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1 p of DNA is protected against digestion with micrococcal nuclease.
2 bited by a specific competitive inhibitor of micrococcal nuclease.
3 DNA fragments resulting from digestions with micrococcal nuclease.
4 the sensitivity of chromatin to digestion by micrococcal nuclease.
5 al DNA ladders sharper than those created by micrococcal nuclease.
6 d treatment of lysates with Ca(2+)-dependent micrococcal nuclease.
7 s even after digestion of the chromatin with micrococcal nuclease.
8  component is sensitive to cycloheximide and micrococcal nuclease.
9 iation to treatment with ethidium bromide or micrococcal nuclease.
10  decreased rate of digestion of chromatin by micrococcal nuclease.
11 ated by treatment with proteinase K, but not micrococcal nuclease.
12 leosomal DNA to Dam methyltransferase and to micrococcal nuclease.
13 the primary chromatin structure is probed by micrococcal nuclease.
14 tects approximately 11 bp of linker DNA from micrococcal nuclease.
15 c mRNA length) were found to be resistant to micrococcal nuclease (69%) or to remain suspended in ass
16 nization but were found to be susceptible to micrococcal nuclease (85%) or to sediment to a pellet in
17            Pretreatment of the U1 snRNP with micrococcal nuclease abolished the assembly of galectin-
18 vage activity is sensitive to treatment with micrococcal nuclease, also consistent with an activity a
19          Linker DNA was freely accessible to micrococcal nuclease, although the oligomers remained pa
20                              High-resolution micrococcal nuclease analyses revealed that a positioned
21                                              Micrococcal nuclease analysis revealed that the heteroch
22 sults demonstrate increased DNA laddering by micrococcal nuclease and an increased amount of DNA inte
23  units are equally accessible to DNase I and micrococcal nuclease and contain similar levels of histo
24 n vitro and in vivo assays of sensitivity to micrococcal nuclease and dam methyltransferase, respecti
25 tivity of wild-type nuclei to digestion with micrococcal nuclease and deoxyribonuclease I, indicating
26 ecreased accessibility of their chromatin to micrococcal nuclease and DNase I digestion and increased
27 s of chromatin structure by accessibility to micrococcal nuclease and DNase I digestion demonstrated
28  core region of the insulator as revealed by micrococcal nuclease and DNase I digestion studies.
29  T118-I) are more accessible to digestion by micrococcal nuclease and do not constrain DNA in a preci
30 s with defined ends, bulk NCPs prepared with micrococcal nuclease and molecular modelling to reassess
31 s no hypersensitivity to either DNase I or a micrococcal nuclease and no translational positioning of
32  complex, as supported by its sensitivity to micrococcal nuclease and proteinase K.
33 e of ribosomal chromatin was investigated by micrococcal nuclease and psoralen photocrosslinking.
34 undaries were determined by assays combining micrococcal nuclease and restriction endonuclease digest
35  region for several days, as demonstrated by micrococcal nuclease and restriction enzyme accessibilit
36 tuted mononucleosomes using exonuclease III, micrococcal nuclease and restriction enzymes demonstrate
37                                              Micrococcal nuclease and short-recognition-sequence blun
38 erformance liquid chromatography analysis of micrococcal nuclease and spleen phosphodiesterase-digest
39                                           In micrococcal nuclease and supercoiling assays, addition o
40 eabilization and digestion of chromatin with micrococcal nuclease and then compared tumor necrosis fa
41 digestion by DNAse, restriction enzymes, and micrococcal nuclease, and an increased affinity for GAL4
42                                     DNase I, micrococcal nuclease, and exonuclease III footprinting s
43                        By combining DNase I, micrococcal nuclease, and specific restriction endonucle
44 atin in the spt6 mutant is hypersensitive to micrococcal nuclease, and this hypersensitivity is suppr
45 e flexibility and strongly blocked access of micrococcal nuclease as contour lengths shortened, consi
46 om human metaphase chromosomes digested with micrococcal nuclease associate spontaneously forming mul
47                 The RTC becomes permeable to micrococcal nuclease but not to antibodies.
48 osome leading to an asymmetric protection to micrococcal nuclease cleavage of linker DNA relative to
49 itional perturbation is marked by changes in micrococcal nuclease cleavage patterns, restriction endo
50  chromatin nor to differences in the in vivo micrococcal nuclease cleavage sites in individual genes
51 10-bp periodicity in WW dinucleotides and in micrococcal nuclease cleavage, providing evidence for ro
52  caused by either linker histone addition or micrococcal nuclease cleavage.
