ライフサイエンスコーパス: DNase

1 DNase 1 was given to assess the effects of extracellular

2 DNase 1, which disrupts NETs, accelerated wound healing

3 DNase Hi-C uses DNase I for chromatin fragmentation, lea

4 DNase I and Tn5 transposase assays require thousands to

5 DNase I hypersensitive sites (DHSs) are a hallmark of ch

6 DNase I hypersensitive sites (DHSs) provide important in

7 DNase I is a secreted enzyme whose function has been pre

8 DNase I is a useful biomarker.

9 DNase II digests DNA in endolysosomes.

10 single intracoronary infusion of 1 x 10(13) DNase-resistant particles of AAV1/SERCA2a or placebo.

11 00 constructs, corresponding to roughly 3500 DNase I hypersensitive (DHS) sites, into the mouse retin

12 ing affinity to Im7 but was inactivated as a DNase.

13 The Lockd promoter contains a DNase-hypersensitive site, binds numerous transcription

14 This variant lies in a DNase 1 hypersensitivity site (DHS) upstream of both the

15 In silico analyses located a DNase I hypersensitivity site to rs7692387 and predicted

16 Herein, the construction of a DNase-mimetic artificial enzyme (DMAE) for anti-biofilm

17 The structure reveals a DNase-I-type fold with a hydrophobic track leading to th

18 motif, with reduced SNP density, and with a DNase footprinting signal in all tested cells.

19 Biallelic mutations abrogating DNase activity cause autoimmunity by allowing immunogeni

20 Accordingly, DNase I footprinting analysis confirmed that AbrB bound

21 own by caspase-3 cleavage, caspase-activated DNase levels, and terminal deoxynucleotidyl transferase-

22 The 3'11-mer CpG-A fragment activates DNase II-deficient DCs.

23 binary complex functioned as a highly active DNase to destroy a large excess DNA substrate, which cou

24 Nuclease activity (DNase, RNase, dsRNase) was concentrated in the salivary

25 We adapted DNase-seq to nuclei isolated from C. elegans embryos and

26 In plants, adding DNase I to root tips eliminates border cell extracellula

27 ient thrombi was more successful when adding DNase 1 to standard t-PA.

28 In addition, DNase I significantly reduced IL-6 and TNF-alpha levels

29 Deletion of sda1 or all DNase genes in M1T1 strain MGAS2221 did not alter emerge

30 for transcription factors (TFs) binding and DNase-seq experiments.

31 ipitation sequencing and microarray data and DNase I hypersensitive site sequencing data.

32 ive trait loci (eQTLs) for AHI1 and DEXI and DNase hypersensitivity sites in FOXP3(+) regulatory T ce

33 EMSAs and DNase I footprinting showed that the [4Fe-4S] form of Sc

34 n start and termination sites, enhancers and DNase I hypersensitive sites.

35 pression quantitative trait loci (eQTLs) and DNase I sensitivity quantitative trait loci (dsQTLs) in

36 f genes and enriched at enhancers, exons and DNase I hypersensitivity sites.

37 In the vicinity of active genes and DNase I hypersensitive sites nucleosomes are organized i

38 ree hypothetical protein-encoding genes, and DNase I footprint analysis identified the specific nucle

39 nce of NET-dissolving drugs like heparin and DNase I, already in clinical use, and recent development

40 nt downregulation of those encoding Hsf4 and DNase IIbeta, which are implicated in the denucleation p

41 Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues d

42 ng DNA methylation, histone modification and DNase I hypersensitivity profiling as well as Hi-C to in

43 as positions of 4 histone modifications and DNase hypersensitive sites, Wilson et al reveal many mor

44 A variants in histone modification peaks and DNase hypersensitivity sites in B cells.

45 gel retardation, potassium permanganate and DNase I footprinting, cleavage reactions with protein co

46 protein of L. pneumophila has both RNase and DNase activities, with the RNase activity being more pro

47 have been reported, few combine ChIP-seq and DNase-seq data analysis and quality control in a unified

48 anscription factor binding from ChIP-seq and DNase-seq data, and scores variants by computing the cha

49 ty control and data analyses of ChIP-seq and DNase-seq data.

50 ool to process large batches of ChIP-seq and DNase-seq datasets.

51 ollaborative projects involving ChIP-seq and DNase-seq from different designs.

