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)

Effect of repeated (20 days) exposure to picrotoxin (PTX) on rat liver lysosomal function was evaluated by measuring the free and total activities of acid phosphatase, cathepsin D, ribonuclease II (RNAse II) and deoxyribonuclease II (DNAse II). The free activities of the nucleases (both RNAse II and DNAse II) were increased following PTX exposure. The total DNAse II activity was increased by 2.2-fold whereas the total acid phosphatase activity was decreased by 28%. Consequently, the ratios of total activity / free activity were low in the PTX exposed groups, implying loss of membrane integrity. Cathepsin D activity was completely abolished. The results show that repeated exposure to PTX can lead to lysosomal dysfunction in liver.
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PMID:Effect of repeated intraperitoneal exposure to picrotoxin on rat liver lysosomal function. 1557 32

Activation of NMDA receptors has been shown to induce either neuronal cell death or neuroprotection against excitotoxicity in cultured neurons in vitro. To elucidate in vivo neuroprotective role of NMDA receptors, we investigated the effects of activation of NMDA receptors by endogenous glutamate on kainate-induced neuronal damage to the mouse hippocampus in vivo. The systemic administration of the K+ channel blocker 4-aminopyridine (4-AP, 5 mg/kg, i.p.) induced expression of c-Fos in the hippocampal neuronal cell layer, which expression was completely abolished by the noncompetitive NMDA receptor antagonist MK-801, thus indicating that the administration of 4-AP would activate NMDA receptors in the hippocampal neurons. The prior administration of 4-AP at 1 h to 1 day before significantly prevented kainate-induced pyramidal cell death in the hippocampus and expression of pyramidal cells immunoreactive with an antibody against single-stranded DNA. Further immunohistochemical study on deoxyribonuclease II revealed that the pretreatment with 4-AP led to complete abolition of deoxyribonuclease II expression induced by kainate in the CA1 and CA3 pyramidal cells. The neuroprotection mediated by 4-AP was blocked by MK-801 and by the adenosine A1 antagonist 8-cyclopenthyltheophylline. Taken together, in vivo activation of NMDA receptors is capable of protecting against kainate-induced neuronal damage through blockade of DNA fragmentation induced by deoxyribonuclease II in the murine hippocampus.
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PMID:In vivo treatment with the K+ channel blocker 4-aminopyridine protects against kainate-induced neuronal cell death through activation of NMDA receptors in murine hippocampus. 1582 53

Acid endonucleases of the deoxyribonuclease II (DNase II, EC 3.1.22.1) family have been implicated in the degradation of DNA from apoptotic cell corpses formed in the process of normal mammalian development. Although a predicted DNase II has been detected in the chicken through expressed sequence tag (EST) analysis, to date no homolog of these important enzymes has been identified in vivo in any avian species. Here we report the cloning and expression of DNase II from the chicken, Gallus gallus. When expressed, the 363 amino acid glycoprotein is observed to be approximately 45 kDa in size and to exhibit DNA hydrolytic activity at pH 5 consistent with DNase II in other species. Furthermore, chicken DNase II sequence is compared with an identified partial sequence from the zebra finch, Taeniopygia guttata, as well as the previously identified homologs found in the fowlpox and canarypox viruses and the previously cloned mammalian DNases II. Through analysis of its amino acid sequence, comparative gene structure, and conserved synteny, chicken DNase II appears to represent a member of the DNase IIbeta subfamily and the apparent lack of a DNase IIalpha homolog in the chicken has important evolutionary implications for the study of this gene family.
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PMID:Cloning and expression of deoxyribonuclease II from chicken. 1650 43

Many endonucleases have been identified in cells, but which are involved in apoptosis remains controversial. We detected and characterized an endonuclease as deoxyribonuclease II. Its most important characteristic is its acidic pH optimum that requires decreased intracellular pH for activation. Intracellular acidification has been observed during apoptosis in a number of systems. This acidification results from a selective loss of pH regulation, and is likely due to dephosphorylation of proton exchangers. The fact that growth factors normally prevent apoptosis and also phosphorylate ion exchangers suggests the critical role of intracellular kinase cascades for preventing apoptosis.
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PMID:Deoxyribonuclease II in apoptosis and the significance of intracellular acidification. 1718 1

SUMMARYNewborn larvae (NBL) and adult (Ad) stage-specifically expressed genes or members of gene families of Trichinella spiralis were identified by suppression subtractive hybridization (SSH). Six cDNA clones were identified as NBL stage-specific, including 1 member of the T. spiralis gene family encoding glutamic acid-rich proteins, 2 clones encoding novel serine proteases, 2 closely related clones encoding proteins that are members of a deoxyribonuclease II (DNase II)-like family and 1 clone with no similarity to known genes. Four stage-specific clones encoding homologues of retinoid X receptor, caveolin, C2H2 type zinc finger protein and a putative protein with no homology to known sequences were obtained from 3-day-old adult worms. One gene specifically up-regulated in the 5-day-old adult worms encoding a putative cuticle collagen was also identified.
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PMID:Identification of stage-specifically expressed genes of Trichinella spiralis by suppression subtractive hybridization. 1747 93