53 clei sorting; 3) preparation of chromatin by micrococcal nuclease digest; 4) ChIP for open chromatin-
54                                Separation of micrococcal nuclease-digested chromatin by sucrose gradi
55          Low resolution Southern analysis of micrococcal nuclease-digested chromatin from untreated r
56                                We begin with micrococcal nuclease-digested non-cross-linked chromatin
57                       The protection against micrococcal nuclease digestion afforded to chromatosomal
58 gradient sedimentation, thermal disassembly, micrococcal nuclease digestion and atomic force microsco
59  examined HSV-1 during lytic infection using micrococcal nuclease digestion and chromatin immunopreci
60 of S. cerevisiae nucleosome lengths based on micrococcal nuclease digestion and paired-end sequencing
61 er DNA, stabilizing an additional 20 bp from micrococcal nuclease digestion and restrict nucleosome m
62 e demonstrate by single-molecule approaches, micrococcal nuclease digestion and small-angle X-ray sca
63 e center of the DNA sequence, protected from micrococcal nuclease digestion by incorporation into a p
64 HBc 149, 154, and 157) remained intact after micrococcal nuclease digestion by native gel electrophor
65 region of the capsid pgRNA is susceptible to micrococcal nuclease digestion during its isolation and
66  replicative aging using spike-in controlled micrococcal nuclease digestion followed by sequencing.
67 ammalian linker histone H1 and have a unique micrococcal nuclease digestion footprint that allows the
68 ound histone H3 and increased sensitivity to micrococcal nuclease digestion in WHS patient-derived ce
69                                      Partial micrococcal nuclease digestion indicated that the sequen
70                                              Micrococcal nuclease digestion indicated the presence of
71 itivity of bulk chromatin from sin4 cells to micrococcal nuclease digestion is strikingly increased r
72                                              Micrococcal nuclease digestion of active promoters in nu
73  of genomic DNA species, produced by partial micrococcal nuclease digestion of chromatin, can be sequ
74 of a 166 bp chromatosome intermediate during micrococcal nuclease digestion of chromatin.
75 me-length DNA ( approximately 166 bp) during micrococcal nuclease digestion of chromatin.
76 itation, we developed a novel strategy using micrococcal nuclease digestion of cross-linked chromatin
77         Capsid disassembly can be induced by micrococcal nuclease digestion of encapsidated RNA.
78 445 nucleotide human telomerase RNA (hTR) by micrococcal nuclease digestion of partially purified hum
79   In this study, we use a procedure based on micrococcal nuclease digestion of reconstituted nucleoso
80                                          The micrococcal nuclease digestion pattern of chromatin from
81 pause at approximately 168 base pairs in the micrococcal nuclease digestion pattern of the chromatin.
82 ure on the transient template as measured by micrococcal nuclease digestion pattern.
83 rther, we found that A-T cells had different micrococcal nuclease digestion patterns compared to norm
84  structure as DNaseI-hypersensitive sites or micrococcal nuclease digestion patterns.
85                   Despite these changes, the micrococcal nuclease digestion profile of this promoter
86  from the Rb-/- cells is more susceptible to micrococcal nuclease digestion than that from Rb+/+ fibr
87  the exon 1 region is much more sensitive to micrococcal nuclease digestion than the exon 2 and exon
88                              A major site of micrococcal nuclease digestion was identified by mapping
89 obes were used to capture RNA targets, and a micrococcal nuclease digestion was performed to remove a
90                          Similar kinetics of micrococcal nuclease digestion were seen for all three t
91  nucleosome position in follicle cells using micrococcal nuclease digestion with Ilumina sequencing.
92  and loss of a regular nucleosomal ladder on micrococcal nuclease digestion, addition of TSA relieves
93 leosomes, produce a chromatosome stop during micrococcal nuclease digestion, and aggregate chromatin.