52 ChIP-seq and DNase-seq further revealed that DNA hypermethylation in

53 ChIP-seq and DNase-seq have become the standard techniques for studyi

54 presents the most comprehensive ChIP-seq and DNase-seq related quality metric resource currently avai

55 derived from over 23,677 public ChIP-seq and DNase-seq samples (11,265 datasets) from eight literatur

56 g-based genomics assays such as ChIP-seq and DNase-seq, the epigenomic characterization of a cell typ

57 c datasets from these mice using RNA-Seq and DNase-Seq.

58 el on publicly available transcriptomics and DNase-seq data and assessed the predictive power of the

59 Tn5 transposase and DNase I sequencing-based methods prefer native or high c

60 In this study, we applied DNase-seq (DNase I hypersensitive site sequencing) to st

61 DNA-cleaving enzymes such as DNase I have been used to probe accessible chromatin.

62 ions negatively correlated with LLD, such as DNase I hypersensitivity sites (DHSs).

63 taking into account epigenomic data such as DNase I sensitivity or histone modification data.

64 chromatin, as detected by techniques such as DNase-seq and FAIRE-seq.

65 ccessibility and DNA methylation patterns at DNase hypersensitive sites (DHSs).

66 exploits information from H3K27ac signal at DNase I hypersensitive sites identified from published h

67 ly respond to RNA-associated ligands because DNase II-mediated degradation of self-DNA is required fo

68 NETs degradation by DNase I promoted NET-protein clearance and protected aga

69 ation is blocked by a TLR7/8/9 inhibitor, by DNase, and by the PDE4 inhibitor rolipram.

70 de regulatory element activities measured by DNase I hypersensitivity (DH).

71 le genomic sites mapped in 164 cell types by DNase-seq, and demonstrate greater predictive accuracy t

72 ultrasensitive strategy, called single-cell DNase sequencing (scDNase-seq) for detection of genome-w

73 Single-cell DNase sequencing (scDNase-seq) is a method of detecting

74 of size-selected DNase I-treated chromatin (DNase-seq) allows high-resolution measurement of chromat

75 rivate disruptive mutations within fetal CNS DNase I hypersensitive sites (i.e., putative regulatory

76 The colicin DNase-Im interaction is a model system for the study of

77 An assay combining DNase I digestion and CMV quantitative polymerase chain

78 n this study, we report that some commercial DNase preparations are contaminated with proteases.

79 ugh a combination of mammalian conservation, DNase hypersensitivity, and histone modification from EN

80 m reveals strong enhancer regions containing DNase I hypersensitive sites overlapping the rs874040 li

81 Conventional DNase sequencing (DNase-seq) for genome-wide DHSs profil

82 s that cannot be analyzed using conventional DNase I sequencing because of the requirement for millio

83 f ChIP-seq and chromatin accessibility data (DNase-seq and ATAC-seq) published before January 1, 2016

84 tory region type, motif sequence degeneracy, DNase accessibility and pairing genomic distance.

85 tors and those within frontal cortex-derived DNase I hypersensitivity sites are significantly enriche

86 ntibodies, brefeldin A, diphenyleneiodonium, DNase or blocking F(ab')2 fragments to CD16, CD18, CD32

87 e hundred thousand genomic loci that display DNase I hypersensitivity in one or more ENCODE cell line

88 Specifically, exploiting a distinctive DNase I cleavage profile within nucleosome-associated DN

89 These structures represent divergent DNase-Im subfamilies and are important in extending our

90 s for identifying regulatory regions in DNA (DNase-seq, ChIP-seq, FAIRE-seq, ATAC-seq).

91 4)-10(-17) M) complex between the Colicin E7 DNase (CE7) and its inhibitor, Immunity protein 7 (Im7).

92 hylogenetic conservation as well as elevated DNase I hypersensitivity (DHS) in ENCODE cell lines.

93 Over half of embryonic DNase I hypersensitive sites (DHSs) were annotated as no

94 minant frameshift (fs) mutations that encode DNase-active but mislocalized proteins cause disease.

95 ntegrating conjugative element (ICE)-encoded DNase, which we name IdeA, is necessary and sufficient f

96 romatin, instead relying on the endonuclease DNase I.

97 the current high-throughput sequencing era, DNase I has mainly been used to study genomic regions de

98 f divalent metal ions, similar to eukaryotic DNase II.

