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Click here for the function of DNASE1. Edit this page in Wiki Genes - DNASE1 or see Wiki Gene. Mutation of DNASE1 in people with systemic lupus erythematosus. Paper-8852853. Novel DNASE I mutations related to systemic lupus erythematosus. Paper-11432873. Results confirm the safety of dornase alfa in CF patients of all ages. Paper-13419838. This is the first report of long-term use of dornase alfa in PCD. Paper-13425889. Mice deficient in deoxyribonuclease I ( Dnase1) develop an SLE-like syndrome. Paper-8852853. Levels of DNase I <7.79 ng ml(-1) are more represented in patients with SLE. Paper-13625808. Five major DNase-I hypersensitive sites (HS) were mapped in the tal-1 locus. Paper-7993387. Characterization of DNASE I hypersensitive sites in the 120kb 5' to the CFTR gene. Paper-251770. Study of DNASE I gene polymorphisms in systemic lupus erythematosus susceptibility. Paper-13154253. DNase X is the first mammalian DNase to be isolated that is homologous to DNase I. Paper-13271781. Dornase alfa cleaves DNA and improves sputum viscosity in CF. Paper-9307975. The binding of 9D7 to PGK-1 was not affected by DNase I but was inhibited by thymus dsDNA. Paper-12174023. Biochemical studies indicate that it is a pepsin destroyed protein, unaffected by Rnase and Dnase. Paper-2265188. Total RNA was treated with 0.5 units of Rnase-free Dnase/mg of RNA to remove any contaminating DNA. Paper-141695. In this report, we describe the long-term use of nebulized dornase alfa in two siblings with PCD. Paper-13425889. We suggest that both cofilin and gelsolin are essential in modulating the release of DNase I from actin. Paper-10806829. Complement, C-reactive protein ( CRP), and serum DNase I act as back-up molecules in the clearance process. Paper-12018761. Moreover, ChIP and DNase I footprinting analysis revealed that HDGF binds this 80 bp DNA fragment specifically. Paper-13440272. OBJECTIVE: To determine the benefit of nasally inhaled dornase alfa in cystic fibrosis ( CF) sinusitis. Paper-2203903. In contrast, molecular crowding did not significantly affect the Michaelis constant of DNase I or exonuclease I. Paper-13332659. DNASE I mutation and systemic lupus erythematosus in a Spanish population: comment on the article by Tew et al. Paper-9176943. Two DNase I hypersensitive sites appeared in the TNF-alpha promoter after LPS stimulation of THP-1 cells. Paper-12313493. Distinct DNase-I hypersensitive sites are associated with TAL-1 transcription in erythroid and T-cell lines. Paper-7993387. Specific enzymes include BAL 31 nuclease, S1 nuclease, mung bean nuclease, micrococcal nuclease and DNase I. Paper-12733692. Human beta-globin locus control region ( LCR) is composed of five DNase I hypersensitive sites (HSs). Paper-12878099. In patients with AITD, a novel mutation (1218G>A, exon 5) and multiple polymorphisms were identified in the DNASE1 gene. Paper-13600362. CONCLUSIONS: Pulmonary function as measured by FEV1 and FVC improved significantly in the dornase alfa-treated patients. Paper-713476. Physicochemical properties of IL-13 ASO/cEL complex were examined by DNA retardation and DNase I protection assay. Paper-13564230. However, the Gln244Arg genotype did not correlate with DNase I activity in sera from SLE patients or from controls. Paper-12048850. CSA protein was detected in the DNase I-insoluble fraction, indicating that it was translocated to the nuclear matrix. Paper-13153199. Here we report that IRE-ABP and SRY bind to IRE-A DNA with comparable specificity in a DNase-I footprinting assay. Paper-7015085. Patients were excluded for hospitalization for complications of CF within 2 months and use of dornase alfa within 6 months. Paper-8885074. Both mobility shift assay and DNase-I footprint analysis showed that P2 had much higher Pit-1 binding affinity than P1. Paper-1832010. Within this region, a 275-bp fragment displaying liver-specific DNase I hypersensitivity was bound by HNF1. Paper-12066021. Further, we demonstrate coimmunoprecipitation of the All1/Af4 and All1/Af9 fusions with Drosha, disrupted by treatment with DNase I. Paper-13317716. Chromosomal assignment of the human deoxyribonuclease I gene, DNASE 1 ( DNL1), to band 16p13.3 using the polymerase chain reaction. Paper-266780. The MPO concentration in CF sputum was approximately double after in vitro treatment with dornase alfa (P < 0.0001). Paper-9033818. Recombinant ACTC inhibits