94 NA and multiples of approximately 60 bp from micrococcal nuclease digestion, and immunoprecipitation
95  nucleosomes prepared by partial and maximum micrococcal nuclease digestion, coupled with Western blo
96 niques along with such laboratory methods as micrococcal nuclease digestion, predicting the genomic l
97 H3 nucleosomes protect 90-100 bp of DNA from micrococcal nuclease digestion, sufficient for only a si
98 some maps generated by chemical cleavage and micrococcal nuclease digestion, the chemical map shows c
99                                        Using micrococcal nuclease digestion, we probed the chromatin
100 CTD antibodies from chromatin solubilized by micrococcal nuclease digestion.
101 ved from K562 human erythroleukemic cells by micrococcal nuclease digestion.
102 . thermophila mononucleosomes were stable to micrococcal nuclease digestion.
103 ity, and chromatin that is hypersensitive to micrococcal nuclease digestion.
104 ome segment protected by the polymerase from micrococcal nuclease digestion.
105 chromatin results in increased resistance to micrococcal nuclease digestion.
106                                           In micrococcal-nuclease digestion experiments, nucleosomes
107  size differences between repeats in partial micrococcal nuclease digests and by trypsin treatment of
108                                  Analysis of micrococcal nuclease digests of chromatin using hybridiz
109  a typical pattern of nucleosomal repeats in micrococcal nuclease digests, the Tec element chromatin
110 by Snf-Swi, by a high resolution analysis of micrococcal nuclease digests.
111 rmal global chromatin density as assessed by micrococcal nuclease digests; and expressed normal level
112                                              Micrococcal nuclease, DNase I, and restriction enzymes s
113 f nuclease probes including exonuclease III, micrococcal nuclease, DNase I, and restriction enzymes.
114 e)--a protein containing five staphylococcal/micrococcal nuclease domains and a tudor domain--is a co
115        Pretreatment of nuclear extracts with micrococcal nuclease eliminated the phosphorylation of C
116 tivity () was solubilized by Triton X-100 or micrococcal nuclease extraction, whereas hTSH2B was rela
117 osomal protections in Drosophila cells using Micrococcal Nuclease followed by sequencing.
118                                              Micrococcal nuclease footprinting shows that after track
119                                  DNase I and micrococcal nuclease footprinting, of both 5' and 3' 32P
120  examined salt-soluble chromatin released by micrococcal nuclease from a 15-day-old chicken embryo er
121 letion of both tails, a lethal event, alters micrococcal nuclease-generated nucleosomal ladders, plas
122 sed sensitivity of chromatin to digestion by micrococcal nuclease; however, phosphorylation of H2A an
123 ested chromatin from untreated rats revealed micrococcal nuclease hypersensitive regions in the proxi
124              The TBP gene comprises a 220 bp micrococcal nuclease hypersensitive site corresponding t
125 ional responses to cold tend to contain more micrococcal nuclease hypersensitive sites in their promo
126  adjacent to the TATAA box and an additional micrococcal nuclease-hypersensitive site in the linker D
127                The position and intensity of micrococcal nuclease-hypersensitive sites correlate poor
128 ma regions undergoes dramatic alterations in micrococcal nuclease hypersensitivity as cells cross the
129         Both hotspot sequences were sites of micrococcal nuclease hypersensitivity in meiotic chromat
130                                              Micrococcal nuclease hypersensitivity in the PBRU was la
131                        We report DNase I and micrococcal nuclease hypersensitivity, chromatin immunop
132 s associated with increased accessibility to micrococcal nuclease, i.e. nucleosome depletion.
133 histone promoters and transcribed regions to micrococcal nuclease, implicating UBTF1/2 in mediating D
