ライフサイエンスコーパス: DNase I

1 DNase I and Tn5 transposase assays require thousands to

2 DNase I DNA footprint assays show that AerR containing B

3 DNase I footprint analysis further defined the sequences

4 DNase I footprinting located the most proximal DNA bindi

5 DNase I footprinting showed that the VpsT binding site a

6 DNase I footprinting showed that this sequence lies with

7 DNase I footprinting with these sequences confirmed trip

8 DNase I footprints for these regulators were indicative

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

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 assays demonstrated that the CO-assoc

17 DNase I protection studies as well as promoter fusion an

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

19 00 constructs, corresponding to roughly 3500 DNase I hypersensitive (DHS) sites, into the mouse retin

20 nkyrin 1 (ANK1E) core promoter contains a 5' DNase I hypersensitive site (HS) with barrier insulator

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

22 6-GATAC, was mapped to its own promoter by a DNase I footprint analysis.

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

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

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

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

27 Accordingly, DNase I footprinting analysis confirmed that AbrB bound

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

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

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

31 saline, provided partial protection against DNase I digestion and exhibited the highest gene transfe

32 trol region (LCR), was revealed by analyzing DNase I hypersensitive sites, H3K4 trimethylation marks

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

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

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

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

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

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

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

40 ctrophoretic mobility shift assay (EMSA) and DNase I protection.

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

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

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

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

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

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

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

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

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

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

51 Chromatin immunoprecipitation and DNase I digestion assays indicate that BAF250a regulates

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

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

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

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

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

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

58 anges in both local nucleosome occupancy and DNase I hypersensitivity.

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

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

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

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

63 onsisting of the RNase H, S1, 5'-sensor, and DNase I subdomains) of E. coli NRne.

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

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

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

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

68 ormatic analyses using H3K4Me1, H3K4Me3, and DNase-I hypersensitivity chromatin signatures and evolut

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

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

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

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

73 ot hypersensitive to nuclease probes such as DNase I.

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

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

76 We associated DNase I hypersensitive sites (DHSs) with genes, and trai

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

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

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

80 By DNase I and hydroxyl radical footprinting experiments, w

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

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

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

84 cts the underlying sequence from cleavage by DNase I, leaving nucleotide-resolution footprints.

85 ologous structural framework as confirmed by DNase I and hydroxyl radical footprinting, the two compl

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

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

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

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

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

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

92 Here it is shown, by DNase I footprinting and site-directed mutagenesis, that

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

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

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

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

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

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

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

100 ucers did not yield identical CbbR-dependent DNase I footprints, indicating that the coinducers cause

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

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

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

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

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

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

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

108 romatin, instead relying on the endonuclease DNase I.

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

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

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

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

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

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

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

116 27 k Illumina array, and with enrichment for DNase-I Hypersensitivity sites across the full range of

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

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

119 er also show a high level of protection from DNase I digestion genome-wide, and likely have important

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

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

122 Using genomic DNase I footprinting across 41 diverse cell and tissue t

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

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

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

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

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

128 egulatory DNA marked by deoxyribonuclease I (DNase I) hypersensitive sites (DHSs).

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

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

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

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

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

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

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

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

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

138 with myocardial infarction exhibit increased DNase I activity.

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

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

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

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

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

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

145 g bacteria by prophylaxis with intravascular DNase I alone.

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

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

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

149 ained a total of 2.7 billion uniquely mapped DNase I-sequencing (DNase-seq) reads, which allowed us t

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

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

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

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

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

155 We previously defined novel DNase I hypersensitive sites (hs) 5, 6, 7 immediately do

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

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

158 nrelated to changes in nucleosome occupancy, DNase I hypersensitivity dynamics are also predictive of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 uccess of this strategy is the unique use of DNase I digestion to remove unwanted ssDNA from the memb

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

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

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

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

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

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

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

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

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

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

208 acing and sequence, and was marked by phased DNase I hyperactivity and protection patterns consistent

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

210 Previously, DNase I hypersensitivity sites were reported to explain

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

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

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

214 High-resolution DNase I cleavage patterns mirror nucleotide-level evolut

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

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

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

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

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

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

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

222 ed and exhibits a plasmacytoma cell-specific DNase I-hypersensitive site in chromatin, henceforth ter

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 vestigated the conditions that inhibited the DNase I activity.

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

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

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

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

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

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

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

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

250 ococcus mutans and DNA binding sites through DNase I footprinting and electrophoretic mobility shift

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

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

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

254 tin of pluripotency genes more accessible to DNase I.

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

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

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

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

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

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

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

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

263 co-activated elements, and the transcellular DNase I sensitivity pattern at a given region can predic

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

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

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

267 utionarily and show distinct footprints upon DNase I digestion.

268 We used DNase I sequencing to measure chromatin accessibility in

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

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

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

272 Analyses using DNase I hypersensitivity assay and chromosome conformati

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

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

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

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

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

278 ved from the membrane containing HBcAg using DNase I digestion and gradient wash with urea buffers.

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

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

281 We call such variants 'DNase I sensitivity quantitative trait loci' (dsQTLs).

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

283 In vitro DNase I footprinting and restriction endonuclease access

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 Treatment with DNase I significantly degraded NETs and reduced citrulli

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

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