Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human papillomavirus type 6 (HPV-6) DNA was detected in a rapidly growing vulvar verrucous carcinoma and two recurrent tumor samples. The viral DNA (HPV-6vc) was molecularly cloned and found to have a high degree of DNA sequence homology to HPV-6b DNA. Comparison of restriction endonuclease cleavage patterns between HPV-6b and HPV-6vc genomes and DNA sequencing analysis demonstrated an additional 106 bases in the HPV-6vc genome. These additional nucleotides were located in the noncoding region of the viral genome which contains the putative viral DNA replication and early gene transcriptional control elements. Seventy-four of the additional 106 nucleotides were found as one insert in the purine-thymidine-rich region 3' to the end of the L1 open reading frame. This 74-base-pair addition had homology with viral sequences immediately upstream to it and to poly(dG-dT) sequences found in the human genome including the conserved repeated sequences in human DNA (EC1) and in the human cardiac muscle actin gene. Two smaller inserts, 19 and 15 nucleotides, were found upstream from the transcriptional control elements and demonstrate homology with regions of human alpha and gamma interferon genes.
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PMID:Isolation and characterization of a novel human papillomavirus type 6 DNA from an invasive vulvar carcinoma. 300 57

The binding of aflatoxin B1, AFB1, a potent hepatocarcinogen, to various high molecular weight (HMW) DNAs from human normal liver and two liver cancer cell lines, Alexander primary liver carcinoma (PLC) and Mahlavu hepatocellular carcinoma (hHC) and from NIH/3T3 cell have been investigated. The kinetics of AFB1 binding to these DNAs showed similar initial rates but the extents of binding to the PLC and hHC DNAs seemed to be slightly higher. Preferential AFB1 bindings were identified in both PLC and hHC DNAs compared to normal liver DNA when analyzed by restriction endonuclease digestions and agarose gel electrophoresis. A critical AFB1 binding dosage, ranging 100 to 460 fmole/microgram DNA, was found to activate the carcinogenic effect of the Mahlavu hHC HMW DNA, but not normal liver HMW DNA, rendering it capable of inducing focal transformation in NIH/3T3 cell. Excessive AFB1 binding on the hHC and PLC HMW DNAs resulted in an "over-kill" of both cell transformation capability and templating activity of the DNA.
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PMID:Dose dependency of aflatoxin B1 binding on human high molecular weight DNA in the activation of proto-oncogene. 300 75

Autodigestion of nuclei isolated from the androgen-dependent Shionogi mouse mammary carcinoma revealed the presence of endogenous endonuclease activity which was stimulated by Ca2+ and Mg2+ and generated a repeating pattern of DNA fragments with an average monomeric size of 179 base pairs. The nuclear concentration of endonuclease activity declined rapidly after castration to a level 45% of that measured in tumours from non-castrated hosts. Most of the endonuclease activity (80%) could be extracted in a soluble form after sonication of the nuclei and subsequent centrifugation. The reduced concentration of endonuclease activity in regressing tumours following castration was not due to changes in chromatin template conformation and could be restored to normal levels within 1 day of androgen treatment. Examination of DNA synthetic activity and the concentration of nuclear androgen receptors during tumour regression indicated that the decrease in endonuclease activity paralleled the declining rate of DNA synthesis but was preceded by a loss of nuclear androgen receptors. Together these results suggest that the endonuclease activity of the Shionogi carcinoma is more likely involved with androgen-stimulated cell proliferation rather than with the autophagic mechanism responsible for tumour regression and cell death.
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PMID:Changes in endonuclease activity during growth and regression of the Shionogi mammary carcinoma. 301 60

