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)

When activated with either Con A, a CD3-specific mAb, or Ag-pulsed B lymphoma (LK35.2) cells, CD4 (Th1) clones quickly induce DNA fragmentation in target cells followed by release of 51Cr-labeled intracellular materials. Both activated CD4 clones and CD8 (CTL) cells fragment target DNA into electrophoretically identical "ladder" pattern made of approximately 200 bp. The effect of various metabolic inhibitors on the ability of CD4 and CD8 cells to induce target DNA fragmentation was studied. Little effect was observed with the DNA synthesis inhibitor, mitomycin C. The RNA synthesis inhibitor, actinomycin D, and the protein synthesis inhibitor, cycloheximide, strongly inhibited the ability of CD4 cells, but not CD8 cells, to induce target DNA fragmentation. In contrast, target DNA fragmentation by CD8 cells, but not by CD4 cells, was inhibited by cholera toxin. Although cyclosporin A inhibited CD4 cells to fragment target DNA during the early phase (90 min) of E:T interaction, this inhibition was not sustained in the later phase (210 min) of the assay. Zinc ions inhibited the ability of both CD4 and CD8 cells to fragment target DNA. Treatment of effectors and targets with these inhibitors, followed by washings, demonstrated that the action of these inhibitors on effector cells alone is sufficient to inhibit target DNA fragmentation. The strong correlation among these parameters of DNA fragmentation and Cr-release assays supports the hypothesis of programed cell death. Although distinct cytolytic pathways are used by CD4 and CD8 cells to kill targets, both pathways deliver a signal that activates endonuclease(s), fragments target DNA, causes Cr-release, and lyses target cells. Taken together with our previous studies, the present findings demonstrate that activated cytolytic CD4 clones do not use perforin, serine proteases, and TNF as mediators for resistant target DNA fragmentation.
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PMID:Distinct pathways of CD4 and CD8 cells induce rapid target DNA fragmentation. 167 Oct 51

Mycosis fungoides, a rare form of cutaneous T cell leukemia/lymphoma, is suspected of having a viral etiology on the basis of certain similarities to adult T cell leukemia, which is associated with human T cell leukemia/lymphoma virus type I (HTLV-I) infection. Cell lines were established from peripheral blood mononuclear cells (PBMC) of an HTLV-I-seronegative patient with mycosis fungoides. DNA hybridization analysis revealed the presence of HTLV-I-related sequences with unusual restriction endonuclease sites. Sequence analysis of subcloned fragments demonstrated the presence of a monoclonally integrated provirus with a 5.5-kilobase deletion involving large regions of gag and env and all of pol. Additional evidence for the presence of deleted proviruses was found by polymerase chain reaction (PCR) amplification of DNA from cutaneous lesions of five other HTLV-I-seronegative patients. The findings suggest that HTLV-I infection may be involved in the etiology of at least certain cases of mycosis fungoides.
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PMID:Deleted HTLV-I provirus in blood and cutaneous lesions of patients with mycosis fungoides. 845 46

Tumors formed from wild type P1798 mouse lymphoma cells undergo regression when treated with pharmacological doses of natural and synthetic glucocorticoids in vivo. Variants have been selected that are insensitive to the cytolytic effects of glucocorticoids in vivo. Although the response of wild type and insensitive tumors is markedly different in vivo, the manner in which cells from such tumors respond to glucocorticoids is indistinguishable in culture under routine conditions. Glucocorticoids inhibit proliferation of wild type cells as well as those that are insensitive to glucocorticoids in vivo. Although neither cell line dies when exposed to dexamethasone in culture in the presence of fetal bovine serum, both sensitive and insensitive cell lines undergo cytolysis when exposed to dexamethasone in serum-free medium. Sensitive cells die more quickly, with 50% cell death observed within 6 h. Insensitive cells exhibit less than 10% cell death within 6 h. Sensitive cells continue to die after transitory exposure to dexamethasone, whereas insensitive cells do not. Thus, growth in serum-free medium mimics the response that prevails in vivo. Cell death is associated with rapid, internucleosomal chromatin degradation. The rate of DNA fragmentation is comparable to that of cell death. About 30% of the DNA in sensitive cells is degraded to fragments of less than 10 kilobases within 2 h after addition of dexamethasone, and 70-80% of the DNA is degraded within 6 h. There is no significant degradation observed when insensitive cells are treated for 6 h. P1798 cell lines express an endonuclease that is capable of degrading chromatin in vitro. Basal expression of this activity does not correlate with glucocorticoid sensitivity, and insensitivity does not appear to be attributable to a decrease in expression of the enzyme(s) thought to be responsible for glucocorticoid-mediated chromatin degradation. The data suggest that glucocorticoid insensitivity is associated with delayed activation and/or induction of some lytic principle. Alternatively, resistance may be due to enhanced ability to repair the damage induced by transitory exposure to glucocorticoids in vivo.
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PMID:Insensitivity to the cytolytic effects of glucocorticoids in vivo is associated with a novel "slow death" phenotype. 191 73