DNase-I and binds myosin S1, indicative of proper folding. Paper-12504221. These data are consistent with the hypothesis that a direct connection exists between low activity of DNASE1 and progression of human SLE. Paper-8852853. Nucleosome and transcription activator antagonism at human beta-globin locus control region DNase I hypersensitive sites. Paper-12509330. The A/T mutation in exon 2 of the DNASE1 gene is not present in Tunisian patients with systemic lupus erythematosus or in healthy subjects. Paper-10145624. DNase I were employed to remove DNA fragments in sera and membrane protein preperation and IgG F(ab')2 was obtained by pepsin digestion. Paper-11053154. DNA polymers bind myeloperoxidase in the sputum, and we speculate that treatment with dornase alfa may remove a source of MPO inhibition. Paper-9033818. This suggests that RNase A and DNase I were not oxidized to lose their activity, but reversibly complexed with Au(III) ions to lose their activity. Paper-12374208. The HSS1 region displayed hypersensitivity to in vivo DNase I digestion in TNFSF6-expressing cells only, including upon T cell activation. Paper-12012627. With the combination of dornase alfa and Tbeta4 at 1.5 mug/mL each, there was a 70% decrease in G*s and a 65% decrease in G' at 1 rad/s (p = 0.013). Paper-12310625. This preliminary study indicates the potential impact of nasally inhaled dornase alfa in controlling postoperative symptoms in CF sinusitis. Paper-2203903. Using DNase I hypersensitivity site (HSS) mapping, we identified two novel HSS mapping to the human CD154 promoter element and just upstream. Paper-13049617. CONCLUSIONS: Treatment of young patients with CF with dornase alfa maintains lung function and reduces the risk of exacerbations over a 96-week period. Paper-8885074. Inhibitory effects of gold(III) ions (Au(III)) on ribonuclease A ( RNase A) and deoxyribonuclease I ( DNase I) were investigated at neutral pH. Paper-12374208. RT-PCR is carried out directly after DNase I treatment of crude bacterial lysates using rTth polymerase for RT-PCR in a single tube. Paper-11144237. DNase I footprint analysis of the fragment revealed a protected region at nt -82/-77, which is in a putative FOXF1/ FOXF2 binding site. Paper-12259665. Dornase alfa also decreased the rate of hospitalizations, the number of days missed from work or school, and the frequency of CF-related symptoms. Paper-176130. DNase I footprinting data and Transfac analyses suggest that the ferritin LCH promoter contains putative GATA, E2F, NIT2, TATA and DPE sites. Paper-11182470. CONCLUSIONS: The combination of DA and NAL exhibits an additive effect for both the viscoelasticity and transportability of CF sputum samples. Paper-9601873. DNase-I footprinting and gel mobility shift studies demonstrated at least three distinct protein-binding sites within the CG beta CRE sequence. Paper-36437. Dnase1 activity was lower in patients with SLE than in the control group: 13.69 +/- 8.52 mug/mL vs 24.75 +/- 12.32 mug/mL, respectively (P < 0.005). Paper-13682852. The binding of TINA-TFOs to the KRAS target has been analysed by electrophoresis mobility shift assays and DNase I footprinting experiments. Paper-12817044. We provide examples of correlation of computational predictions to reported mapped DNase I hypersensitive segments in the HOXA locus in human chromosome 7. Paper-13664838. We have previously reported the mapping of six nuclear DNase-I hypersensitive sites at the PBG-D locus which could contribute to the regulation of the gene. Paper-293769. We show by DNase I footprinting and electophoretic mobility shift assays that the cis-regulatory element within this DHS binds CTCF in vitro. Paper-13651233. dsDNA-, nucleohistone- and DNASE I-reactive T lymphocytes in patients affected by systemic lupus erythematosus: correlation with clinical disease activity. Paper-865938. Dornase alfa has been shown to reduce pulmonary exacerbations and improve lung function and is currently the only mucolytic agent with proven efficacy in CF. Paper-13177258. DNase I hypersensitivity of the TNF-alpha promoter was also analyzed in human monocytes prepared from individuals of different -863C/A genotype. Paper-12313493. PCAF and the nuclear actin- associated HAT activity detected in the DNase I-bound protein fraction could be released by disruption of the actin-hnRNP U complex. Paper-12954837. Serum DNase I, soluble Fas/ FasL levels and cell surface Fas expression