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1                                              DNase 1 was given to assess the effects of extracellular
2                                              DNase I administration significantly diminished plasma c
3                                              DNase I and Tn5 transposase assays require thousands to
4                                              DNase I hypersensitive sites (DHSs) are generic markers
5 -seq data with 1418 histone ChIP-seq and 118 DNase-seq data tracks from the ENCODE project in a moder
6  single intracoronary infusion of 1 x 10(13) DNase-resistant particles of AAV1/SERCA2a or placebo.
7 ase protein that possesses alkaline 5'-to-3' DNase activity and promotes host shutoff at the mRNA lev
8 00 constructs, corresponding to roughly 3500 DNase I hypersensitive (DHS) sites, into the mouse retin
9 tering, molecular dynamics simulations and a DNase I cleavage assay we found that the wild type hTERT
10 ing affinity to Im7 but was inactivated as a DNase.
11                       This variant lies in a DNase 1 hypersensitivity site (DHS) upstream of both the
12 elets, which increased fibrin formation in a DNase-dependent manner.
13                 In silico analyses located a DNase I hypersensitivity site to rs7692387 and predicted
14                Herein, the construction of a DNase-mimetic artificial enzyme (DMAE) for anti-biofilm
15                      The structure reveals a DNase-I-type fold with a hydrophobic track leading to th
16 o built a CRISPR interference system using a DNase-dead Cas12a to significantly repress endogenous ge
17  motif, with reduced SNP density, and with a DNase footprinting signal in all tested cells.
18                                 Accordingly, DNase I footprinting analysis confirmed that AbrB bound
19 own by caspase-3 cleavage, caspase-activated DNase levels, and terminal deoxynucleotidyl transferase-
20 binary complex functioned as a highly active DNase to destroy a large excess DNA substrate, which cou
21                           Nuclease activity (DNase, RNase, dsRNase) was concentrated in the salivary
22                                   We adapted DNase-seq to nuclei isolated from C. elegans embryos and
23                            In plants, adding DNase I to root tips eliminates border cell extracellula
24 ient thrombi was more successful when adding DNase 1 to standard t-PA.
25  despite prior administration of IL-17A, and DNase also disassembled the inflammatory networks.
26  by electrophoretic mobility shift assay and DNase I footprinting.
27 atin-1s) prophylaxis given 1 hour before and DNase I 3 hours after CC injection completely prevented
28 ipitation sequencing and microarray data and DNase I hypersensitive site sequencing data.
29 n start and termination sites, enhancers and DNase I hypersensitive sites.
30 pression quantitative trait loci (eQTLs) and DNase I sensitivity quantitative trait loci (dsQTLs) in
31 nt downregulation of those encoding Hsf4 and DNase IIbeta, which are implicated in the denucleation p
32                  Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues d
33 ription factors, enhancer histone marks, and DNase hypersensitivity) in mouse embryonic stem cells (m
34 atin states, transcription factor motifs and DNase I footprints, providing tools for epigenome-wide a
35 A variants in histone modification peaks and DNase hypersensitivity sites in B cells.
36 sults with RNA-seq data, ChIP-seq peaks, and DNase-seq footprints, we show that MEDEA improves the de
37 f Crosscheck to 8851 ENCODE ChIP-, RNA-, and DNase-seq datasets enabled us to identify and correct do
38      Here, we characterize how the RNase and DNase activities associated with Type III-B immunity in
39 c repeat (CRISPR) system with both RNase and DNase activity.
40 anscription factor binding from ChIP-seq and DNase-seq data, and scores variants by computing the cha
41 ty control and data analyses of ChIP-seq and DNase-seq data.
42 ollaborative projects involving ChIP-seq and DNase-seq from different designs.
43                                 ChIP-seq and DNase-seq have become the standard techniques for studyi
44 presents the most comprehensive ChIP-seq and DNase-seq related quality metric resource currently avai
45 derived from over 23,677 public ChIP-seq and DNase-seq samples (11,265 datasets) from eight literatur
46 c datasets from these mice using RNA-Seq and DNase-Seq.
47 F binding profiles based on DNA sequence and DNase-seq footprints, but to what extent a model can be
48 hromatin immunoprecipitation sequencing, and DNase sequencing datasets to establish the relationship
49                                Gel shift and DNase I footprinting assays confirmed the presence and l
50 ned using electrophoretic mobility shift and DNase I footprinting assays.