99 velopment is illustrated by direct evidence: DNase I added to tumor cells eliminates the structures a

100 ranscription factor footprints from existing DNase-seq data derived from central nervous system tissu

101 Treatment with CLI reduced extracellular DNase Sda1 and streptolysin O (SLO) activity in vivo, wh

102 Extracellular DNases (exDNases) of pathogens promote virulence and sys

103 he structure of RecJ, a 5' --> 3' DHH family DNase and other DHH family nanoRNases, Bacillus NrnA has

104 For individual chromatin features, DNase I enables high and consistent predictions.

105 rimetric readout would make the lateral flow DNase I test strip a suitable platform for point-of-care

106 we used potassium permanganate footprinting, DNase I footprinting, and in vitro transcription from th

107 Module genes were also enriched for DNase I hypersensitivity footprints and binding from fou

108 riants at the 20 eGFR loci were enriched for DNase I hypersensitivity sites (DHSs) in human kidney ce

109 27 k Illumina array, and with enrichment for DNase-I Hypersensitivity sites across the full range of

110 site annotation and motif identification for DNase-seq, analysis of nascent transcription from Global

111 with a DNA fragment including only its four DNase I hypersensitive sites (lacking the large spacer r

112 We generated 27 Gb DNase-seq and 67.6 Gb RNA-seq data to investigate chroma

113 We use allelically resolved genomic DNase I footprinting data encompassing 166 individuals a

114 regions of low nucleosome occupancy and high DNase I hypersensitivity.

115 These 6-mer motif sites showed higher DNase I hypersensitivity and are flanked by strongly pha

116 DNA motif pairs exhibit substantially higher DNase accessibility than the background sequences.

117 ility occurs primarily within narrow, highly DNase hypersensitive sites that frequently coincide with

118 However, DNase treatment after nucleic acid extraction to remove

119 ificant co-occurring DNA motifs in 349 human DNase I hypersensitive site datasets.

120 Although deoxyribonuclease I (DNase I) was used to probe the structure of the nucleoso

121 alfa (recombinant human deoxyribonuclease I, DNase), demonstrating DNA degradation and improved NP pe

122 Deoxyribonuclease II (DNase II) is also known as acid deoxyribonuclease becaus

123 Chromatin immunoprecipitation, DNase I hypersensitivity and transposase-accessibility a

124 Importantly, DNase although very effective at DNA removal, and somewh

125 In DNase II-deficient mice, the excessive accrual of undegr

126 sing triple knockout (TKO) mice deficient in DNase II/IFNaR together with deficiency in either stimul

127 We observed significant enrichment in DNase I hypersensitive sites in fetal heart and lung.

128 tify candidate noncoding driver mutations in DNase I hypersensitive sites in breast cancer and experi

129 le of a co-evolved substitution where Pro in DNase loop 4 occupies the volume vacated and removes the

130 he large multiplicity of sequence signals in DNase- or ATAC-seq maps.

131 Enzymatically inactive DNase II mutants cannot rescue CpG-A responses.

132 me-widely using chromatin features including DNase I hypersensitivity, 11 histone modifications (HMs)

133 the accessible chromatin landscape including DNase-seq, FAIRE-seq and ATAC-seq.

134 with myocardial infarction exhibit increased DNase I activity.

135 chromatin structure, resulting in increased DNase I sensitivity, the accumulation of DNA damage, and

136 h LAMP-2(+) lysosomes than CpG-B and induces DNase II localization in LAMP-2(+) lysosomes.

137 Here, we develop a low-input DNase I sequencing (liDNase-seq) method that allows us t

138 Interestingly, DNase II has also been identified in a few genera of bac

139 ing CpG site methylation, CGIs, co-localized DNase I hypersensitive sites, transcription factor bindi

140 reveals that DUX4 binds two classes of loci: DNase accessible H3K27Ac-rich chromatin and inaccessible

141 and plasma cells by inducing and maintaining DNase I hypersensitive sites.

142 while interactions involving actively marked DNase accessible elements are enriched both at short (<5

143 these elements have active chromatin marks, DNase hypersensitivity, and occupancy by multiple transc

144 Current methods of measuring DNase I relies either on an immunochemical assay, which

145 e Illumina 450 k DNA methylation microarray, DNase hypersensitivity sequencing, single-cell ATAC sequ

146 We then mined DNase-seq data to identify putative active CRMs and TF f

147 de maps for 17 TFs, 3 histone modifications, DNase I hypersensitive sites, and high-resolution promot

148 The saliva-induced NETs were more DNase-resistant and had higher capacity to bind and kill

149 Moreover, DNase-seq and chromatin conformation capture (3C) define

150 es identified from published human and mouse DNase-seq data.