in patients with SLE: a possible explanation for the lack of efficacy of hrDNase I treatment. Paper-13625808. Aerosolized recombinant human DNase ( dornase alfa) reduces mucus viscoelasticity in vitro and improves pulmonary function in patients with cystic fibrosis ( CF). Paper-1395560. DNase-I footprint analysis, using nuclear extracts from LNCaP cells, revealed the presence of three DNase-I- protected areas within the DD3 proximal promoter. Paper-8578679. This study examined in patients with autoimmune thyroid disease ( AITD) whether a reduced DNase activity is associated with sequence variations in the DNASE1 gene. Paper-13600362. Phalloidin promotes the dissociation of cofilin from F-actin and slowly reverses the cofilin- induced disorder in the DNase I binding loop of subdomain 2. Paper-12333680. Reduction of serum DNASE1 ( DNase I) activity is supposed to aggravate anti-nuclear autoimmunity, i.e. Systemic Lupus Erythematosus ( SLE) in man and mice. Paper-13616879. Both vitamin D-binding protein and thymosin beta4 inhibit binding by ADF or cofilin, while cofilin or ADF and DNase I bind simultaneously. Paper-12452287. Patients with cystic fibrosis ( CF) receiving dornase-alfa had improved pulmonary function relative to a control group in a large randomized phase III controlled study. Paper-1881469. We show that the high mobility group I(Y) protein binds to one of the DNase-I-protected areas and recruits another, yet unidentified, protein to the DD3 promoter in LNCaP cells. Paper-8578679. This role may contribute to explain the inefficacy of hrDNase I in SLE, a treatment proposed for the ability of DNase I to remove DNA from auto-antigenic nucleoprotein complexes. Paper-13625808. The -77 kb region, which was DNase I hypersensitive in both active and inactive states, conferred equivalent enhancer activities in GATA-1- and GATA-2-expressing cells. Paper-12232599. The function of the SLPI promoter encompassing these DNase-I hypersensitive sites has been studied by deletion analysis with the luciferase gene as a transient expression vector. Paper-1174823. We also show that cofilin stabilises the actin-DNase I complex by forming a ternary complex that prevents N-gelsolin from releasing DNase I from actin. Paper-10806829. P-115- ABP and P-135- ABP present in a crude protein extract prepared from germinating pollen bound to a DNase I affinity column in a Ca(2+)-dependent manner. Paper-11539227. Dornase alfa, also called recombinant human DNase I (rhDNase), cleaves extracellular DNA, which is present in inordinately high concentrations in purulent CF airway secretions. Paper-176130. Some quality-of-life (QOL) domains (mainly cough frequency and chest congestion) have shown modest improvement in patients treated with dornase alfa, mainly those with mild CF. Paper-1186706. DNase I does not correlate with sFas or sFasL, whereas it correlates with T cell surface Fas expression that is higher in patients with active SLE than in healthy controls. Paper-13625808. We first performed DNase I hypersensitive site mapping and demonstrated that the promoter region of ESE-2 is in open chromatin conformation in differentiated keratinocytes. Paper-11411660. Binding of VDR and retinoid X receptor to the promoter region was shown in DNase I footprinting, electrophoretic mobility shift and chromatin immunoprecipitation assays. Paper-12158734. MATERIALS AND METHODS: Valve-bearing segments of human allogeneic great saphenous veins (GSVs) were decellularised using sodium deoxycholic acid ( SD) and treated with DNase I. Paper-13491834. In vitro DNase I footprinting analysis identified a protected region that corresponds to a conserved, predicted binding site for hepatocyte nuclear factor 1 ( HNF1). Paper-13773604. GATA-1 is an erythroid activator that binds beta-globin gene promoters and DNase I hypersensitive sites (HSs) of the beta-globin locus control region (LCR). Paper-12901877. We report here preliminary results of a study of dornase alfa delivered by two different nebulizer systems to patients with mild lung disease in CF and near normal lung function. Paper-1178705. The results demonstrated that the para-derivative has the greatest affinity for its cognate sequence, as indicated via thermal denaturation, CD, ITC, SPR analyses, and DNase I footprinting. Paper-13773090. As assayed by DNase I protection, DNA binding by TFIIIA ( transcription factor IIIA, prototypical Cys(2)His(2) zinc finger protein), was