51 el on publicly available transcriptomics and DNase-seq data and assessed the predictive power of the
52                          Tn5 transposase and DNase I sequencing-based methods prefer native or high c
53      Target recognition activates RNases and DNases that may either destroy foreign DNA directly or e
54                    In this study, we applied DNase-seq (DNase I hypersensitive site sequencing) to st
55 regulatory DNA elements can be identified as DNase I hypersensitive sites (DHSs).
56 ions negatively correlated with LLD, such as DNase I hypersensitivity sites (DHSs).
57 chromatin, as detected by techniques such as DNase-seq and FAIRE-seq.
58      Restriction enzyme accessibility assay, DNase I footprinting and AFM experiments reveal perturbe
59 ccessibility and DNA methylation patterns at DNase hypersensitive sites (DHSs).
60  exploits information from H3K27ac signal at DNase I hypersensitive sites identified from published h
61  3 groups: control (group 1), one i.v. bolus DNase I before CPB start (group 2) and a second DNase I
62 e to both soluble DNase I and membrane-bound DNase on cells.
63    Surprisingly, 22% MHSs are not covered by DNase-seq or ATAC-seq reads, which are referred to "spec
64                          NETs degradation by DNase I promoted NET-protein clearance and protected aga
65 de regulatory element activities measured by DNase I hypersensitivity (DH).
66        Mechanistically, digestion of NETs by DNase I significantly diminished NETs-dependent upregula
67 thelial cell damage that can be prevented by DNase.
68  the open chromatin identified previously by DNase-seq and ATAC-seq.
69 le genomic sites mapped in 164 cell types by DNase-seq, and demonstrate greater predictive accuracy t
70 ting of circulating cell-free DNA (cfDNA) by DNases might represent a feasible therapeutic strategy t
71                                  Single-cell DNase sequencing (scDNase-seq) is a method of detecting
72  of size-selected DNase I-treated chromatin (DNase-seq) allows high-resolution measurement of chromat
73                           An assay combining DNase I digestion and CMV quantitative polymerase chain
74 ugh a combination of mammalian conservation, DNase hypersensitivity, and histone modification from EN
75 m reveals strong enhancer regions containing DNase I hypersensitive sites overlapping the rs874040 li
76 s that cannot be analyzed using conventional DNase I sequencing because of the requirement for millio
77 f ChIP-seq and chromatin accessibility data (DNase-seq and ATAC-seq) published before January 1, 2016
78 tory region type, motif sequence degeneracy, DNase accessibility and pairing genomic distance.
79  factor footprints, we produced high-density DNase I cleavage maps from 243 human cell and tissue typ
80 ensors are vulnerable to deoxyribonucleases (DNases) which cells may express on cell membrane or secr
81 ase that also possesses target RNA-dependent DNase and cyclic oligoadenylate (cOA) synthetase activit
82 tors and those within frontal cortex-derived DNase I hypersensitivity sites are significantly enriche
83   Here, we introduced a previously described DNase-inactivating Glu129His (Q129H) mutation into the O
84 alleys exhibit concordance with differential DNase signal at cell line specific valleys.
85 ntibodies, brefeldin A, diphenyleneiodonium, DNase or blocking F(ab')2 fragments to CD16, CD18, CD32
86 e hundred thousand genomic loci that display DNase I hypersensitivity in one or more ENCODE cell line
87       Specifically, exploiting a distinctive DNase I cleavage profile within nucleosome-associated DN
88 s for identifying regulatory regions in DNA (DNase-seq, ChIP-seq, FAIRE-seq, ATAC-seq).
89 4)-10(-17) M) complex between the Colicin E7 DNase (CE7) and its inhibitor, Immunity protein 7 (Im7).
90                       Over half of embryonic DNase I hypersensitive sites (DHSs) were annotated as no
91          We then applied MEDEA to 610 ENCODE DNase-seq data sets, where it revealed significant motif
92 romatin, instead relying on the endonuclease DNase I.
93 nnate immune cells and digested by endosomal DNase II to generate an immune response.
94 binds to PF4-NET complexes, further enhances DNase resistance.
95  the current high-throughput sequencing era, DNase I has mainly been used to study genomic regions de
96 f divalent metal ions, similar to eukaryotic DNase II.
