methyltransferase)
 4,983 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies employed the synthetic linear DNA, poly dGdC, in the B and cobalt hexammine chloride (Co)-induced Z form to determine the effect of conformation on protein-DNA interactions. The rate of the reaction of the restriction endonucleases, Hha I and Cfo I, are reduced with Z DNA as compared to B DNA. The ability of both restriction endonucleases to react with an aggregate form of Z DNA (Z* DNA) is found to depend upon how the Z* DNA is formed. When Z* DNA is induced by low concentrations of Co (50 microM), the endonucleases remain active. In the presence of 100 microM Co, which causes increased aggregation, the endonucleases are inactive. The Hha I DNA methyltransferase reacts at equal rates with the B, Z and low cobalt Z* forms and at a greatly reduced rate with the high cobalt Z* form. These results are significantly different than those observed with Z form dGdC tracts inserted into circular DNA molecules.
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PMID:Methylation and restriction endonuclease cleavage of linear Z-DNA in the presence of hexamminecobalt (III) ions. 302 May 10

The class-IIS restriction endonuclease, R.MmeI, was isolated from Methylophilus methylotrophus. It was originally described as a monomeric enzyme, with the native Mr 105000+/-7000, which did not cleave DNA efficiently [Boyd et al. (1986) Nucleic Acids Res. 14, 5255-5274; Tucholski et al. (1995) Gene 157, 87-92]. However, it was discovered that R.MmeI endonucleolytic activity is enhanced by S-adenosyl-l-methionine (AdoMet) and sinefungin, an analogue of AdoMet. Surprisingly, the purified R.MmeI endonuclease was found to have a second enzymatic activity, namely methylation of the adenine residue to N6-methyladenine in the top strand of the MmeI-recognition sequence, 5'-TCCR*AC-3' (*A=meA. The R.MmeI methylating activity requires AdoMet and is increased in the presence of several divalent cations, 20-fold by Mg2+ or Ca2+, and less by Mn2+, Zn2+ and Co2+; however, methylation is inhibited entirely by sinefungin, at concentrations above 9microM. The latter observation shows that the enhancing effect of AdoMet or sinefungin on the DNA cleavage was not related to the process of DNA methylation. Furthermore, a second component of the MmeI restriction-modification system, a M.MmeI methyltransferase, was isolated and purified. The M.MmeI protein was found to have an Mr of 48000+/-2000 (under denaturing conditions) and to methylate both adenine residues (*A) in the MmeI-recognition sequence 5'-TCCR*AC-3'/3'-*AGGYTG-5'. Methylation of the top strand does not inhibit the DNA cleavage by R.MmeI, whereas methylation of both DNA strands blocks the cleavage process.
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PMID:Two intertwined methylation activities of the MmeI restriction-modification class-IIS system from Methylophilus methylotrophus. 985 52

Epidemiological studies suggest an important link between obesity and thyroid cancer. The adipose tissue-derived polypeptide leptin acting via leptin receptor may modulate cell migration of thyroid cancer cells. Previously we have demonstrated that leptin receptor is overexpressed in papillary thyroid cancer and is associated with tumor aggressiveness. The present study was undertaken to explore the possible regulatory factors which would influence leptin receptor expression in papillary thyroid cancer cells. We found that DNA methyltransferase inhibitor (5-Aza-2'-deoxycytidine) and histone deacetylase inhibitor (trichostatin A) reduced leptin receptor expression. Conversely, insulin upregulated leptin receptor expression in a time- and dose-dependent manner. Hypoxia-mimicking agent (cobalt chloride) had no effect on leptin receptor expression. Taken together, our study provides evidence that epigenetic events and insulin stimulation take part in regulation of leptin receptor expression in papillary thyroid cancer cells.
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PMID:Regulation of leptin receptor expression in human papillary thyroid cancer cells. 2256 Mar 41