151 characterization of the most highly mutated DNase I hypersensitive sites in breast cancer (using in

152 he high environmental sensitivity of natural DNase in anti-biofilm applications, DMAE exhibited a muc

153 Nevertheless, DNase somewhat reduces responses to some Ags with alum.

154 NFAT and AP-1 which created thousands of new DNase I-hypersensitive sites (DHSs), enabling ETS-1 and

155 was completely diminished by RNase, but not DNase.

156 arget protein and the inhibitor, and a novel DNase protection assay measured chemical inhibition of p

157 s are responsible for most of the ability of DNase preparations to inhibit alum's adjuvant activity.

158 In the absence of DNase II, undigested DNA activates cytoplasmic DNA-sensi

159 se increases were enhanced by the actions of DNase I.

160 Interestingly, addition of DNase I reduced the numbers of EPEC bacteria recovered a

161 NETs were depleted by administration of DNase I to mice.

162 Global analyses of DNase I-hypersensitive sites and 3D genome architecture,

163 orms a comprehensive k-mer-based analysis of DNase footprints to determine any k-mer's potential for

164 The effect of DNase is independent of its ability to cleave DNA, sugge

165 ture Hi-C with target-sequence enrichment of DNase I hypersensitive sites.

166 se effectors, RhsA, belongs to the family of DNase enzymes, the activity of the other was not apparen

167 uired for chromatin binding and induction of DNase I hypersensitive sites.

168 localize with, and maintain the intensity of DNase I hypersensitive sites genome wide, in resting but

169 ion of association tests, prior knowledge of DNase-I hypersensitivity sites or other relevant biologi

170 tations in DNASE2, associated with a loss of DNase II endonuclease activity.

171 s-regulatory elements; therefore, mapping of DNase I hypersensitive sites (DHSs) enables the detectio

172 q) method that allows us to generate maps of DNase I-hypersensitive site (DHS) of mouse preimplantati

173 immunochemical assay for the measurement of DNase I activity on the test strip.

174 atomic structure and catalytic mechanism of DNase II.

175 ity genes-those with a large total number of DNase-mapped enhancers across the lineage-differ archite

176 AS or eQTL phenotypes are located outside of DNase-seq footprints.

177 The presence of DNase I would cleave the reporter probe and lead to redu

178 Deep sequencing of DNase-seq libraries and computational analysis of the cu

179 e, we use a recent comprehensive data set of DNase I sequencing-identified cis-regulatory binding sit

180 te lung injury (ALI) and assessed the use of DNase I, for the treatment of ALI.

181 on of extracellular DNA through secretion of DNases.

182 It relies on DNase I-mediated detachment of chromatin from the nuclea

183 VM accurately predicts the impact of SNPs on DNase I sensitivity in their native genomic contexts and

184 Instead, ORC binds nonspecifically to open (DNase I-hypersensitive) regions containing active chroma

185 t was negated by either a TLR9 antagonist or DNase treatment.

186 PAD4 deficiency or DNase 1 similarly protected hearts from fibrosis.

187 sequencing experiments (such as ChIP-seq or DNase-seq) and models the change in enhancer signature u

188 including at enhancers, promoters, and other DNase hypersensitive regions not marked with canonical h

189 t require genetically modified histones, our DNase-based approach is easily applied in any organism,

190 Here we present PlantDHS, a plant DNase I hypersensitive site (DHS) database that integrat

191 Previously, DNase I hypersensitivity sites were reported to explain

192 the experiments used commercially purchased DNase and showed that coinjection of these DNase prepara

193 CMV quantitative polymerase chain reaction (DNase-CMV-qPCR) was developed to differentiate free nake

194 systemic lupus erythematosus exhibit reduced DNase I activity, and patients with myocardial infarctio

195 1 and therefore endosomal TLRs, also require DNase II deficiency in both donor and host compartments,

196 egions in various cells using Encode Roadmap DNase-hypersensitive site data.

197 Deep sequencing of size-selected DNase I-treated chromatin (DNase-seq) allows high-resolu

198 In this study, we applied DNase-seq (DNase I hypersensitive site sequencing) to study changes

199 ell technologies (e.g. single-cell ATAC-seq, DNase-seq or ChIP-seq) have made it possible to assay re

200 ly accumulating publicly available ChIP-seq, DNase-seq and ATAC-seq data are a valuable resource for

201 g (ChIP-Seq), histone modification ChIP-Seq, DNase-Seq and RNA-Seq.