97 ranscription factor footprints from existing DNase-seq data derived from central nervous system tissu
98  Sequencing data were compared with existing DNase-seq, ChIP-seq, and RNA-seq data to evaluate librar
99     Treatment with CLI reduced extracellular DNase Sda1 and streptolysin O (SLO) activity in vivo, wh
100 ls, it has been shown that the extracellular DNase, DNASE1L3, plays a role in the fragmentation of pl
101 he structure of RecJ, a 5' --> 3' DHH family DNase and other DHH family nanoRNases, Bacillus NrnA has
102 ally categories based on chromatin features, DNase hypersensitivity and transcription factor localiza
103           For individual chromatin features, DNase I enables high and consistent predictions.
104                                    Following DNase treatment, 5/39 DS specimens yielded HIV sequences
105 we used potassium permanganate footprinting, DNase I footprinting, and in vitro transcription from th
106 ated hypermethylation signature enriched for DNase Hypersensitive Sites in acute myeloid leukemia.
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 mputational method that integrates data from DNase-seq and ChIP-seq of TFs and histone marks.
113                           We generated 27 Gb DNase-seq and 67.6 Gb RNA-seq data to investigate chroma
114                                      Genomic DNase I footprinting enables the quantitative, nucleotid
115 ut experiment methods (e.g. H3K4me1/H3K27ac, DNase-seq/ATAC-seq, P300, POLR2A, CAGE, ChIA-PET, GRO-se
116 ch for human silencers, we utilized H3K27me3-DNase I hypersensitive site (DHS) peaks with tissue spec
117 DNA motif pairs exhibit substantially higher DNase accessibility than the background sequences.
118                                     However, DNase treatment after nucleic acid extraction to remove
119                Although deoxyribonuclease I (DNase I) was used to probe the structure of the nucleoso
120                        Deoxyribonuclease II (DNase II) is also known as acid deoxyribonuclease becaus
121               Chromatin immunoprecipitation, DNase I hypersensitivity and transposase-accessibility a
122                                           In DNase II-deficient mice, the excessive accrual of undegr
123        We observed significant enrichment in DNase I hypersensitive sites in fetal heart and lung.
124 ree uncharacterized DNA motifs identified in DNase footprinting assays.
125 tify candidate noncoding driver mutations in DNase I hypersensitive sites in breast cancer and experi
126 e-reporting capability and remains stable in DNase-expressing cells.
127 the accessible chromatin landscape including DNase-seq, FAIRE-seq and ATAC-seq.
128                Several techniques, including DNase-seq, which is based on nuclease DNase I, and ATAC-
129                           TRACE incorporates DNase-seq data and PWMs within a multivariate hidden Mar
130                 Here, we develop a low-input DNase I sequencing (liDNase-seq) method that allows us t
131                               Interestingly, DNase II has also been identified in a few genera of bac
132 ing sites in promoter regions that intersect DNase I hypersensitive sites (DHSs).
133  terminal subunit is loosely tethered by its DNase-1 loop to the third subunit, because its monomer-l
134 ion, little is known about the impact of its DNase activity on the KSHV genome and life cycle and the
135 ed Q129H mutant virus that selectively lacks DNase activity but retains host shutoff activity, we pro
136 reveals that DUX4 binds two classes of loci: DNase accessible H3K27Ac-rich chromatin and inaccessible
137 cluding expression quantitative trait locus, DNase I sensitivity quantitative trait locus and functio
138 and plasma cells by inducing and maintaining DNase I hypersensitive sites.
139            We generated regulatory DNA maps (DNase-seq) and paired gene expression profiles (RNA-seq)
140 while interactions involving actively marked DNase accessible elements are enriched both at short (<5
141  these elements have active chromatin marks, DNase hypersensitivity, and occupancy by multiple transc
142  genome annotations including histone marks, DNase hypersensitivity, and transcription factor binding
143 ine-scale structure within about 1.6 million DNase I-hypersensitive sites and show that the overwhelm
144                                We then mined DNase-seq data to identify putative active CRMs and TF f
145 de maps for 17 TFs, 3 histone modifications, DNase I hypersensitive sites, and high-resolution promot
146                                    Moreover, DNase-seq and chromatin conformation capture (3C) define
147 es identified from published human and mouse DNase-seq data.
