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1 n vitro with treatments with HCl, pepsin, or sarkosyl.
2 t became solubilized in the presence of 0.2% Sarkosyl.
3 tially extracted with salt, Triton X-100, or sarkosyl.
4 ingle round with low levels of the detergent Sarkosyl.
5 ernary complex with buffers containing 0.25% Sarkosyl.
6 lternatively, it can be extracted using 0.3% sarkosyl.
7 RNA synthesis in the presence of heparin and sarkosyl.
8 ssed DTP from isolated inclusion bodies with Sarkosyl, 28 mg of DTP was obtained per liter of E. coli
9 e of RNA synthesis to high concentrations of sarkosyl after formation of one or two phospho-diester b
10 ty was strongly inhibited by the detergents, Sarkosyl and deoxycholate, even at 0.025%, but it was no
11 urified elongation complexes treated with 1% Sarkosyl and paused at U(14)/G(16) on an HIV-1 template
12 ce the elongation complexes were released by sarkosyl but not by SII, these complexes apparently did
13 f early steps in initiation as revealed by a sarkosyl challenge assay that exploited the resistance o
14                                              Sarkosyl disruption of preinitiation complex formation f
15 fication process was developed that included Sarkosyl extraction followed by affinity purification on
16                            Our workflow uses sarkosyl fractionation to extract the pathological tau s
17 without schizophrenia were subjected to cold sarkosyl fractionation, separating proteins into soluble
18                                              Sarkosyl has been used by others to purify B. burgdorfer
19 cur upon dissociation of nucleosomes with 1% sarkosyl, indicating that the RNA polymerases were not d
20 We characterized the aqueous extractable and sarkosyl insoluble fibrillar tau species derived from hu
21  knockdown of USP13 reduces the abundance of sarkosyl insoluble mTDP-43 in both our HEK293 model and
22         This complex preferentially degrades Sarkosyl insoluble Tau and phosphorylated Tau.
23 seed competent tau can be distinguished from sarkosyl insoluble tau by the presence of overlapping, b
24 ce integral outer membrane (OM) proteins are Sarkosyl insoluble, this is consistent with our previous
25                      This included abundant, sarkosyl-insoluble 4R-tau in both gray and white matter
26 tic alpha-synuclein strains and also between sarkosyl-insoluble alpha-synuclein extracted from two su
27 rom PD and MSA brains are those that contain Sarkosyl-insoluble alpha-synuclein.
28 ther U1 small nuclear ribonucleoproteins are Sarkosyl-insoluble and associate with Tau neurofibrillar
29          The most potent fractions contained Sarkosyl-insoluble assemblies enriched in filaments.
30 reacted with a 64-kDa antigen present in the Sarkosyl-insoluble cell envelope fraction of H. ducreyi
31 ing of endogenous tau in both oligomeric and sarkosyl-insoluble forms in the hippocampal region.
32  but not full-length tau, was present in the Sarkosyl-insoluble fraction and formed thioflavin-S-posi
33             Endogenous Tau11i is enriched in Sarkosyl-insoluble fraction in AD hippocampus and forms
34 ysis showed the expected ~30 kDa band in the sarkosyl-insoluble fraction of frontal cortex tissue in
35 oped antibody to detect TMEM106B CTFs in the sarkosyl-insoluble fraction of post-mortem human brain t
36 tissues revealed that tau was present in the sarkosyl-insoluble fraction, and composed of three- and
37 her molecular weight species, is enriched in Sarkosyl-insoluble fraction, and exhibits greater protei
38 olubility in various reagents, including the sarkosyl-insoluble fraction.
39 ses, and the amount of phosphorylated tau in sarkosyl-insoluble fractions is inversely proportional t
40 study, we have inoculated well-characterized sarkosyl-insoluble fractions of sporadic Alzheimer's dis
41 nts correlated with the presence of a 29-kDa sarkosyl-insoluble fragment and globular cytoplasmic inc
42 s Abeta fibrils were identical to those from sarkosyl-insoluble homogenates.
43 sary for the evolution of tau oligomers into Sarkosyl-insoluble inclusions even though it is not exte
44 of active GSK3beta leads to the formation of Sarkosyl-insoluble inclusions.
45  neither Tau-D421 nor full-length tau formed Sarkosyl-insoluble inclusions.
46                             We have purified sarkosyl-insoluble NFTs and performed liquid chromatogra
47           Subchronic MPTP exposure increased sarkosyl-insoluble p-Tau in striatum of WT but not alpha
48                                              Sarkosyl-insoluble PHFs were visualized by electron micr
49                                     However, sarkosyl-insoluble phosphorylated tau levels and ubiquit
50    In Nrf2-knockout mice, phosphorylated and sarkosyl-insoluble tau accumulates in the brains concurr
51 ectants, R406W had the highest proportion of sarkosyl-insoluble tau by day 7.