Feline leukemia virus (FeLV) is a horizontally transmitted agent of the domestic cat which is known to be associated with wide spectrum of diseases of the hematopoietic system. In the present study, proviral DNAs of FeLV proviruses were examined in the tumor cells of natural killer cell lineage which is very rare in cats. In the chromosomal DNA of the tumor cells, 5 distinct bands corresponding to exogenous FeLV provirus genomes were detected by digestion with EcoRI which does not cut most FeLV isolates. Five clones of pLC1, pLC2, pLC3, pLC4, and pLC5 obtained from the 5 respective bands were analysed by restriction endonuclease mapping and Southern blot hybridization using gene-specific probes of FeLV. The results have clearly demonstrated that pLC4 and pLC5 contained large deletions in the pol and part of gag regions, while the full-length proviruses could be observed in pLC1 and pLC2. Furthermore, pLC3 contained part of a variant FeLV genome having an EcoRI site in its gag region. The molecular clones of defective and variant FeLV in this study may be useful for the further examination of tumorigenesis of large granular lymphoma in the cat.
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PMID:Molecular cloning of feline leukemia provirus genomes integrated in the feline large granular lymphoma cells. 216 59

The methylation patterns of the gag, pol, env, pX and LTR regions of proviral DNA of human T-cell leukemia/lymphoma virus type I (HTLV) in fresh leukemic cells and established cell lines were examined using HpaII/MspI endonuclease. Peripheral blood lymphocytes (PBL) isolated from patients with adult T-cell leukemia/lymphoma (ATL) did not express viral antigens of HTLV, but PBL that had been cultured for 2 days did express these viral antigens. Most parts of the gag, pol and env regions of the HTLV provirus in PBL isolated from 12 ATL patients and PBL cultured for 2 days were hypermethylated as reported by others. In contrast, in 10 established cell lines that harbored HTLV genomes and expressed viral antigens, HTLV proviruses were hypomethylated. In one cell line, ATL-IK, which harbored an HTLV genome but did not produce viral antigens, the gag, pol and env regions were hypermethylated. However, two HpaII sites, one in the middle of the gag region and the other in the middle of the pol region, were not methylated even in PBL from most ATL patients. Furthermore, the pX and LTR regions were hypomethylated not only in established cell lines but also in PBL of ATL patients. The hypomethylation of the pX and LTR regions detected in fresh leukemic cells of ATL patients may have some etiological significance in cell transformation by controlling the level of transcription of these regions, or modulating the binding of some factors to these regions.
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PMID:Methylation pattern of human T-cell leukemia virus in vivo and in vitro: pX and LTR regions are hypomethylated in vivo. 258 3

Recent studies based upon immunophenotypic data have provided strong evidence that nodular lymphocyte predominant Hodgkin's disease (NLPHD) represents an entity that is distinct from other subtypes of Hodgkin's disease (HD). In contract to other forms of HD, the predominance of B-lymphocytes in NLPHD has prompted the thesis that this lesion is actually an atypical B-cell hyperplasia or follicular center cell lymphoma. Three cases of NLPHD by restriction endonuclease analysis were studied in an attempt to identify a clonal B-cell or T-cell expansion in this disorder. DNA was extracted from these tumors and hybridized to probes for the immunoglobulin genes (C kappa, C lambda, JH) and the T-cell receptor beta chain gene. Gene rearrangements were not detectable in any of the cases. The results provide genotypic evidence that there is not a monoclonal or oligoclonal proliferation of small B-lymphocytes or T-lymphocytes in NLPHD. The possibility that the L&H Reed-Sternberg cells are monoclonal cannot be excluded because their small number is below the level of sensitivity of this technique.
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PMID:Absence of B-cell or T-cell clonal expansion in nodular, lymphocyte predominant Hodgkin's disease. 313 Dec 33