With the use of the isoschizomeric restriction endonucleases HpaII and MspI, we found that mouse tumour ornithine decarboxylase (ODC; EC 4.1.1.17) genes are extensively methylated. ODC genes in L1210 mouse leukaemia cells were apparently more methylated than in Ehrlich ascites carcinoma, as revealed by the use of HpaII endonuclease, yet the digestion of genomic DNA isolated from these two murine tumour cell lines with MspI, which cleaves at a CCGG sequence, also with internally methylated cytosine, resulted in an apparently identical restriction pattern. It is possible that the amplification of ODC genes in Ehrlich ascites-carcinoma cells in response to 2-difluoromethylornithine (DFMO) was associated with hypomethylation, or that less-methylated genes were amplified. A human myeloma (Sultan) cell line only revealed three separate hybridization signals when cleaved with HpaII. One of these signals was amplified under the pressure of DFMO. When cleaved with MspI, these three HpaII fragments disappeared and were replaced by a double signal of 2.3-2.4 kilobase-pairs (kbp) in size. The amplified ODC sequences in the Sultan myeloma cell line apparently originated from chromosome 2, as indicated by a unique hybridization signal in a 5.8 kbp HindIII fragment specific for the human ODC locus on chromosome 2. A comparison of different human cells, the Sultan myeloma, a lymphocytic B-cell leukaemia (Ball), normal mononuclear leucocytes and leucocytes obtained from leukaemia patients, revealed interesting differences in the methylation of ODC genes. The use of two restriction endonucleases (HpaII and CfoI), the cleavage site for both of which contains a CG sequence and which only cleave when cytosine is unmethylated, indicated that ODC genes in the lymphocytic leukaemia cells were much less methylated than those in the normal leucocytes or in the Sultan cells.
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PMID:Mouse and human ornithine decarboxylase genes. Methylation polymorphism and amplification. 303 86

We have examined Blym expression in 11 human tumor cell lines. Increased Blym expression was observed in one of three osteosarcoma cell lines relative to nontransformed human foreskin fibroblasts. In addition, enhanced Blym expression was observed in a melanoma cell line and in 2 of 6 squamous carcinoma cell lines relative to nontransformed, low passage human epithelial cells. We found no evidence of gene amplification or rearrangements of Blym sequences in any of the cell lines we have examined. We further analyzed the state of methylation of the Blym gene in several of the tumor cell lines by Msp I/Hpa 11 restriction endonuclease digestion. All cell lines examined had similar Msp I digestion patterns. However, the different tumor cell lines had different Hpa 11 digestion patterns. Therefore, our results indicate that the Blym gene is differentially expressed and methylated in human tumor cell lines.
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PMID:Expression and methylation of the Blym gene in human tumor cell lines. 303 38

We have compared warts and carcinomas from cottontail and domestic rabbits for the presence of cottontail rabbit papillomavirus (CRPV) and the status of the viral DNA genome. Our studies indicate that benign warts from cottontail rabbits, whether found naturally or induced in the laboratory, contain large amounts of virus and on the average 1000 copies of the virus genome per cell. Both benign warts and carcinomas from domestic rabbits contain significantly reduced levels of virus relative to cottontail rabbit warts and an average of 100 copies of the virus genome per cell. A single sample of a naturally occurring cottontail rabbit carcinoma contained approximately 80 copies of the viral genome per cell. None of the tumors that we have analyzed thus far appear to have integrated viral genomes by Southern blot analysis of undigested and restriction endonuclease-digested DNA samples. Furthermore, the CRPV genome present in domestic rabbit carcinomas and a cottontail rabbit carcinoma appears identical by restriction endonuclease mapping to that present in papillomas of cottontail and domestic rabbits indicating that no major deletions or rearrangements of the CRPV genome had occurred during the progression of benign to malignant tumors nor was a variant of wild-type CRPV responsible for this phenomenon. Finally, we have demonstrated morphological transformation in vitro of NIH 3T3 and C127 cells upon infection with purified CRPV and upon transfection with purified CRPV DNA. Furthermore, single cell clones derived from transformed foci contain free forms of CRPV DNA that persist through continued passage in culture. Cells transformed by CRPV grow in soft agar in vitro and produce tumors in athymic nude mice.
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PMID:Free cottontail rabbit papillomavirus DNA persists in warts and carcinomas of infected rabbits and in cells in culture transformed with virus or viral DNA. 629 3

A human transforming gene present in T24 bladder carcinoma cells has been molecularly cloned. The transforming sequences have been located within a 4.6 kilo base pair (kbp) DNA fragment that transforms NIH/3T3 cells with a specific activity of 5 X 10(4) focus-forming units/pmol. Homologous sequences present in normal human DNA have also been molecularly cloned. Comparison of the restriction endonuclease maps of the normal and transforming genes did not reveal any significant differences. These results suggest that subtle molecular changes are responsible for the acquisition of malignant properties by this gene in T24 cells. The T24 oncogene was found to be unrelated to transforming genes present in a variety of human tumors other than bladder carcinomas. In contrast, the T24 oncogene is highly related to the onc genes of the BALB and Harvey strains of murine sarcoma viruses ( MSVs ). Preliminary characterization of the transcriptional and translational products of the T24 oncogene suggests that this gene is transcribed into a 1.2-kbp poly(A)-containing RNA whose translation yields a 23,000-dalton protein antigenically related to the transforming gene products of BALB and Harvey MSVs .
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PMID:Characterization of a human transforming gene isolated from T24 bladder carcinoma cells. 632 52