inhibited by micromolar amounts of ebselen. Paper-13617318. DESIGN: In this multicenter, double-blind, placebo-controlled study, CF patients with advanced lung disease were randomized to receive either dornase alfa or placebo once a day for 12 weeks. Paper-713476. DNase I-footprinting assays were carried out with the topoisomerase IIalpha-promoter sequence, which contains five ICB sites; of these, ICB1 and ICB5 are similar to the ICB site of MDR1. Paper-11527929. Gel shift, DNase I, and chemical cross-linking assays with TATA box-binding protein ( TBP) and Rep68 indicate that both proteins interact with each other and with the promoter at adjacent sites. Paper-12038828. By cleaving neutrophil-derived DNA, dornase alfa (recombinant human deoxyribonuclease I) decreases the adhesiveness and visco-elasticity of sputum in the infected lungs of patients with CF. Paper-1186706. Home intravenous (IV) antibacterial therapy and recombinant human DNase (rhDNase; dornase alfa) treatment are the two main therapeutic strategies most often evaluated in health economic studies of CF. Paper-10159612. Recent data investigating the use of dornase alfa (recombinant human deoxyribonuclease I) in patients with acute exacerbations of COPD were disappointing and failed to demonstrate a mortality benefit. Paper-822569. In conclusion, our findings confirm that DNase I is low in SLE and suggest that it may play a role in apoptosis in SLE by regulating the surface expression of the cell death molecule Fas. Paper-13625808. Analysis of DNase I hypersensitive sites indicated that only two of these map to highly accessible chromatin, one of which, SNP rs2981578, has previously been implicated in up-regulating FGFR2 expression. Paper-13712352. OBJECTIVE: Our objective was to determine whether long-term treatment of young patients with cystic fibrosis ( CF) with dornase alfa maintains lung function and reduces respiratory tract exacerbations. Paper-8885074. DNA mapping with a probe for a delta-globin fragment showed a 27-kb deletion of DNA that included the beta-globin gene and the 3' deoxyribonuclease I hypersensitive site 1 (3'HS1) sequence downstream. Paper-12016811. However, binding of myosin heads (S1) shifted the population of 6nSLADP toward the more highly restricted cone, while binding of DNase-I shifted it toward the less restricted cone. Paper-116812. Dornase alfa has been found to increase the pourability and reduce the viscoelasticity of CF sputum in vitro and, in an animal model, to increase its mucociliary transportability. Paper-176130. Gene expression and protein analysis identified significantly lower levels of deoxyribonuclease (DNase) I and reduced nuclear translocation and biological activity of DNase I in GSN(-/-) mice. Paper-13712115. OBJECTIVE: Dnase1-deficient mice with the 129 x C57BL/6 genetic background develop symptoms of systemic lupus erythematosus, such as high titers of antinuclear autoantibodies directed against nucleosomes. Paper-10285354. Its relationship with SLE susceptibility, serum DNase I activity, anti-ribonucleoprotein (RNP), anti-double-stranded DNA (dsDNA), anti-nucleosome and anti-single-stranded DNA (ssDNA) antibodies was determined. Paper-12048850. Pituitary-specific DNase I hypersensitive site I ( HSI), the dominant hGH LCR element, is separated from the hGH-N promoter by a 14.5 kb span that encompasses the B-lymphocyte-specific CD79b gene. Paper-11994430. The action of basonuclin is mediated through three pairs of evolutionarily conserved zinc fingers, which produce three DNase I footprints on the promoters of rDNA and the basonuclin gene. Paper-12199675. We show here by DNase-I footprint and gel shift assay in presence of recombinant transcription factors and their antibodies that NF-1/CAAT and C/ EBP like transcription factors bind to this region of the promoter. Paper-7844253. These glycolipids showed no effect even on the activities of plant pols, prokaryotic pols and other DNA metabolic enzymes such as T4 polynucleotide kinase, T7 RNA polymerase and deoxyribonuclease I. Paper-13191470. STUDY OBJECTIVE: The 12-week efficacy and safety of aerosolized recombinant human DNase ( dornase alfa) were evaluated in previously untreated patients with cystic fibrosis ( CF) with advanced lung disease. Paper-713476. Twenty-eight of 15,865 SAEs (0.18%), occurring in 26 of 6,829 patients ever treated with dornase alfa (0.38%), and no deaths were reported as possible SADRs: most were typical complications of cystic fibrosis ( CF). Paper-13419838. In both human and mouse cells, repression was accompanied by the loss of multiple DNase I hypersensitive sites at the TERT promoters and their upstream regions, revealing positions of potential regulatory elements. Paper-13757541. Loss of GATA-1 in HS2 did not compromise interaction of NF-E2, a second activator that binds to HS2, nor was DNase I hypersensitivity at HS2 or the promoter of a linked epsilon-globin gene altered. Paper-12901877. Subsequently, the influence of sera from Dnase1-deficient and wild-type mice as well as the influence of purified enzymes present in the culture medium on the process of necrotic chromatin breakdown was investigated. Paper-10285354. Dornase alfa (Pulmozyme) treatment for patients with cystic fibrosis ( CF) has been shown to improve pulmonary function and reduce exacerbations of infection in a number of placebo-controlled double-blind studies. Paper-10012100. DNase-I hypersensitive sites were detected within 1 kbp upstream of exon I in chromatin structures of type II pneumocyte cell line A549 and utero-cervical cell line HeLa, both of which express SLPI mRNA transcripts. Paper-1174823. Our investigation concludes that gelsolin is an important contributor to heart failure progression through novel mechanisms of HIF-1alpha and DNase I activation and downregulation of antiapoptotic survival factors. Paper-13712115. The DNA conveyance ability of MPS was examined by evaluating properties such as particle size, zeta potential, complex formation, protection of plasmid DNA against DNase-I, and the release of DNA upon cell entry. Paper-12822844. The identified new mutation and numerous polymorphisms, noted for the first time in AITD patients, may alter transcription and translation of the DNASE1 gene, thereby decreasing the stability and activity of the corresponding enzyme. Paper-13600362. The patients with severe RSTS all had deletions comprising telomeric neighbor genes of CREBBP, including DNASE1, a dominant gene encoding a nuclease that has been associated with systemic lupus erythematodes. Paper-12171428. RESULTS: Our results showed a >90% decrease in the viability of HeLa and HEp-2 cells, and >50%<90% decline in Calu-1, SK-MES-1 and L-929 cell viability, incubated with 9 mg/ml of DNase-I in comparison with control cells (p<0.05). Paper-13594408. Electrophoretic mobility shift assay and DNase I footprinting analysis revealed that Prop-1 binds to six positions, -1038/-1026, -942/-928, -495/-479, -338/-326, -153/-146, and -131/-124 bp, that comprise the A/T cluster. Paper-12265304. Sequence analysis combined with gel retardation and Dnase 1 footprinting assay identified multiple cis and trans elements for this fragment, including Sp1, PEA3, cyclic AMP response element (CRE)-like sequence, and E-boxes. Paper-298825. An apparent synergy of Tbeta4 on actin and dornase on DNA may be explained by the combined effect of actin depolymerization and DNA filament severing or by virtue of actin depolymerization increasing the effectiveness of dornase alfa. Paper-12310625. By cleaving neutrophil-derived DNA present in the infected lungs of patients with cystic fibrosis ( CF), dornase alfa (recombinant human deoxyribonuclease I) reduces the adhesiveness and viscoelasticity of CF sputum. Paper-8245255. Electron microscopy and sedimentation analysis after digestion with DNase I or proteinase K indicate that complex is composed of an intact phage head with a genome-sized linear DNA molecule attached at the collar-tail region. Paper-12795516. However, DNase-I treatment partly reduced this binding, whereas after purification of MoAb by protein-A sepharose chromatography under dissociative conditions, all clones completely lost their binding capacity to HS and HSPG. Paper-6802922. Gel mobility-shift assays and DNase I footprinting analyses indicated that MobR binds as a homodimer to an imperfect inverted repeat within the mobA-mobR intergenic region, with an apparent dissociation constant of 11.5(+/-0.5) nM. Paper-12330401. It also proposes two different methods that could be used to overcome DNA contamination: (i) DNase I treatment prior to PCR amplification; and (ii) the use of a highly purified Taq DNA polymerase which was devoid of detectable contamination. Paper-11369348. The Au(III)-inhibited RNase A and DNase I were renatured to exhibit 80% and 60% of their intrinsic activity, when the bound