DNA was isolated from 20 fine needle aspiration (FNA) biopsies from lymphomas, hyperplastic lymph nodes and nonlymphoid malignant tumors. Small aliquots (0.2 microgram to 2.0 micrograms) of DNA from each sample were digested to completion with restriction endonuclease Eco RI and/or Bam HI and electrophoresed in 0.8% agarose minigels. DNA was transferred to a nylon filter after brief treatment in HCl and subsequent denaturation and neutralization. Filters were hybridized to radiolabeled JH, C kappa, TCR beta or bcl-2 probes to determine if these genes were in germline or rearranged configurations in each of the samples. It was possible to demonstrate rearrangement of at least one immunoglobulin gene in each of the samples diagnosed as lymphoma, while all samples derived from hyperplastic lymph nodes and nonlymphoid malignant tumors exhibited a germline pattern for each probe tested. Thus, FNA biopsies can provide suitable and sufficient DNA for genotypic analysis using molecular probes that detect gene rearrangement.
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PMID:Genotypic analysis of DNA isolated from fine needle aspiration biopsies. 321 71

Avian leukosis viruses (ALV) induce malignant lymphoma of the bursa of Fabricius. Viral DNA in tumors and normal tissues from infected birds were analyzed by using restriction endonucleases. Viral DNA fragments diagnostic of the exogenous ALV were easily detected in tumors, uninvolved bursal tissue, kidney, and erythrocyte nuclei. Exogenous viral DNA was more difficult to detect in liver. Using a restriction endonuclease (SacI) which cleaves linear unintegrated ALV DNA in a single site to define integration sites in DNA from the various tissues, we were able to detect ALV DNA only in tumor tissue. We concluded that the proviral DNA detected in the various nontumor tissue must be integrated in multiple sites. The appearance of ALV integration sites uniquely in tumors suggests that they are clonal growths. Furthermore, the data suggested the presence of a single exogenous integration site for the ALV provirus in each of six early neoplastic bursal nodules. This provirus appeared to retain the organization of EcoRI and BamHI recognition sequences present in the genome of virus used to infect the birds. The ALV integration site appeared different in each of the tumors studied. In a widespread metastatic lymphoma, multiple ALV integration sites were found as well as structural alterations in at least some copies of the ALV provirus.
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PMID:Viral DNA in bursal lymphomas induced by avian leukosis viruses. 624 53

Neocarzinostatin (NCS) induces alkali-labile sites in DNA which are stabilized by NaBH4 reduction. The stabilized sites are sensitive to an AP endonuclease from human lymphoma cells. NCS-induced degradation of supercoiled Col E1 DNA proceeds in stepwise fashion with apurinic/apyrimidinic (AP) sites as intermediates. Degradation is increased when reaction occurs in the presence of AP endonuclease, and DNA reacted with NCS can be shown to have numerous AP endonuclease sensitive sites.
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PMID:Apurinic/apyrimidinic endonuclease sensitive sites as intermediates in the in vitro degradation of deoxyribonucleic acid by neocarzinostatin. 625 58

Neocarzinostatin (NCS) induces repair in a xeroderma pigmentosum lymphoblastoid line deficient in the ability to repair DNA damage induced with (acetoxyacetyl-amino)fluorene. Repair was demonstrated by the induction of repair synthesis and by the disappearance of NCS-induced single-strand breaks and/or alkaline-labile sites in DNA. Estimation of NCS-induced repair patch size, based on the density shift induced in DNA by extensive shear after incubation of treated cells in medium with bromodeoxyuridine or by calculation from the extent of restoration of DNA sedimentation profiles in alkaline sucrose gradients and the amount of repair synthesis measured by the BND cellulose method, indicated that only a few nucleotides were inserted per repaired region. NCS-treated bacteriophage T7 DNA requires incubation with alkaline phosphatase to make it a substrate for DNA polymerase I. NCS-reacted T7 DNA, even after phosphatase treatment, is not a substrate for a DNA polymerase alpha obtained from human lymphoma cells. NCS-treated T7 DNA did serve as a substrate for the DNA polymerase alpha when incubated with an apurinic/apyrimidinic (AP) endonuclease with associated 5'-3'-exonuclease activity. The results suggest that NCS-induced AP sites could be intermediates for the in vivo repair synthesis.
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PMID:Repair of neocarzinostatin-induced deoxyribonucleic acid damage in human lymphoblastoid cells: possible involvement of apurinic/apyrimidinic sites as intermediates. 625 59


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