52 u, and an equimolar mixture of the two using sarkosyl-insoluble tau extracted from AD brain and deter
53              In this study, we first derived sarkosyl-insoluble tau fractions from post-mortem brains
54 In addition, fisetin decreased the levels of sarkosyl-insoluble tau in an active GSK-3beta-induced ta
55             In contrast, formation of either sarkosyl-insoluble tau or paired helical filaments was n
56 ikely accounts for our previous finding that sarkosyl-insoluble tau protein extracted from the filame
57                Low levels of phosphorylated, sarkosyl-insoluble tau were detected at 2 months, with a
58                  Treatment nearly eliminated Sarkosyl-insoluble Tau with the most prominent effect on
59                  Furthermore, the content of Sarkosyl-insoluble tau, a measure of abnormal tau aggreg
60 cord, where it had no impact on the level of sarkosyl-insoluble tau.
61 ically relevant epitopes and accumulation of sarkosyl-insoluble tau.
62    By immunoblotting, it was not detected in sarkosyl-insoluble tau.
63 c formyl thiophene acetic acid positive) and sarkosyl-insoluble tau.
64   Our findings suggest that the formation of sarkosyl-insoluble TMEM106B CTFs is an age-related featu
65   Here, we investigated proteins that become sarkosyl-insoluble with age and identified hyaluronan an
66 ontrol brain or recombinant U1-70K to become Sarkosyl-insoluble.
67 merase will initially resume elongation when Sarkosyl is added but loses this capacity within minutes
68 cription in isolated nuclei is stimulated by sarkosyl or high salt.
69                    Complexes treated with 1% Sarkosyl remain elongation-competent but demonstrate a 5
70 ue to increased efficiency of formation of a Sarkosyl-resistant pre-initiation complex.
71 sembled from all six Tau isoforms as well as Sarkosyl-resistant Tau aggregates extracted from cell cu
72 n the other hand, purifying the PFs by using Sarkosyl resulted in no FlaA in the isolated PFs.
73 n, where transcriptional activity acquires a sarkosyl sensitive component in the adult.
74 ied a novel Ets-1 site (at -50), and a novel Sarkosyl-sensitive DNase I-hypersensitive site generated
75 ed DNA and does not require ATP-dependent or Sarkosyl-sensitive factors.
76 tions in the initiator element increased the sarkosyl sensitivity of the rate of elongation and decre
77 n of M. xanthus membranes with the detergent sarkosyl showed that CarR was associated with the inner
78 ranscription experiments using the detergent Sarkosyl showed that this stimulation is due to increase
79  electrophoretic mobility, immunoreactivity, Sarkosyl solubility, and, as a novel approach, resistanc
80  transition of accumulating tau species from Sarkosyl soluble 55 kDa to insoluble hyperphosphorylated
81 phorylated tau aggregates were predominantly sarkosyl soluble and migrated in the light sucrose densi
82 ast, proteinase K-treated AD homogenates and Sarkosyl-soluble AD fractions were unable to induce U1-7
83  trachomatis serovar L2 434/Bu EB, COMC, and Sarkosyl-soluble EB fractions to identify proteins enric
84  studies showed that p76 predominated in the Sarkosyl-soluble fraction of the bacterial cell pellet.
85 he HMW IgBPs were found predominantly in the Sarkosyl-soluble fraction of the culture supernatant.
86 evious studies were strongly enriched in the Sarkosyl-soluble fraction, suggesting that these protein
87 lated tau profiles, with markedly suppressed sarkosyl-soluble phosphorylated tau isoforms.
88 II appear to be paused, in that they display sarkosyl-stimulated trancription in a nuclear run-on tra
89 owing exposure to guanidine hydrochloride or Sarkosyl than was RML PrP27-30.
90 t dodecylmaltoside and the anionic detergent sarkosyl that a linear relationship between detergent qu
91                    Addition of the detergent Sarkosyl to cell lysates solubilized PrPSc106, which ret
92  low concentrations of the anionic detergent Sarkosyl to limit cell-free transcription to a single ro
93                                        Using Sarkosyl to limit transcription to a single-round, we co
94 opy associated with the use of the detergent sarkosyl to solubilize microtubule doublets suggests tha
95  sensitivity of RNAP IIO in both control and Sarkosyl-treated elongation complexes is dependent on th
96                            The incubation of Sarkosyl-treated elongation complexes with nuclear extra
97  resistant to low (0.015%) concentrations of Sarkosyl was accelerated on templates containing either
98                  Sodium lauroyl sarcosinate (sarkosyl) was applied to enhance the dead bacterial perm
99 er, addition of recombinant Xenopus TFIIS to Sarkosyl-washed pol I elongation complexes had no effect
100                  Subsequent elongation by 1% Sarkosyl-washed U(14)/G(16) complexes is unaffected by p
101 sed particles are unstable in the detergent, sarkosyl, which does not disrupt wild-type phage.

 
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