Au(III) ions were eliminated from the nucleases by addition of thiourea, which forms a strong complex with gold ions. Paper-12374208. In a previously reported large multicenter trial, dornase alfa improved pulmonary function and decreased the need for hospitalization in patients with CF over 5 years of age and with forced vital capacity greater than 40% predicted. Paper-1178705. The expression of soluble heat-labile toxin is subject to catabolite ( glucose) activation, and three binding sites for cAMP receptor protein ( CRP or CAP) were identified upstream and within the toxin promoter by DNase I footprinting. Paper-13580517. A history of gastrointestinal complications attributed to cystic fibrosis and the use of histamine H2-receptor blockers, corticosteroids, or recombinant human DNase ( dornase alfa) were associated with a higher incidence of fibrosing colonopathy. Paper-969912. In vitro transcribed/translated ERRalpha and ERRgamma bound to the NRE(SP-A); DNase I footprinting using bacterially expressed ERRalpha revealed a single DNase I protected region that included NRE(SP-A). Paper-12273647. We have mapped using DNase I footprinting and mobility shift assays three putative heat shock elements and one AP-1 binding domain (ARE) in the 5' intergenic region shared by PbMDJ1and PbLON (ML) from Paracoccidioides brasiliensis. Paper-13162309. Short-term (10-day) Phase I and II clinical trials showed dornase alfa to be safe and effective in improving pulmonary function in clinically stable CF patients with mild to moderate pulmonary disease (FVC > or = 40% of predicted value). Paper-176130. However, in the absence of guidance from definitive cost-effectiveness analyses, individual healthcare providers must make their own decisions about how best to provide dornase alfa to patients with CF in a rational and cost-justifiable manner. Paper-1186706. Plasminogen bound to the cytoskeleton and nuclear structures, was activated to plasmin by either tissue-type or urokinase-type plasminogen activator, and degraded histone H1, thereby facilitating internucleosomal DNA cleavage by Dnase1. Paper-10285354. Treatment of rat hepatoma cells with insulin, glucagon, thyroxine ( T4) and triiodothyronine ( T3) caused a concentration-dependent decrease in the monomeric actin content as measured by the deoxyribonuclease-I inhibition assay. Paper-4850816. Data in the Epidemiologic Registry of Cystic Fibrosis (ERCF) in November 1998 were used to assess the long-term effectiveness in routine clinical practice of dornase alfa in terms of pulmonary function and frequency of acute pulmonary exacerbations in CF. Paper-10012100. Sputum rheology, cough and ciliary transportability, and interfacial tension were measured before and after the addition of dornase alfa at 30 mug/mL; Tbeta4 at 0.3, 3, 30, and 150 mug/mL; and Tbeta4 with dornase alfa at 1.5 mug/mL each. Paper-12310625. As compared to proliferative keratinocytes, calcium stimulation specifically associates with increased local DNase I hypersensitivity around PIE, and increased physical proximity of PIE and PADI3 as assessed by Chromosome Conformation Capture. Paper-13037251. Enzymatic degradation assays revealed that only the DMA homopolymer provided effective DNA protection against DNase I degradation, while other highly condensed copolymer complexes, as judged from TEM and gel electrophoresis, only partially protected the DNA. Paper-11491510. In conclusion, the acquisition cost of dornase alfa is partially offset by savings gained by reducing resource utilisation in patients with mild to moderate CF, and the drug appears to improve quality of life in some patients, mostly those with less severe disease. Paper-1186706. OBJECTIVE: To investigate the effect of dornase alfa ( DA), Nacystelyn (NAL) and their combination on mucociliary transportability and mucus viscoelasticity of cystic fibrosis ( CF) sputum, and to assess whether the combination possesses an additive effect. Paper-9601873. Moreover, kinetic analysis showed that the maximum velocity for the reaction of DNase I at 25 degrees C was increased from 0.1 to 2.7 microM/min by molecular crowding with 20% (w/v) PEG, whereas that of exonuclease I at 37 degrees C decreased from 2.2 to 0.4 microM/min. Paper-13332659. MATERIAL AND METHODS: In this work, we evaluated cell viability (violet crystal stain), cell proliferation (tritiated thymidine) and DNA degradation of tumoral cells ( Calu-1, SK-MES-1, HeLa, HEp-2, L-929) incubated with different concentrations of DNase I. Paper-13594408. In summary, aerosolised dornase alfa offers modest improvements in lung function and, importantly, a reduced risk of respiratory exacerbations in patients with CF and an FVC > or = 40% of the predicted value, thus representing an important adjunct agent in this patient group. Paper-8245255. The expression pattern of HIF-1alpha was similar to that of gelsolin, and HIF-1alpha was detected in the gelsolin complex by coprecipitation and HIF-1alpha bound to the promoter of DNase I in both gel-shift and promoter activity assays. Paper-13712115. The gel mobility and particle size of polyplex with Man-alpha-CDE conjugate (G3, DSM10) were relevant to those with alpha-CDE conjugate (G3), but zeta-potential, DNase I stability, pDNA condensation of the former polyplex were somewhat different from those of the latter one. Paper-12334503. A biochemical assay employing DNase-I affinity chromatography, two-dimensional peptide analysis and SDS polyacrylamide gel electrophoresis was used to isolate, identify, and assess the amount of actin from gonial cells of the crane fly, Nephrotoma suturalis. Paper-3599979. There was more DNase I mRNA expression in the hypoxic group than in the control group (P<0.05) in vitro, and the expression of Endo G mRNA in the hypoxic groups was significantly higher than that in the control groups both in vitro and in vivo (P<0.05). Paper-13739885. By using 5' deletion mutants of promoter II fused to the bacterial chloramphenicol acetyltransferase (CAT) gene, the DNA mobility shift assay and the DNase I footprinting assay, the authors have identified the 30 bp from -389 to -359 as the TNF responsive element in promoter II. Paper-12792598. For four complexes, LIR-1/HLA-A2, Actin/ DNase I, CDK2/ cyclin, and CDK6/p16(INK4a), the motions calculated for the monomer exhibiting the largest conformational change, in its unbound (free) form, correlate with the experimentally observed structural changes upon binding. Paper-11175673. Strong in vivo topo II cleavage sites and DNase I hypersensitive sites often co-localize with each other and also with many of the BCRs in most of these genes, whereas SARs are associated with BCRs in MLL, AF4, AF9, AML1, ETO and ABL, but not in the BCR gene. Paper-12204414. Biofilms of C. albicans were also partially detached by treatment with proteinase K, chitinase, DNase I, or beta-N-acetylglucosaminidase, whereas C. tropicalis biofilms were only affected by lipase type VII or chitinase. Paper-12068221. The binding sites for actin depolymerising factor ( ADF) and cofilin on G-actin have been mapped by competitive chemical cross- linking using deoxyribonuclease I ( DNase I), gelsolin segment 1 ( G1), thymosin beta4 ( Tbeta4), and vitamin D-binding protein (DbP). Paper-12452287. For example, the differentially methylated 5 -portion of the human SNRPN gene-a sequence element that controls imprinting in the Prader-Willi and Angelman syndromes' domain on chromosome 15q11- q13-has strong DNase-I hypersensitive sites on the unmethylated paternal chromosome (4). Paper-11439056. In this study, DNase I footprinting and EMSA also revealed binding of transcription factors, specificity protein 1 (Sp1) and octamer-binding transcription factor 1 ( Oct-1) to the P2 promoter, and site-directed mutagenesis confirmed that these factors contribute to the basal P2 promoter activity. Paper-13561333. Beta toxin belongs to the DNase I folding superfamily; in addition to sphingomyelinases, the proteins most structurally related to beta toxin include human endonuclease HAP1, Escherichia coli endonuclease III, bovine pancreatic DNase I, and the endonuclease domain of TRAS1 from Bombyx mori. Paper-12544815. The objectives of the study are to evaluate DNase I serum levels and their correlation with soluble Fas (sFas) and soluble Fas ligand (sFasL) and with cell surface Fas expression in patients with systemic lupus erythematosus ( SLE), thus contributing to the dysregulated apoptosis typical of the disease. Paper-13625808. Using DNA affinity, electrophoretic mobility shift assay, DNase I footprinting, and chromatin immunoprecipitation (ChIP), we found that CTCF binds both in vitro and in vivo to the EBV genome between OriP and Cp, with an approximately 50-bp footprint at EBV coordinates 10515 to 10560. Paper-12021059. Using DNase I footprinting performed with in vitro reconstituted human