148  characterization of the most highly mutated DNase I hypersensitive sites in breast cancer (using in
149 he high environmental sensitivity of natural DNase in anti-biofilm applications, DMAE exhibited a muc
150 of NETs by secreting a deoxyribonuclease (Nb-DNase II) to degrade the DNA backbone.
151 vitro, which was enhanced by neutralizing Nb-DNase II.
152                               Homologs of Nb-DNase II are present in other nematodes, including the h
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 nd target RNA-activated sequence-nonspecific DNase and RNase activities.
156 arget protein and the inhibitor, and a novel DNase protection assay measured chemical inhibition of p
157 luding DNase-seq, which is based on nuclease DNase I, and ATAC-seq, which is based on transposase Tn5
158 se increases were enhanced by the actions of DNase I.
159                   Interestingly, addition of DNase I reduced the numbers of EPEC bacteria recovered a
160                        The administration of DNase, a NET inhibitor, significantly reduced hepatic da
161                           Global analyses of DNase I-hypersensitive sites and 3D genome architecture,
162 orms a comprehensive k-mer-based analysis of DNase footprints to determine any k-mer's potential for
163                                  Analysis of DNase I hypersensitive sites sequencing data revealed an
164 600 times the physiological concentration of DNase I.
165 se effectors, RhsA, belongs to the family of DNase enzymes, the activity of the other was not apparen
166 dentified in chicken lung overlapped half of DNase-I hypersensitive sites, coincided with active hist
167 gated the effects of loss or inactivation of DNase activity on viral genome replication, cleavage, an
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  atomic structure and catalytic mechanism of DNase II.
174 AS or eQTL phenotypes are located outside of DNase-seq footprints.
175 respectively, displayed distinct patterns of DNase I hypersensitivity, histone acetylation and NFAT1
176 te-specific periodic cleavage, regulation of DNase cleavage activity, and autoimmunity suppression.
177                           Deep sequencing of DNase-seq libraries and computational analysis of the cu
178 ed autoinhibitory conformation suggestive of DNase activity regulation.
179  an accessible material for the synthesis of DNase-resistant tension sensor that retains the force-re
180 A/RNA, were tested and evaluated in terms of DNase resistance, cellular force imaging ability and mat
181 te lung injury (ALI) and assessed the use of DNase I, for the treatment of ALI.
182  Instead, ORC binds nonspecifically to open (DNase I-hypersensitive) regions containing active chroma
183 t was negated by either a TLR9 antagonist or DNase treatment.
184                           PAD4 deficiency or DNase 1 similarly protected hearts from fibrosis.
185  4 (PAD4, a key enzyme for NET formation) or DNase 1 treatment (which cleaves NETs) also prolonged al
186  sequencing experiments (such as ChIP-seq or DNase-seq) and models the change in enhancer signature u
187 pproaches initially designed for ChIP-seq or DNase-seq, without considering the transposase digested
188 t were not identified by H3K27ac ChIP-seq or DNase-seq.
189 including at enhancers, promoters, and other DNase hypersensitive regions not marked with canonical h
190 t require genetically modified histones, our DNase-based approach is easily applied in any organism,
191                                  Previously, DNase I hypersensitivity sites were reported to explain
192 hese results indicated that ORF37's proposed DNase activity is essential for viral genome processing
193  the experiments used commercially purchased DNase and showed that coinjection of these DNase prepara
194  CMV quantitative polymerase chain reaction (DNase-CMV-qPCR) was developed to differentiate free nake
195 urokinase, or DNA digestion with recombinant DNase I all prevented arterial occlusions, GFR loss, and
196 1 and therefore endosomal TLRs, also require DNase II deficiency in both donor and host compartments,
197 egions in various cells using Encode Roadmap DNase-hypersensitive site data.
198    This led to the identification of ORF37's DNase activity as a potential target for antiviral thera
199 se I before CPB start (group 2) and a second DNase I dose before reperfusion (group 3).
200             Humans and mice lacking secreted DNase DNASE1L3 develop rapid anti-dsDNA antibody respons
201             Deep sequencing of size-selected DNase I-treated chromatin (DNase-seq) allows high-resolu
202         In this study, we applied DNase-seq (DNase I hypersensitive site sequencing) to study changes
203 n immunoprecipitation sequencing (ChIP-seq), DNase I hypersensitive sites sequencing (DNase-seq), and
204 ell technologies (e.g. single-cell ATAC-seq, DNase-seq or ChIP-seq) have made it possible to assay re
205  By integrating previously published BS-seq, DNase-seq, ATAC-seq, and RNA-seq data collected during m
206 egulatory information derived from ChIP-seq, DNase-seq and ATAC-seq chromatin profiling assays, which
207 ly accumulating publicly available ChIP-seq, DNase-seq and ATAC-seq data are a valuable resource for
208 activities in bulk samples such as ChIP-seq, DNase-seq and FAIRE-seq cannot analyze samples with smal
209  to better utilize the large-scale ChIP-seq, DNase-seq, and ATAC-seq data.
