ライフサイエンスコーパス: DNase I

1 DNase I administration significantly diminished plasma c

2 DNase I and Tn5 transposase assays require thousands to

3 DNase I DNA footprint assays show that AerR containing B

4 DNase I footprint analysis further defined the sequences

5 DNase I footprinting located the most proximal DNA bindi

6 DNase I footprinting showed that the VpsT binding site a

7 DNase I footprinting showed that this sequence lies with

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

9 DNase I hypersensitive sites (DHSs) are generic markers

10 DNase I hypersensitive sites (DHSs) provide important in

11 DNase I injected into experimental animals, moreover, re

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

13 DNase I is a sequence-specific enzyme, with a specificit

14 DNase I is a useful biomarker.

15 DNase I is an enzyme which cuts duplex DNA at a rate tha

16 DNase I protection studies as well as promoter fusion an

17 DNase I-hypersensitive site I (HSI) of the LCR is essent

18 00 constructs, corresponding to roughly 3500 DNase I hypersensitive (DHS) sites, into the mouse retin

19 e image analysis, electron microscopy, and a DNase I assay to show that hyperosmotic conditions (>400

20 tering, molecular dynamics simulations and a DNase I cleavage assay we found that the wild type hTERT

21 6-GATAC, was mapped to its own promoter by a DNase I footprint analysis.

22 slocation breakpoints in t-AMLs cluster in a DNase I hypersensitive region, which possesses cryptic p

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

24 This association requires a DNase I hypersensitive region (RHS6) at the Th2 locus.

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

26 Accordingly, DNase I footprinting analysis confirmed that AbrB bound

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

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

29 Administering DNase I to dissolve NETs, which have a high DNA content,

30 by electrophoretic mobility shift assay and DNase I footprinting.

31 r, electrophoretic mobility shift assays and DNase I footprinting revealed that OhrR binds directly t

32 l, electrophoretic mobility shift assays and DNase I footprinting showed that the ArcA and IscR bindi

33 by the use of gel mobility shift assays and DNase I footprinting.

34 atin-1s) prophylaxis given 1 hour before and DNase I 3 hours after CC injection completely prevented

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

36 re evaluated in DNA thermal denaturation and DNase I footprinting assays, and the ability to inhibit

37 located in GC-rich, nucleosome-depleted, and DNase I sensitive regions, flanked by well-positioned nu

38 , micrococcal nuclease (MNase) digestion and DNase I digestion, followed by deeply sequencing the res

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

40 results were referenced against enhancer and DNase I hypersensitive regions from ENCODE and Roadmap E

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

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

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

44 n of the activities of 3'-5' exonuclease and DNase I in cell lysates.

45 r agreement of DMRs with gene expression and DNase I hypersensitivity.

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

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

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

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

50 els of H3K4me2 and H3K27ac histone marks and DNase I hypersensitivity--signifying accessible, permiss

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

52 nhancer-associated histone modifications and DNase I hypersensitive sites.

53 atin states, transcription factor motifs and DNase I footprints, providing tools for epigenome-wide a

54 We utilized mutagenesis and DNase I footprinting to characterize YqjI regulation of

55 le in the dynamic changes of the numbers and DNase I sensitivity of DH sites during development.

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

57 d to DNA in combination with DMS probing and DNase I footprinting results supported the CoMA data.

58 e also significantly protected from MI/R and DNase I treatment had no further beneficial effect.

59 hese hypotheses, and promoter resections and DNase I footprinting assays revealed a single CepR2 bind

60 firmed by electrophoretic mobility shift and DNase I footprint assays.

61 Gel shift and DNase I footprinting assays confirmed the presence and l

62 ned using electrophoretic mobility shift and DNase I footprinting assays.

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

64 even histone marks, one histone variant, and DNase I hypersensitivity sites in seven cell lines.

65 cluding protein-coding genes, enhancers, and DNase-I hypersensitive sites in over 100 tissues and cel

66 occupied by the insulator protein CTCF, are DNase I hypersensitive and represent only a small minori

67 regulatory DNA elements can be identified as DNase I hypersensitive sites (DHSs).

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

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

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

71 ot hypersensitive to nuclease probes such as DNase I.