papillomavirus (HPV) chromatin and nucleosome-free DNA templates, we found that Brd4 facilitates E2 binding to its cognate sequences in chromatin depending on bromodomains and the E2- interacting region of Brd4. Paper-13587535. At the beta-globin locus, well-established DNase I hypersensitive sites stand out against a background in which actively transcribed gene sequences (e.g., beta-adult and beta-hatching) are no more sensitive than the nearby constitutive heterochromatin that has previously been shown to form the 30-nm fibre structure. Paper-13607256. PATIENTS: A total of 320 patients in clinically stable condition with documented CF and an FVC less than 40% of predicted were recruited from 65 CF Foundation care centers in the United States. The dornase alfa and placebo groups were comparable with respect to age (range, 7 to 57 years), height, and weight. Paper-713476. These results support the idea that GATA-1 interaction in HS2 has a prominent and direct role in co-activator and pol II recruitment conferring active histone tail modifications and transcription activation to a target gene but that it does not, by itself, play a major role in establishing DNase I hypersensitivity. Paper-12901877. Surprisingly, we found that human and bovine RPE expressed not only OTX2 but also CRX, the CRX genomic region in bovine RPE was hypersensitive to DNase I, consistent with active transcription, and that both OTX2 and CRX bound to the BEST1 proximal promoter in vivo. Paper-13495146. Well designed clinical studies performed in patients with CF and mild to moderate pulmonary disease [ forced vital capacity (FVC) > or = 40% of predicted value] show that aerosolised dornase alfa improves lung function, achieving a 6 to 7% increase from baseline in forced expiratory volume in 1 second (FEV1) after 6 months' therapy. Paper-8245255. After the blocking with bovine serum albumin, the immunosensor in flow-injection mode was used to detect the antibodies to dsDNA in purified protein solutions of antibodies to dsDNA and to single-stranded DNA, monoclonal human immunoglobulin G, DNase I and in blood serum of patients with bronchial asthma and systemic lupus erythematosus. Paper-13204630. Expression of a portion of the C terminus of NuMA that shares sequence similarity with the chromatin regulator HPC2 is sufficient to inhibit acinar differentiation and results in the redistribution of NuMA, chromatin markers acetyl-H4 and H4K20m, and regions of deoxyribonuclease I-sensitive chromatin compared with control cells. Paper-13099338. There was a 44% increase in cough transportability of sputum in vitro (p = 0.037) and a 71% increase in mucociliary transportability of sputum in vitro (p = 0.013) relative to control with the combination of dornase alfa and Tbeta4, but no significant change with dornase alfa or Tbeta4 alone at any concentration. Paper-12310625. The histone deacetylase inhibitor trichostatin A, but not the DNA methylation inhibitor 5'-aza-2'-deoxycytidine, re-established the expression of GATA4 and/or GATA6 in A2780 and HIO-114 cells, correlating with increased histone H3 and H4 acetylation, histone H3 lysine K4 methylation and DNase I sensitivity at the promoters. Paper-12203430. Deletion analysis of the distal GATA site and its neighboring sequence and DNase-I footprinting/EMSA ( electrophoretic mobility shift assay) analysis indicated that induced nuclear factor binding to GATA-1 and its neighboring sequence may be required for expression during MEL cell differentiation induced by dimethyl sulfoxide treatment. Paper-599395. These synonyms are used for gene DNASE1 (deoxyribonuclease I): FLJ44902, FLJ38093, DRNI, DNL1, DNase I, DKFZp686H0155, Deoxyribonuclease I, Deoxyribonuclease-1. These accession numbers are used for gene DNASE1: Q14UU9 (UNIPROT__AC), CAC12813 (NCBI_GENBANK__AC), BAA11841 (NCBI_GENBANK__AC), B4DV35 (UNIPROT__AC). DNASE1 is a homologue of zgc:92440 (zgc:92440) from Danio rerio. DNASE1 is a homologue of DNASE1 (deoxyribonuclease I) from Bos taurus. DNASE1 is a homologue of DNASE1 (deoxyribonuclease I) from Pan troglodytes. DNASE1 is a homologue of DNASE1 (deoxyribonuclease I) from Gallus gallus. DNASE1 is a homologue of DNASE1 (deoxyribonuclease I) from Canis lupus familiaris. DNASE1 is a homologue of Dnase1 (deoxyribonuclease I) from Mus musculus. DNASE1 is a homologue of Dnase1 (deoxyribonuclease I) from Rattus norvegicus. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann. |