134               The chromatin accessibility to micrococcal nuclease in the MFA2 promoter is unaffected
135  DNA and stabilize it against digestion with micrococcal nuclease, in a similar manner to histone H1.
136 fragility, manifested as high sensitivity to micrococcal nuclease, in contrast to the common presumpt
137 ith increased resistance to both DNase I and micrococcal nuclease, indicating that the silenced state
138 P knockout) brain homogenate with RNase A or micrococcal nuclease inhibited hamster but not mouse PrP
139 ocalization of Cse4 in chromatin digested by micrococcal nuclease is consistent with the potential as
140 cribe a Hi-C-based method, Micro-C, in which micrococcal nuclease is used instead of restriction enzy
141 mic DNA is either sonicated or digested with micrococcal nuclease, making it possible that current pr
142 reconstituted branch migration substrates by micrococcal nuclease mapping and exonuclease III and hyd
143            Chromatin immunoprecipitation and micrococcal nuclease mapping studies reveal that Knirps
144                                              Micrococcal nuclease mapping studies revealed that a nuc
145                         With high-resolution micrococcal nuclease mapping, we show that the HMRa locu
146 r, since the activities in the extracts were micrococcal nuclease (MN) sensitive.
147 scription elongation complex to digestion by micrococcal nuclease (MN).
148 activity of the S. aureus secreted nuclease, micrococcal nuclease (MN).
149 ly in situ single cell chromatin imaging and micrococcal nuclease (MNase) assay to show that Brd4 dep
150 ructure of chromatin in cereal species using micrococcal nuclease (MNase) cleavage showed nucleosomal
151     Chromatin immunoprecipitation (ChIP) and micrococcal nuclease (MNase) digest assays were performe
152           We combined low and high levels of micrococcal nuclease (MNase) digestion along with core h
153 accessibility of nucleosomes, as measured by micrococcal nuclease (MNase) digestion and ATAC-seq (ass
154 uch as chromatin immunoprecipitation (ChIP), micrococcal nuclease (MNase) digestion and DNase I diges
155                We performed a time-course of micrococcal nuclease (MNase) digestion and measured the
156 emodelling analysis at gene promoters, using micrococcal nuclease (MNase) digestion followed by deep
157                                 We have used micrococcal nuclease (MNase) digestion followed by deep
158              We introduce a metric that uses micrococcal nuclease (MNase) digestion in a novel manner
159                    We have combined standard micrococcal nuclease (MNase) digestion of nuclei with a
160 erential nuclease sensitivity assay based on micrococcal nuclease (MNase) digestion to discover open
161 al DNA was significantly less protected from micrococcal nuclease (MNase) digestion up to 6 h postinf
162 erepressed ESs show increased sensitivity to micrococcal nuclease (MNase) digestion, and a decrease i
163                                              Micrococcal nuclease (MNase) digests the linker to yield
164                                              Micrococcal nuclease (MNase) is commonly used to map nuc
165                                              Micrococcal nuclease (MNase) is extensively used in geno
166 ely digested to mononucleosomes using either micrococcal nuclease (MNase) or caspase-activated DNase
167 re-RC) assembly, replication initiation, and micrococcal nuclease (MNase) sensitivity at different ce
168                                              Micrococcal nuclease (MNase) sequence-based profiles of
169              Digestion of the chromatin with micrococcal nuclease (MNase) shows a nucleosome array wi
170 ome-wide mapping of nucleosomes generated by micrococcal nuclease (MNase) suggests that yeast promote
171 method to measure chromatin accessibility to micrococcal nuclease (MNase) that is normalized for nucl
172 hEC) uses fusion of a protein of interest to micrococcal nuclease (MNase) to target calcium-dependent
173                                         Like micrococcal nuclease (MNase), MPE-Fe(II) preferentially
174   In this review, we compare the traditional micrococcal nuclease (MNase)-based approach with a chemi
175                                  Compared to micrococcal nuclease (MNase)-based methods that map nucl
176 bind one or both full nucleosomes that flank micrococcal nuclease (MNase)-defined nucleosome-free pro
177 tes at nucleotide resolution by footprinting micrococcal nuclease (MNase)-sensitive sites.
178 inaccessible to DNA-binding factors, such as micrococcal nuclease (MNase).
179 e extent to which chromatin is digested with micrococcal nuclease (MNase).
180 n these mutants has reduced accessibility to Micrococcal nuclease (MNase).
181                                          The micrococcal nuclease Nuc1 is one of the major S. aureus
182 chromatic sequences become hypersensitive to micrococcal nuclease, nucleoli fail to form, and transcr
183                               Treatment with micrococcal nuclease of highly purified mtRNase P confir
184  products, similar to the well-characterized micrococcal nuclease of Staphylococcus aureus.