72 Restriction enzyme accessibility assay, DNase I footprinting and AFM experiments reveal perturbe

73 , transcriptional fusions, gel-shift assays, DNase I footprinting, and in vitro transcription, it was

74 lator that was analyzed by gel-shift assays, DNase I footprinting, and UV-vis spectroscopy.

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

76 TF DNA-binding sites obtained from the B1H, DNase I and SELEX methodologies are presented.

77 However, GATA-1 binding, DNase I hypersensitive site formation and several histon

78 3 groups: control (group 1), one i.v. bolus DNase I before CPB start (group 2) and a second DNase I

79 ficant reduction in CXCL8 levels achieved by DNase I treatment.

80 closed conformation of CNS-1, as assessed by DNase I hypersensitivity, along with enhanced accumulati

81 show that the intrinsic rate of cleavage by DNase I closely tracks the width of the minor groove.

82 of sequence preference spanning sites cut by DNase I in a number of published data sets.

83 ally in accessible regulatory DNA defined by DNase I hypersensitive sites.

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

85 alysis of Pol II-nucleosome intermediates by DNase I footprinting suggest that efficient O-loop forma

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

87 Furthermore, preprocessing of NETs by DNase I facilitated their clearance by macrophages.

88 Mechanistically, digestion of NETs by DNase I significantly diminished NETs-dependent upregula

89 Meanwhile, negatively charged DNase I was encapsulated in a positively charged acid-de

90 rved sequence element mapping to a chromatin DNase I hypersensitive site located within intron 1.

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

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

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

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

95 By correlating DNase I signal and gene expression, we predicted regulat

96 factor footprints, we produced high-density DNase I cleavage maps from 243 human cell and tissue typ

97 imarily used to identify nucleosome-depleted DNase I hypersensitive (DHS) sites genome-wide that corr

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

99 Here we describe DNase I-released fragment-length analysis of hypersensit

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

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

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

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

104 romatin, instead relying on the endonuclease DNase I.

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

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

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

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

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

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

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

112 27 k Illumina array, and with enrichment for DNase-I Hypersensitivity sites across the full range of

113 of a well characterized LCR containing four DNase I hypersensitive sites (HSs).

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

115 Genomic DNase I footprinting enables the quantitative, nucleotid

116 n regulatory evolution, we performed genomic DNase I footprinting of the mouse genome across 25 cell

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

118 ch for human silencers, we utilized H3K27me3-DNase I hypersensitive site (DHS) peaks with tissue spec

119 Additionally, sequence reads in HepG2 DNase-I-hypersensitivity and CEBPB ChIP-seq signals span

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

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

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

123 Employing deoxyribonuclease I (DNase I) as a model enzyme template, we prepared surface

124 Deoxyribonuclease I (DNase I) is an important enzyme that cleaves both double

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

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

127 f altered nucleosome occupancy or changes in DNase I hypersensitivity.

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

129 thirds act through binding events located in DNase I hypersensitive sites.

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

131 oteins were partially purified and tested in DNase I footprinting experiments with the excisive attac

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

133 with myocardial infarction exhibit increased DNase I activity.

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

135 signal reduction as a function of increasing DNase I concentration.

136 t formation along the gradient of increasing DNase I concentrations is used to determine the accessib

137 Here, we show that hormone-induced DNase I hypersensitivity changes (DeltaDHS) are highly p

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

139 Care must be taken when interpreting DNase I results, especially when looking at the precise

140 ing sites in promoter regions that intersect DNase I hypersensitive sites (DHSs).

141 g bacteria by prophylaxis with intravascular DNase I alone.

142 tor binding sites are derived from intrinsic DNase I cleavage bias rather than from specific protein-

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

144 cluding expression quantitative trait locus, DNase I sensitivity quantitative trait locus and functio

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

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

147 ine-scale structure within about 1.6 million DNase I-hypersensitive sites and show that the overwhelm

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

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

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

151 Through a nonbiased DNase I hypersensitivity assay, four novel regulatory re

152 luding DNase-seq, which is based on nuclease DNase I, and ATAC-seq, which is based on transposase Tn5

153 , AP endonuclease, duplex-specific nuclease, DNase I, or T7 exonuclease.