202 nctional genomic assays, including ChIP-seq, DNase-seq, FAIRE-seq and others.

203 Using HTS data from a variety of ChIP-seq, DNase-seq, FAIRE-seq, and ATAC-seq experiments, we show

204 A-seq, nucleosome positioning for MNase-seq, DNase hypersensitive site mapping, site annotation and m

205 sets including ChIP-seq, RNA-seq, MNase-seq, DNase-seq, GRO-seq, and ATAC-seq data.

206 ity relative to existing methods in RNA-seq, DNase-seq and ChIP-seq data.

207 Conventional DNase sequencing (DNase-seq) for genome-wide DHSs profiling is limited by

208 ility experiments such as DNaseI sequencing (DNase-seq) and Assay for Transposase Accessible Chromati

209 favorably with published DNaseI sequencing (DNase-seq) results and it requires less than 50 000 nucl

210 Sasquatch only requires a single DNase-seq data set per cell type, from any genotype, and

211 nteractions supported by CTCF binding sites, DNase accessibility, and/or active histone marks.

212 Libraries generated by in situ DNase Hi-C have a higher effective resolution than tradi

213 Importantly, in situ DNase Hi-C obviates the dependence on a restriction enzy

214 Like traditional Hi-C protocols, in situ DNase Hi-C requires that chromatin be chemically cross-l

215 re using a novel 3C protocol, termed in situ DNase Hi-C.

216 ions induced expression and activity of SLO, DNase, and Streptococcus pyogenes cell envelope protease

217 Here we profile parental allele-specific DNase I hypersensitive sites in mouse zygotes and morula

218 ntify 76 genes with paternal allele-specific DNase I hypersensitive sites that are devoid of DNA meth

219 regions and in particular in tissue-specific DNase I hypersensitivity sites (DHSs).

220 Surprisingly, DNase-accessible euchromatin is protected from UV, while

221 tiviral single guide RNA libraries to target DNase I hypersensitive sites surrounding a gene of inter

222 We applied targeted DNase Hi-C to characterize the 3D organization of 998 la

223 We identify ten DNase I hypersensitive sites that are significantly muta

224 Each monomer of B. thailandensis DNase II exhibits a similar overall fold as phospholipas

225 The crystal structure of B. thailandensis DNase II shows a dimeric quaternary structure which appe

226 that recombinant Burkholderia thailandensis DNase II is highly active at low pH in the absence of di

227 Moreover, we demonstrate that DNase II is required for TLR9 activation by bacterial ge

228 g studies have instead yielded evidence that DNase I plays a central role in newly defined dynamics o

229 We found that DNase treatment of poliovirus RNA followed by random rev

230 This could imply that DNase-seq footprinting is too insensitive an approach to

231 Here we show that DNase II is required for TLR9.

232 Here, we reveal for the first time that DNase I can be used to precisely map the (translational)

233 mutation of the HD motif only abolished the DNase activity in vitro.

234 By analyzing the DNase I hypersensitive sites under 349 experimental cond

235 hment folds from 1.36 to 3.1) as well as the DNase hypersensitive sites (1.58-2.42 fold), H3K4Me1 (1.

236 e superantigens SSA and SpeC, as well as the DNase Spd1.

237 erated by complementary substitutions at the DNase-Immunity protein binding interface.

238 variants, and DNA methylation changes in the DNase I hypersensitivity based regulatory network.

239 vestigated the conditions that inhibited the DNase I activity.

240 due to the extensive characterization of the DNase hypersensitivity sites, modification of chromatin,

241 cleosomal DNA; the oscillatory nature of the DNase I cleavage profile within nucleosomal DNA enables

242 s between receptor loading, lifetimes of the DNase I hypersensitivity sites (DHSs), long-range intera

243 Recent reports point to limitations of the DNase-based genomic footprinting approach and call into

244 changes in the structure and dynamics of the DNase-I loop, alterations in the structure of the H73 lo

245 g three chromatography steps, over which the DNase activity was largely separated from the dNTPase ac

246 d DNase and showed that coinjection of these DNase preparations with alum and Ag reduced the host's i

247 ond the need for guide-target pairing, this "DNase H" activity has no apparent sequence requirements,

248 il loci drive gene-expression changes though DNase-I hypersensitive sites (DHSs) near transcription s

249 nce and protected against ALI in mice; thus, DNase I may be a new potential adjuvant for ALI therapy.