Our earlier study demonstrated that in vivo acute treatment with trimethyltin chloride (TMT) produces severe neuronal damage in the dentate gyrus and cognition impairment in mice. In the present study, we assessed whether TMT was capable of causing neuronal degeneration in the olfactory bulb (OB) and anterior olfactory nucleus (AON) of the mouse brain. An intraperitoneal injection of TMT at the dose of 2.8 mg/kg led to a dramatic increase in the number of degenerating cells, which were reactive with antibody against single-stranded DNA, in the granule cell layer (GCL) of the OB and AON 1 day and 2 days later, respectively. TMT treatment produced a marked translocation of phospho-c-Jun-N-terminal kinase from the cytoplasm to the nucleus in the AON. Expectedly, a marked increase in phospho-c-Jun-positive cells was seen in the AON after the treatment. In addition to the AON, the mitral cell layer of the olfactory bulb showed the presence of phospho-c-Jun-positive cells after the treatment. However, the GCL had no cells positive for either phospho-c-Jun-N-terminal kinase or phospho-c-Jun at any time after the treatment with TMT. Similarly, TMT-induced nuclear translocation of the lysosomal enzyme deoxyribonuclease II was seen in the AON, but not in the GCL. On the other hand, TMT elicited the expression of activated caspase 3 in the GCL but not in the AON. Taken together, our results suggest that TMT is capable of causing neuronal degeneration in the murine OB and AON through different cascades in the two structures.
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PMID:In vivo acute treatment with trimethyltin chloride causes neuronal degeneration in the murine olfactory bulb and anterior olfactory nucleus by different cascades in each region. 1818 23

Different fragments of promoters of deoxyribonuclease II (DNAse II) and calcium-modulating cyclophilin ligand (CAML) associated with Alu family repeats have been inserted into a luciferase reporter vector. These constructions were introduced into A549 and HEK293 cell lines and after transient transfection we lysed cells and analysed luciferase activities in these lysates. It has been shown that Alu repeats localized in constructions influence expression of luciferase. Therefore, Alu copies which are associated with cis-regulatory modules of protein-coding genes have biological activity.
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PMID:[Retroposons of Alu family from cis-regulatory modules of DNAse II and CAML genes effect gene expression in A549 and HEK293 cells]. 1866 27

Several recent reports proposed that astrocyte death might precede neuronal demise after focal ischemia, contrary to the conventional view that astrocytes are more resistant to injury than neurons. Interestingly, there are findings supporting each of these opposing views. To clarify these controversies, we assessed astrocyte viability after 2-h middle cerebral artery occlusion in mice. In contrast to neighboring neurons, astrocytes were alive and contained glycogen across the ischemic area 6 h after reperfusion, and at the expanding outer border of the infarct at later time points. These glycogen-positive astrocytes had intact plasma membranes. Astrocytes lost plasmalemma integrity much later than neurons: 19 +/- 22 (mean +/- standard deviation), 58 +/- 14 and 69 +/- 3% of astrocytes in the perifocal region became permeable to propidium iodide (PI) at 6, 24, 72 h after ischemia, respectively, in contrast to 81 +/- 2, 96 +/- 3, 97 +/- 2% of neurons. Although more astrocytes in the cortical and subcortical core regions were PI-positive, their numbers were considerably less than those of neurons. Lysosomal rupture (monitored by deoxyribonuclease II immunoreactivity) followed a similar time course. Cytochrome-c immunohistochemistry showed that astrocytes maintained mitochondrial integrity longer than neurons. EM confirmed that astrocyte ultrastructure including mitochondria and lysosomes disintegrated much later than that of neurons. We also found that astrocytes died by a delayed necrosis without significantly activating apoptotic mechanisms although they rapidly swelled at the onset of ischemia.
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PMID:Astrocytes are more resistant to focal cerebral ischemia than neurons and die by a delayed necrosis. 1894 34

Neural progenitor cells play an essential role in both the developing embryonic nervous system and in the adult brain, where the capacity for self-renewal would be important for normal brain functions. In the present study, we used embryonic cortical neural progenitor cells to investigate the effects of trimethyltin chloride (TMT) on the survival of neural progenitor cells. In cultures of cortical neural progenitor cells, the formation of round neurospheres was observed in the presence of epidermal growth factor and basic fibroblast growth factor within 9 days in vitro. The neurospheres were then harvested for subsequent replating and culturing for assessment of cell viability in either the presence or absence of TMT at the concentration of 5microM. Lasting exposure to TMT produced not only nuclear condensation in the cells in a time-dependent manner over a period of 6-24h, but also the release of lactate dehydrogenase into the culture medium. Immunoblot and immunocytochemical analyses revealed that TMT had the ability to activate both caspase-3 and calpain, as well as to cause nuclear translocation of deoxyribonuclease II, which is located within cytoplasm in intact cells. Additionally, treatment with a calpain inhibitor [trans-epoxysuccinyl-l-leucylamido-(4-guanidino) butane] and a caspase inhibitor [Z-Val-Ala-Asp(OMe)-CH2F] produced a significant reduction in damaged cells induced by TMT. Taken together, our data indicate that neural progenitor cells are highly susceptible to TMT in undergoing cell death via the activation of 2 parallel pathways, ones involving calpain and the other, caspase-3.
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PMID:High susceptibility of cortical neural progenitor cells to trimethyltin toxicity: involvement of both caspases and calpain in cell death. 1952 17

A procedure is described for the purification of salmon testis deoxyribonuclease II by means of acid extraction, fractional precipitation with ammonium sulfate, heat denaturation of extraneous proteins, and ethanol fractionation. This process separates the deoxyribonuclease activity from that of ribonuclease, phosphatase, phosphodiesterase, and protease. Over 50 per cent of the activity is retained with an over-all enrichment of 20,000-fold. The enzyme degrades both native and heat-denatured DNA, but the rate of degradation of the latter is only one-tenth that of the former. It does not hydrolyze apurinic acid. The enzyme is most stable in the pH range 4 to 5. Electrolytes are essential for the expression of its activity: monovalent ions satisfy the requirement, but divalent ones are much more effective. Above a certain optimum concentration, each electrolyte is inhibitory. The pH of maximal activity, under conditions of optimal ionic strength, is 4.8; the temperature optimum is near to 55 degrees C.
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PMID:Deoxyribonuclease from Salmon Testes : I. Purification and properties. 1987 45


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