154 and affects the organization of nucleosomes, DNase I hypersensitivity, and the transcriptional profil

155 Bound regions covered 80% of DNase I hypersensitive sites including 99.7% of TSS and

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

157 In an acidic environment, the activity of DNase I was activated through the acid-triggered sheddin

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

159 The addition of DNase I to growth medium significantly reduced biofilm f

160 Administration of DNase I to mice reduced neutrophil infiltration and tiss

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

162 We observed that physiological amounts of DNase I do not suffice to completely degrade NETs in vit

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

164 Analysis of DNase I hypersensitive sites sequencing data revealed an

165 However, an extended analysis of DNase I-hypersensitive sites (DHSs) spanning the entire

166 tudies have created genome-scale catalogs of DNase I hypersensitive sites (DHSs), which demark potent

167 We first defined more than 1800 clusters of DNase I hypersensitive sites (DHSs) with similar tissue

168 Both monotherapies and coadministration of DNase I and rhADAMTS13 revealed a cardioprotective effec

169 In contrast, quantitative comparison of DNase I hypersensitivity between states can predict tran

170 erformed the first genome-wide comparison of DNase I sensitivity of chromatin in mitosis and interpha

171 600 times the physiological concentration of DNase I.

172 olymeric nanogel to facilitate decoration of DNase I into the NCl by electrostatic interactions.

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

174 robed by digesting nuclei with a gradient of DNase I followed by locus-specific PCR.

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

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

177 displayed significantly different levels of DNase I sensitivity within the two tissues.

178 port consistent patterns of gain and loss of DNase I-hypersensitive sites (DHSs) as cells progress fr

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

180 Genome-wide mapping of DNase I hypersensitive sites revealed an open chromatin

181 rate that it enables simultaneous mapping of DNase I hypersensitivity and regional DNA methylation le

182 enerated genome-wide high-resolution maps of DNase I hypersensitive (DH) sites from both seedling and

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

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

185 The LCR is composed of a number of DNase I-hypersensitive sites (HSs), which are believed t

186 scription start sites, reduces the number of DNase I-hypersensitive sites genome wide, and decreases

187 atory element located in an adjacent pair of DNase I HS located 5.6 kb 3' of the ANK1E promoter at th

188 respectively, displayed distinct patterns of DNase I hypersensitivity, histone acetylation and NFAT1

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

190 Sequencing of DNase I hypersensitive sites (DNase-seq) is a powerful t

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

192 gulated by two partially overlapping sets of DNase I hypersensitive sites (HSs) that constitute the p

193 apped the location and allele-specificity of DNase I hypersensitive (DH) sites within the PWS-IC in b

194 c identification of hundreds of thousands of DNase I hypersensitive sites (DHS) per cell type has bee

195 The use of DNase I accessibility to define proximal promoter border

196 Through use of DNase I footprinting, we demonstrate that BpaB binds the

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

198 dentified in chicken lung overlapped half of DNase-I hypersensitive sites, coincided with active hist

199 degradation including a direct inhibition of DNase-I by C1q.

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

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

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

203 entified binding sites for >700 TFs from one DNase I hypersensitivity analysis followed by sequencing

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

205 e of these seven loci lay within enhancer or DNase I hypersensitivity regions in lung fibroblasts or

206 ped, based mostly on histone modification or DNase I hypersensitivity data in conjunction with DNA mo

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

208 Previously, DNase I hypersensitivity sites were reported to explain

209 okines, which is characterized by four Rad50 DNase I hypersensitive sites (RHS4-7).

210 urokinase, or DNA digestion with recombinant DNase I all prevented arterial occlusions, GFR loss, and

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

212 We call these regions DNase I annotated regions of nucleosome stability (DARNS

213 Here we demonstrate that high-resolution DNase I cleavage profiles can provide detailed informati

214 oclew (NCl) embedded with an acid-responsive DNase I nanocapsule (NCa) was developed for targeted can

215 We developed a robust DNase I-polymerase chain reaction (PCR) protocol for the

216 se I before CPB start (group 2) and a second DNase I dose before reperfusion (group 3).