185  moderately greater sequence preference than micrococcal nuclease or DNase I, and the sites attacked
186 essed by sedimentation and by digestion with micrococcal nuclease or DNase I.
187 prepared from chromatin digested with either micrococcal nuclease or DNaseI and are restricted in the
188 deed induce sites hypersensitive to DNase I, micrococcal nuclease, or restriction enzymes on either s
189 th Cse4 and H2A are precisely protected from micrococcal nuclease over the entire CDE of all 16 yeast
190                                              Micrococcal nuclease partial digestion generated a ladde
191          Treatment of the polyribosomes with micrococcal nuclease prior to salt extraction solubilize
192                           Use of DNase I and micrococcal nuclease probes further indicated that the s
193                                  DNase I and micrococcal nuclease probes show that GATA-1 binding cau
194  nt stagger is explained by the finding that micrococcal nuclease produces NCPs not with flush ends,
195                                              Micrococcal nuclease protection analysis showed that les
196 ich antibody-targeted controlled cleavage by micrococcal nuclease releases specific protein-DNA compl
197 ent protein-tagged H1 variants, we show that micrococcal nuclease-resistant chromatin is specifically
198 ift assay, this protein produced a discrete, micrococcal nuclease-resistant complex with an approxima
199                 Characterization of the most micrococcal nuclease-resistant DNA indicates that micron
200 visiae, obtained by paired-end sequencing of micrococcal nuclease-resistant DNA.
201 s that the centromeric nucleosome contains a micrococcal nuclease-resistant kernel of 123-135 bp, dep
202 ementing activity was protease-sensitive and micrococcal nuclease-resistant, had a native molecular m
203           This Asf1p/H3/H4 complex generated micrococcal nuclease--resistant DNA in the absence of DN
204  be produced by pretreatment with DNase I or micrococcal nuclease, respectively.
205 table for analysis of chromatin structure by micrococcal nuclease, restriction endonuclease or by imm
206 ive and inactive CEN chromatin digested with micrococcal nuclease revealed that periodic nucleosome a
207 e of exons 1, 2, and 5 of the DHFR gene with micrococcal nuclease revealed that the exon 1 region is
208 nctional significance of this association, a micrococcal nuclease-sensitive component, i.e., an snRNP
209           PELP1 overexpression increased the micrococcal nuclease sensitivity of estrogen response el
210 he human protamine cluster were subjected to Micrococcal Nuclease-seq.
211                                              Micrococcal nuclease studies revealed that TRs are embed
212                                Consistently, micrococcal nuclease susceptibility analysis revealed al
213 pressed CFS, the FRA3B, is more resistant to micrococcal nuclease than that of the flanking non-fragi
214           Consistently, the accessibility of micrococcal nuclease to chromatin was generally inhibite
215 a cell extracts, which were pre-treated with micrococcal nuclease to degrade the endogenous RNase P R
216 riments where the extracts were treated with micrococcal nuclease to digest endogenous snRNAs, the ef
217 acO/GFP-LacI plants were lysed, treated with micrococcal nuclease to digest the DNA to fragments of a
218                                              Micrococcal nuclease-treated cell extracts are fully com
219                                        Using micrococcal nuclease-treated chromatin, we find that Cse
220 ng to successive salt-extracted fractions of micrococcal nuclease-treated Drosophila chromatin.
221  by incubating human 32P-labeled U2 snRNP in micrococcal nuclease-treated HeLa nuclear extracts, foll
222                           Addition of DNA to micrococcal nuclease-treated samples restored interactio
223                                              Micrococcal nuclease-treated TAP preparations were devoi
224 that the 3' ends of capsid pgRNA isolated by micrococcal nuclease treatment are heterogeneously dispe
225 ted by using an established method involving micrococcal nuclease treatment demonstrated reduced leve
226 as not bridged by nucleic acids, as shown by micrococcal nuclease treatment of the proteins prior to
227 A (vRNA) has been depleted by treatment with micrococcal nuclease, was used to study transcription in
228                                     By using micrococcal nuclease, which has both endo- and exo-nucle
229 eosome cores were liberated using an enzyme (micrococcal nuclease) with a strong preference for cleav

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