Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nuclear ADP-ribosyltransferase is present in cells from the chick lens throughout embryonic development. The activity does not decrease when the cells become post-mitotic and commence terminal differentiation but declines slowly in both epithelia and fibre cells. At all stages studied the enzyme retains its ability to be activated by DNA strand breaks induced either by X-irradiation or by the action of an endogenous endonuclease. There is no correlation between the enzyme activity or the levels of its substrate NAD+ and the changes in DNA repair capacity which have been observed during the development of the lens.
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PMID:Nuclear ADP-ribosylation in the chick lens during embryonic development. 298 94

It has been recently shown that in developing chicken embryonic nuclear extracts there is a 5-methyldeoxycytidine excision repair activity (Jost, J. P. (1993) Proc. Natl. Acad. Sci. U. S. A. 90, 4684-4688). We show that in differentiating mouse myoblasts, a similar enzymatic reaction may be responsible for the genome-wide DNA demethylation (up to 50% of all CmCGG) occurring between the 3rd and 5th days of differentiation. Furthermore, in differentiating myoblasts, there is first a 50% transient decrease in DNA methyltransferase activity and a 90% drop in the rate of DNA synthesis, followed by an increase in 5-methyl-CpG endonuclease and 5-methyldeoxycytidine excision repair activities. As tested in vitro, the maximal activity of the 5-methyldeoxycytidine excision repair coincides with the maximal in vivo genome-wide DNA demethylation. We also find that 3-aminobenzamide, a potent inhibitor of ADP-ribosyltransferase, blocks the differentiation of myoblasts, the 5-methyldeoxycytidine excision repair activity, and the genome-wide demethylation.
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PMID:Transient DNA demethylation in differentiating mouse myoblasts correlates with higher activity of 5-methyldeoxycytidine excision repair. 814 2