Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.25.1 (deoxyribonuclease)
1,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed a host cell reactivation assay of DNA repair utilizing UV-treated plasmid vectors. The assay primarily reflects cellular repair of transcriptional activity of damaged DNA measured indirectly as enzyme activity of the transfected genes. We studied three plasmids (pSV2cat, 5020 base pairs; pSV2catSVgpt, 7268 base pairs; and pRSVcat, 5027 base pairs) with different sizes and promoters carrying the bacterial cat gene (CAT, chloramphenicol acetyltransferase) in a construction that permits cat expression in human cells. All human simian virus 40-transformed cells studied expressed high levels of the transfected cat gene. UV treatment of the plasmids prior to transfection resulted in differential decrease in CAT activity in different cell lines. With pSV2catSVgpt, UV inactivation of CAT expression was greater in the xeroderma pigmentosum group A and D lines (D0 = 56 J X m-2) than in the other human cell lines tested (normal, ataxia-telangiectasia, Lesch-Nyhan, retinoblastoma)(D0 = 680 J X m-2)(D0 is the dose that reduces the percentage of CAT activity by 63% along the exponential portion of the dose-response curve). The D0 of the CAT inactivation curve was 50 J X m-2 for pSV2cat and for pRSVcat in the xeroderma pigmentosum group A cells. The similarity of the D0 data in the xeroderma pigmentosum group A cells for three plasmids of different size and promoters implies they all have similar UV-inactivation target size. UV-induced pyrimidine dimer formation in the plasmids was quantified by assay of the number of UV-induced T4 endonuclease V-sensitive sites. In the most sensitive xeroderma pigmentosum cells, with all three plasmids, one UV-induced pyrimidine dimer inactivates a target of about 2 kilobases, close to the size of the putative CAT mRNA.
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PMID:One pyrimidine dimer inactivates expression of a transfected gene in xeroderma pigmentosum cells. 299 75

The incidence of hematoxyphilic extracellular deposits in 159 cases of retinoblastoma was found to be 18%. Six other features of these tumors also were examined. In the majority of eyes with these deposits, the tumors were composed solely of anaplastic cells. None was well differentiated with preponderantly rosette formation. The hematoxyphilic deposits were Feulgen-positive, and this staining was diminished but not abolished by pretreatment with purified deoxyribonuclease (DNase), which did abolish nuclear staining. Feulgen staining of the deposits was totally blocked by pronase--DNase pretreatment--suggesting that the deposits may represent DNA-protein complexes. Ultrastructurally, these deposits were electron dense and finely vacuolar. The deposits may originate from degenerating tumor cell nuclei, and the possibility that they may represent immune complexes warrants future study in view of occasional spontaneous regression of this tumor.
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PMID:Feulgen-positive deposits in retinoblastoma. Incidence, composition, and ultrastructure. 700 79