210 kit can determine the most similar ChIP-seq, DNase-seq, and ATAC-seq samples in terms of genomic inte
211   Using HTS data from a variety of ChIP-seq, DNase-seq, FAIRE-seq, and ATAC-seq experiments, we show
212 A-seq, nucleosome positioning for MNase-seq, DNase hypersensitive site mapping, site annotation and m
213 sets including ChIP-seq, RNA-seq, MNase-seq, DNase-seq, GRO-seq, and ATAC-seq data.
214 ity relative to existing methods in RNA-seq, DNase-seq and ChIP-seq data.
215 ility experiments such as DNaseI sequencing (DNase-seq) and Assay for Transposase Accessible Chromati
216  favorably with published DNaseI sequencing (DNase-seq) results and it requires less than 50 000 nucl
217 q), DNase I hypersensitive sites sequencing (DNase-seq), and whole-genome bisulfite sequencing (WGBS
218  the many-body functional landscape and show DNase accessibility, POLR2A binding, and decreased H3K27
219             Sasquatch only requires a single DNase-seq data set per cell type, from any genotype, and
220 nteractions supported by CTCF binding sites, DNase accessibility, and/or active histone marks.
221                         Importantly, in situ DNase Hi-C obviates the dependence on a restriction enzy
222 re using a novel 3C protocol, termed in situ DNase Hi-C.
223 ions induced expression and activity of SLO, DNase, and Streptococcus pyogenes cell envelope protease
224  exhibited strong resistance to both soluble DNase I and membrane-bound DNase on cells.
225     Here we profile parental allele-specific DNase I hypersensitive sites in mouse zygotes and morula
226 ntify 76 genes with paternal allele-specific DNase I hypersensitive sites that are devoid of DNA meth
227 regions and in particular in tissue-specific DNase I hypersensitivity sites (DHSs).
228 ase) with collateral RNase and single-strand DNase activities.
229                                Surprisingly, DNase-accessible euchromatin is protected from UV, while
230                         Altogether, systemic DNase I administration during CPB efficiently reduced cf
231 tiviral single guide RNA libraries to target DNase I hypersensitive sites surrounding a gene of inter
232                              We identify ten DNase I hypersensitive sites that are significantly muta
233             Each monomer of B. thailandensis DNase II exhibits a similar overall fold as phospholipas
234    The crystal structure of B. thailandensis DNase II shows a dimeric quaternary structure which appe
235  that recombinant Burkholderia thailandensis DNase II is highly active at low pH in the absence of di
236 than did NAC, and it was more effective than DNase in CF sputum ex vivo.
237                                We found that DNase treatment of poliovirus RNA followed by random rev
238                        This could imply that DNase-seq footprinting is too insensitive an approach to
239      Here, we reveal for the first time that DNase I can be used to precisely map the (translational)
240  mutation of the HD motif only abolished the DNase activity in vitro.
241                             By analyzing the DNase I hypersensitive sites under 349 experimental cond
242 ts, the ADP ribosyl transferase PltA and the DNase CdtB, linked to a pentameric B subunit, which is a
243  secreted superantigens SSA and SpeC and the DNase Spd1.
244 hment folds from 1.36 to 3.1) as well as the DNase hypersensitive sites (1.58-2.42 fold), H3K4Me1 (1.
245                       Activation of both the DNase and cOA generation activities require target RNA b
246                       We find that Cas10-the DNase effector of the complex-displays rapid conformatio
247 o found NucDHS, a nucleosome that covers the DNase hypersensitive site, in unintegrated viral DNA.
248 of the C terminus changes so it distorts the DNase binding loop, which allows cofilin binding, and a
249 o mutational analyses reveal that either the DNase activity of Cas10 or the RNase activity of Csx1 ca
250 variants, and DNA methylation changes in the DNase I hypersensitivity based regulatory network.
