Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.1 (S1 nuclease)
 3,660 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes experiments designed to study the organization of the linker DNA in nucleosomes. When rat liver nucleosomes (145 to 188 base pairs in length) were digested by Exonuclease III and then by nuclease S1 a series of bands on sizes 90 - 102 - 112 - 125 - 135 - 142 - 154 - 166 - 172 - 181 - bases was observed in denaturing electrophoretic gels. Digestion of H1-depleted nucleosomes under the same conditions results in a series of products of sizes (10.4) xn in base (n less than or equal to 14) only. This result is interpreted as reflecting a particular arrangement of linker DNA under the influence of histone H1.
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PMID:Involvement of histone H1 in the structure of the linker DNA in nucleosomes as revealed by nucleases. 627 19

Inhibition of the gap-filling, polymerizing step of excision repair by 1-beta-D-arabinofuranosylcytosine (ara-C) after irradiation with ultraviolet light in human diploid fibroblasts resulted in the formation of persistent DNA strand breaks in G1, G2, and plateau phase cells, but not in S phase cells. Addition of hydroxyurea to ara-C resulted in partial inhibition of repair in S phase cells. These observations can be explained either in terms of changing roles in repair for different DNA polymerases throughout the cell cycle or by the presence of a pool of deoxycytidine nucleotides during S phase equivalent to be an external source of deoxycytidine at 50 microM concentration. A similar concentration dependence on ara-C was observed for inhibition of repair in normal human, xeroderma pigmentosum (XP) variant, and Cockayne's syndrome cells but slightly more in XP variant cells. Exonuclease III and S1 nuclease independently both degraded about 50% of the 3H-thymidine incorporated into repaired regions in the presence of ara-C. Sequential digestion with both enzymes degraded nearly 90% of the repaired regions. These observations can be explained if excision repair proceeds by displacing the damaged strand so that both the 3H-labeled patch and the damaged region are still ligated to high molecular weight DNA and compete for the same complementary strand during in vitro incubation with the nucleases. The amount of 3H-thymidine incorporated in DNA by repair decreased with increasing concentrations of ara-C and hydroxyurea, suggesting that the incomplete patches became shorter under these conditions. Extrapolation of the digestion kinetics with exonuclease III permits an estimate of the normal patch size of about 100 nucleotides, consistent with previous estimates.
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PMID:Sensitivity of excision repair in normal human, xeroderma pigmentosum variant and Cockayne's syndrome fibroblasts to inhibition by cytosine arabinoside. 726 70

identify the specific nuclear scaffold-bound DNA sequence in rRNA gene clusters of silkwormAttacus ricini, the detergent-like salt lithium 3', 5' diiodosalicylate (LIS) was used for the preparation of nuclear scaffold. Through Southern hybridization, using different DNA stretches of rRNA gene as the probe, a scaffold-associated region (SAR) in the 5-non transcribed spacer (NTS) of rRNA gene has been identified. Exonuclease III digestion was used to narrow down the sequence of matrix attachment fragment. It was defined as a specific attachment site within the SacII-EcoRI fragment. It is about 1 kb in length and AT-rich (> 70%). Computer analysis of the SAR sequencing data showed that there are topoisomerase II cleavage sites, ATATTT box, and yeast autonomously replication sequence (ARS). The d(AT)(18) specific DNA sequence of the SAR, which was determined previously, was an S1 nuclease hypersensitive site. It might be a cis-element of DNA-signal characteristic for SAR.
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PMID:Identification and characterization of scaffold-associated region (SAR) of rRNA gene of silkwormAttacus ricini. 1872 4