Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.22.1 (DNase II)
 429 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nuclear localization of nerve growth factor (NGF) in HS 294 melanoma cells and SW 707 colorectal carcinoma was determined by indirect immunofluorescence staining and by cell fractionation. NGF receptors were immunoprecipitated from the EcoRI-digested chromatin of HS 294 melanoma cells, of melanocytes proliferating in the presence of 12-O-tetradecanoylphorbol-13-acetate, and of SW 707 colorectal carcinoma cells, using a monoclonal antibody to the Mr 75,000 cell surface NGF receptor. Melanoma cells expressed a receptor species with a molecular weight of 230,000. Proliferating melanocytes expressed a small amount of Mr 230,000 receptor, whereas colorectal carcinoma cells expressed a Mr 35,000 receptor. Scatchard analysis indicated one type of NGF chromatin binding site in HS 294 cells with KD = 241 pM but two types of binding sites in chromatin of SW 707 cells with KD = 333 and 1718 pM, respectively. Both the Mr 230,000 and the 35,000 receptor species were tightly bound to DNase II-sensitive regions, which became DNase II-insensitive after nerve growth factor binding. [125I]NGF was detected in the chromatin in nondegraded form. Chromatin binding of NGF inhibited RNA synthesis and cell proliferation.
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PMID:Nerve growth factor receptors in chromatin of melanoma cells, proliferating melanocytes, and colorectal carcinoma cells in vitro. 246 Dec 54

Cellular uptake, nuclear translocation, and chromatin binding of epidermal growth factor (EGF) and monoclonal antibodies (MAbs) against the protein domain of the EGF surface receptor (MAb 425) and against the carbohydrate Y determinant on the EGF receptor (MAb Br 15-6A) were analyzed in cell lines that express surface EGF receptor. Both EGF and MAb 425 were translocated to the nucleus and bound in nondegraded form to the chromatin of all cells tested. MAb Br 15-6A was taken up only by SW 948 colorectal carcinoma cells which express EGF receptor whereas neither EGF nor MAb 425 was taken up by SW 707 colorectal carcinoma cells which do not express EGF receptor. MAb 425 immunoprecipitated a 230- to 250-kDa chromatin protein, which appears to be the EGF chromatin receptor. EGF was localized in a single EcoRI DNA fragment suggesting that the chromatin binding was highly specific. Binding of EGF to primarily DNase II-sensitive chromatin regions protected these regions from nuclease action. The role of growth factor binding to chromatin in neoplastic transformation is discussed.
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PMID:Epidermal growth factor (EGF) and monoclonal antibody to cell surface EGF receptor bind to the same chromatin receptor. 278 44

The features of histone proteolysis, their carbonylation level and endonucleolysis intensity were studied in the spleen lymphocytes of rats with transplanted Guerin's carcinoma and under the conditions of hydrobromide-5-(5',6' benzocoumaroyl-3')-methylaminouracil (BCU) action. The intensification of oxidizing histone destruction and histone-specific protease activity during oncogenesis and under conditions of BCU action was shown. DNase I and DNase II enzymatic activities of spleen lymphocytes of rats with tumour were decreased on different stages of tumour development, however, they were increased under conditions of chemical compound administration.
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PMID:[Histone specific proteinase and DNase activity of spleen lymphocyte nuclei during oncogenesis and under the effect of hydrobromide-5-(5',6' benzocoumaroyl-3')-methylaminouracil]. 1871 25

Ascorbate and menadione (Apatone) in a ratio of 100:1 kills tumor cells by autoschizis. In this study, vitamin-induced changes in nucleolar structure were evaluated as markers of autoschizis. Human bladder carcinoma (T24) cells were overlain with vitamins or with culture medium. Supernatants were removed at 1-hr intervals from 1 to 4 hr, and the cells were washed with PBS and prepared for assay. Apatone produced marked alterations in nucleolar structure including redistribution of nucleolar components, formation of ring-shaped nucleoli, condensation and increase of the proportion of perinucleolar chromatin, and the enlargement of nucleolar fibrillar centers. Immunogold labeling of the nucleolar rRNA revealed a granular localization in treated and sham-treated cells, and immunogold labeling of the rDNA revealed a shift from the fibrillar centers to the condensed perinucleolar chromatin. Fibrillarin staining shifted from the fibrillar centers and adjacent regions to a more homogeneous staining of the entire nucleolus and was consistent with the percentage of autoschizic cells detected by flow cytometry. Because autoschizis entails sequential reactivation of DNase I and DNase II, and because the fibrillarin redistribution following DNase I and Apatone treatment is identical, it appears that the nucleolar and fibrillarin changes are markers of autoschizis.
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PMID:Nucleolar changes and fibrillarin redistribution following apatone treatment of human bladder carcinoma cells. 2038 87