251 cleosomal DNA; the oscillatory nature of the DNase I cleavage profile within nucleosomal DNA enables
252   Recent reports point to limitations of the DNase-based genomic footprinting approach and call into
253 ouble-helical DNA substrate, positioning the DNase active site for first-strand cleavage.
254 e, we provide experimental evidence that the DNase activity of the SOX protein does not affect viral
255 de experimental evidence confirming that the DNase function of the KSHV SOX protein is essential for
256 ing E. coli that do not perform lysis to the DNase colicin, we found that mass lysis occurs when cell
257  up multiple favorable interactions with the DNase-I binding loop in subdomain 2 of the adjacent subu
258 d DNase and showed that coinjection of these DNase preparations with alum and Ag reduced the host's i
259                                        These DNases can damage the sensors, lower signal-to-noise rat
260 nce and protected against ALI in mice; thus, DNase I may be a new potential adjuvant for ALI therapy.
261 on measurement of chromatin accessibility to DNase I cleavage, permitting identification of de novo a
262 chromatin regions that are not accessible to DNase I or Tn5.
263 open chromatin that may not be accessible to DNase I or Tn5.
264 data define a type I interferonopathy due to DNase II deficiency in humans.
265 were identified based on hypersensitivity to DNase I digestion and association with H3K4me3-modified
266 e small size of the MNase enzyme relative to DNase I or Tn5 allows its access to relatively more cond
267 ompacts NETs, increasing their resistance to DNase I.
268 -containing structures that are resistant to DNase and exclude the general transcription factor TFIIB
269 low salt and up to tenfold more resistant to DNase I digestion than when uncoated.
270 ce of nanoparticles were highly resistant to DNase I endonucleases, and degradation was carried out e
271 elements: short genomic regions sensitive to DNase digestion that are strongly bound by known insulat
272 P. aeruginosa biofilm formation similarly to DNase, suggesting interference with the pyocyanin-depend
273   Specifically, adding a DNA-damaging toxin (DNase colicin) from another strain induced mass cell sui
274 gical inflammation in the joint depends upon DNase II deficiency in both donor hematopoietic cells an
275     To identify cis-acting elements, we used DNase-seq and H3K4me1 and H3K27Ac ChIP-seq to map open a
276 atch, a new computational approach that uses DNase footprint data to estimate and visualize the effec
277                                        Using DNase I hypersensitivity methods and ENCODE data, we hav
278                                        Using DNase-seq data from the ENCODE project, we show that a l
279                                        Using DNase-seq data improved predictions of tissue-specific e
280 recise AioR binding site was confirmed using DNase I foot-printing.
281                           Furthermore, using DNase I in a nuclease degradation assay, G4-T-oligo was
282 with open chromatin regions identified using DNase I hypersensitivity assays, and are enriched in the
283 frozen and all 10 fresh samples tested using DNase-CMV-qPCR.
284 seq data with similar accuracy as when using DNase-seq data.
285  based on cuts in linker regions, we utilize DNase I cuts both outside and within nucleosomal DNA; th
286                      Dissolution of NETs via DNase I did not alter anti-glomerular basement membrane
287                          Removal of NETs via DNase infusion, or in peptidylarginine deiminase-4-defic
288           Enrichment of SNPs associated with DNase I-hypersensitive sites was also found in many tiss
289                        TOP2B associates with DNase I hypersensitivity sites, allele-specific transcri
290 ingle nucleotide resolution, coincident with DNase hypersensitive and ATAC-seq sites at a low sequenc
291                   However, correlations with DNase I hypersensitive sites were different for all vect
292 ries, cells are lysed and then digested with DNase I.
293          The advent of DNA footprinting with DNase I more than 35 years ago enabled the systematic an
294                       Targeting of NETs with DNase 1 might have prothrombolytic potential in treatmen
295 eutrophil elastase or by degrading NETs with DNase protects mice from type-2 immunopathology.
296 hat was prevented by disruption of NETs with DNase.
297  incubation of purified malaria pigment with DNase abrogated IFN-beta induction.
298 ming ex vivo lysis of retrieved thrombi with DNase 1 and t-PA.
299 romatin Model (SCM), which when trained with DNase-seq data for a cell type is capable of predicting
300 o-derived motifs mapped to the genome within DNase I hypersensitivity footprints to characterize regi

 
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