250 on measurement of chromatin accessibility to DNase I cleavage, permitting identification of de novo a

251 data define a type I interferonopathy due to DNase II deficiency in humans.

252 were identified based on hypersensitivity to DNase I digestion and association with H3K4me3-modified

253 d cellular internalization and resistance to DNase I compared to free synthetic nucleic acids, they s

254 low salt and up to tenfold more resistant to DNase I digestion than when uncoated.

255 ce of nanoparticles were highly resistant to DNase I endonucleases, and degradation was carried out e

256 elements: short genomic regions sensitive to DNase digestion that are strongly bound by known insulat

257 P. aeruginosa biofilm formation similarly to DNase, suggesting interference with the pyocyanin-depend

258 ession (GTEx) data using distance from TSSs, DNase hypersensitivity sites, and six histone modificati

259 gical inflammation in the joint depends upon DNase II deficiency in both donor hematopoietic cells an

260 Here, we use DNase-seq in combination with analysis of histone modifi

261 first documentation that plant pathogens use DNases to modulate their biofilm structure for systemic

262 at HRG modulates the contact system, we used DNase, RNase, and antisense oligonucleotides to characte

263 To identify cis-acting elements, we used DNase-seq and H3K4me1 and H3K27Ac ChIP-seq to map open a

264 We used DNase-seq to map accessibility of cis-regulatory element

265 DNase Hi-C uses DNase I for chromatin fragmentation, leading to greatly

266 atch, a new computational approach that uses DNase footprint data to estimate and visualize the effec

267 ed a recently developed Hi-C assay that uses DNase I for chromatin fragmentation to mouse F1 hybrid s

268 Using DNase I hypersensitivity methods and ENCODE data, we hav

269 Using DNase-seq data from the ENCODE project, we show that a l

270 Using DNase-seq data improved predictions of tissue-specific e

271 Genome-wide footprinting analysis using DNase-seq provides little evidence for TR footprints bot

272 recise AioR binding site was confirmed using DNase I foot-printing.

273 s during hematopoietic differentiation using DNase-seq, histone mark ChIP-seq and RNA sequencing to m

274 s for over 50 years, the potential for using DNase I as a clinical tool to prevent or treat cancer re

275 Furthermore, using DNase I in a nuclease degradation assay, G4-T-oligo was

276 with open chromatin regions identified using DNase I hypersensitivity assays, and are enriched in the

277 frozen and all 10 fresh samples tested using DNase-CMV-qPCR.

278 seq data with similar accuracy as when using DNase-seq data.

279 based on cuts in linker regions, we utilize DNase I cuts both outside and within nucleosomal DNA; th

280 acterial competition activity of the type VI DNase toxins Tde1 and Tde2.

281 Dissolution of NETs via DNase I did not alter anti-glomerular basement membrane

282 Removal of NETs via DNase infusion, or in peptidylarginine deiminase-4-defic

283 vely parallel sequencing has enabled in vivo DNase I footprinting on a genomic scale, offering the po

284 Whereas DNase or FVII knockdown had no effect, carotid occlusion

285 Regulatory DNA elements are associated with DNase I hypersensitive sites (DHSs).

286 Enrichment of SNPs associated with DNase I-hypersensitive sites was also found in many tiss

287 TOP2B associates with DNase I hypersensitivity sites, allele-specific transcri

288 ingle nucleotide resolution, coincident with DNase hypersensitive and ATAC-seq sites at a low sequenc

289 However, correlations with DNase I hypersensitive sites were different for all vect

290 ries, cells are lysed and then digested with DNase I.

291 obust and recoverable artificial enzyme with DNase-like activity was obtained, which exhibited high c

292 The advent of DNA footprinting with DNase I more than 35 years ago enabled the systematic an

293 Targeting of NETs with DNase 1 might have prothrombolytic potential in treatmen

294 eutrophil elastase or by degrading NETs with DNase protects mice from type-2 immunopathology.

295 incubation of purified malaria pigment with DNase abrogated IFN-beta induction.

296 ming ex vivo lysis of retrieved thrombi with DNase 1 and t-PA.

297 romatin Model (SCM), which when trained with DNase-seq data for a cell type is capable of predicting

298 Treatment with DNase I significantly degraded NETs and reduced citrulli

299 Upon treatment with DNase, levan aggregates dispersed.

300 sputum, tobramycin NPs both with and without DNase functionalisation, exhibited anti-pseudomonal effe