DNA from T24, a cell line derived from a human bladder carcinoma, can induce the morphological transformation of NIH 3T3 cells. Using techniques of gene rescue to clone the gene responsible for this transformation, we have found that it is human in origin, less than 5 kilobase pairs in size and is homologous to a 1,100-base polyadenylated RNA species found in T24 and HeLa cells. Blot analysis indicates extensive restriction endonuclease polymorphism near this gene, in human DNAs.
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PMID:Isolation and preliminary characterization of a human transforming gene from T24 bladder carcinoma cells. 706 39

Human breast carcinoma (MCF7-MLNr) cells resistant to the bifunctional drugs L-phenylalanine mustard (L-PAM, 5-fold resistance), mechlorethamine (9-fold), cisplatin (3-fold), and BCNU (3-fold) were used to investigate the role of DNA repair in the development of resistance to alkylating agents. We have previously shown that neither L-PAM transport and metabolism nor glutathione-associated enzymes were altered in MCF7-MLNr cells, compared to the sensitive cells MCF7-WT. This study shows that treatment of pRSV-CAT plasmid with L-PAM at concentrations up to 1 microM proportionally inhibit the expression of chloramphenicol acetyl transferase (CAT) activity, while higher concentrations abolished CAT activity. pRSV-CAT reactivation was significantly increased when plasmid was transfected into MCF7-MLNr cells, compared to MCF7-WT cells. This indicates that resistant cells have more efficient capacity to recognize and repair L-PAM induced DNA damage. The mRNA expression of DNA nucleotide excision repair genes ERCC1, XPD (ERCC2), XPB (ERCC3), and polymerase beta was found to be similar in both the MCF7-WT and MCF7-MLNr cells. Western blot analysis also reveals no difference in the expression of ERCC1, AP endonuclease, poly (ADP-ribose) polymerase, and alkyl-N-purine-DNA glycosylase proteins. The lack of correlation between enhanced host cell reactivation capacity in resistant cells, and the expression of these specific DNA repair genes suggests that proteins encoded by these genes are not rate limiting steps for resistance to bi-functional alkylating drugs in human breast cancer cells.
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PMID:Enhanced host cell reactivation capacity and expression of DNA repair genes in human breast cancer cells resistant to bi-functional alkylating agents. 749 Nov 21

The oligonucleosomal pattern of DNA fragmentation is the best-characterized biochemical marker of apoptosis and believed to be generated by a, as yet unidentified, Ca2+, Mg(2+)-dependent endonuclease. All apoptotic cells fragment their genome. However, not every cell type undergoing apoptosis is capable of internucleosomal DNA cleavage. We have analyzed the endonuclease activities and patterns of DNA fragmentation in four established cell lines undergoing apoptosis following serum deprivation, i.e., rat 5123tc hepatoma and PC12 pheochromocytoma, as well as human MCF7 breast and DU145 prostatic carcinoma cells. Whereas apoptotic 5123tc and PC12 cells degraded their DNA into oligonucleosomes, the MCF7 and DU145 cells generated only > 50 kilobase pairs (kbp) DNA fragments. However, when isolated nuclei from all four cell lines were incubated with both Ca2+ and Mg2+ ions, their DNA was cleaved into internucleosomal fragments. Following washing with a low ionic strength buffer, the nuclei could only degrade DNA to > 50-kbp fragments. DNA ladders were produced again in these washed nuclei after reconstitution with the nuclear wash, which contained an endonucleolytic activity of approximately 97 kilodaltons. These experiments showed that cells maintain separate pools of endonucleolytic activities responsible for the high and low molecular mass DNA fragmentation, and depending on the cell type, one or both enzymatic pools become activated during apoptosis.
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PMID:Separate pools of endonuclease activity are responsible for internucleosomal and high molecular mass DNA fragmentation during apoptosis. 765 36


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