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

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

219 n immunoprecipitation sequencing (ChIP-seq), DNase I hypersensitive sites sequencing (DNase-seq), and

220 exhibited strong resistance to both soluble DNase I and membrane-bound DNase on cells.

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

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

223 at the 3' boundary of an erythroid-specific DNase I-sensitive chromatin domain.

224 In modeling the sequence-specific DNase I cutting bias, we found a strong effect that vari

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

226 with several traits, and cell-type-specific DNase-I hypersensitive sites were enriched with SNPs ass

227 Altogether, systemic DNase I administration during CPB efficiently reduced cf

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

229 In mice given taurocholate, DNase I administration also reduced expression of integr

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

231 modes of interaction with chromatin and that DNase I hypersensitivity dynamics provides a general app

232 vasive bioluminescent imaging confirmed that DNase I treatment was sufficient to suppress tumor metas

233 Thus, our studies demonstrate that DNase I hypersensitive sites HS1-2 within the Vkappa-Jka

234 oximately 40 yr ago it was demonstrated that DNase I also digests with a approximately 10-bp periodic

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

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

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

238 tructural and biochemical data implicate the DNase I binding loop (D-loop) of actin in such nucleotid

239 nd disulfide cross-linking of Cys-41 (in the DNase I binding loop) to Cys-374 (C-terminal) but increa

240 s-40-Lys-50 segment of actin, located in the DNase I binding loop.

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

242 vestigated the conditions that inhibited the DNase I activity.

243 est strip, we have successfully measured the DNase I activity and determined the factors that influen

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

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

246 Using the DNase I test strip, we have successfully measured the DN

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

248 up multiple favorable interactions with the DNase-I binding loop in subdomain 2 of the adjacent subu

249 Integration of these DNase I cleavage data with bisulfite sequencing data for

250 Consistent with this, DNase I accessibility in regions flanking the GAA repeat

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

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

253 and H3K27me3, an increased accessibility to DNase I and an induction of euchromatic H3 and H4 histon

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

255 open chromatin that may not be accessible to DNase I or Tn5.

256 chromatin regions that are not accessible to DNase I or Tn5.

257 tin of pluripotency genes more accessible to DNase I.

258 rate that a 650-bp sequence corresponding to DNase I hypersensitive sites HS1-2 within the mouse Igka

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

260 e small size of the MNase enzyme relative to DNase I or Tn5 allows its access to relatively more cond

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

262 ompacts NETs, increasing their resistance to DNase I.

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

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

265 ue-specific demethylation were restricted to DNase I hypersensitive sites within this locus.

266 enylation sites tend to be less sensitive to DNase I.

267 tory proteins is a pronounced sensitivity to DNase I digestion.

268 ENCODE Consortium has mapped transcription, DNase I hypersensitivity, transcription factor binding,

269 ronic sequence containing an uncharacterized DNase I hypersensitivity (DHS) site located 3' to the si

270 with those of enhancers and exhibited unique DNase I hypersensitivity profiles that reflected the pot

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

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

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

274 Analyses using DNase I hypersensitivity assay and chromosome conformati

275 targeting extracellular DNA and VWF by using DNase I with/without rhADAMTS13.

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

277 Additionally, experiments using DNase I showed that purified recombinant H-NS protected

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

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

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

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

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

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

284 While DNase I hypersensitivity (HS) is a good predictor of act

285 eling the magnitude and shape of genome-wide DNase I hypersensitivity profiles to identify transcript

286 tiling microarrays to establish genome-wide DNase I sensitivity landscapes.

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

288 matin, and are significantly associated with DNase I hypersensitivity.

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

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

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

292 ngly, treatment of cancer cell cultures with DNase I to degrade DNA nonspecifically reduced metastati

293 Our data with DNase I footprinting provide mechanistic insights and su

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

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

296 ayed, respectively, by dismantling NETs with DNase I treatment.

297 Treatment with DNase I significantly degraded NETs and reduced citrulli

298 Treatment of biofilms formed in urea with DNase I reduced the biofilm, indicating that extracellul

299 o-derived motifs mapped to the genome within DNase I hypersensitivity footprints to characterize regi

300 In this work, DNase I footprinting measurements were employed to inves