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1 lternatively, it can be extracted using 0.3% 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 RNA synthesis in the presence of heparin and sarkosyl.
7 ssed DTP from isolated inclusion bodies with Sarkosyl, 28 mg of DTP was obtained per liter of E. coli
8 e of RNA synthesis to high concentrations of sarkosyl after formation of one or two phospho-diester b
9 ty was strongly inhibited by the detergents, Sarkosyl and deoxycholate, even at 0.025%, but it was no
10 urified elongation complexes treated with 1% Sarkosyl and paused at U(14)/G(16) on an HIV-1 template
11 ce the elongation complexes were released by sarkosyl but not by SII, these complexes apparently did
12 f early steps in initiation as revealed by a sarkosyl challenge assay that exploited the resistance o
13                                              Sarkosyl disruption of preinitiation complex formation f
14 fication process was developed that included Sarkosyl extraction followed by affinity purification on
15                                              Sarkosyl has been used by others to purify B. burgdorfer
16 cur upon dissociation of nucleosomes with 1% sarkosyl, indicating that the RNA polymerases were not d
17         This complex preferentially degrades Sarkosyl insoluble Tau and phosphorylated Tau.
18 ce integral outer membrane (OM) proteins are Sarkosyl insoluble, this is consistent with our previous
19                      This included abundant, sarkosyl-insoluble 4R-tau in both gray and white matter
20 tic alpha-synuclein strains and also between sarkosyl-insoluble alpha-synuclein extracted from two su
21 ther U1 small nuclear ribonucleoproteins are Sarkosyl-insoluble and associate with Tau neurofibrillar
22 reacted with a 64-kDa antigen present in the Sarkosyl-insoluble cell envelope fraction of H. ducreyi
23  but not full-length tau, was present in the Sarkosyl-insoluble fraction and formed thioflavin-S-posi
24 tissues revealed that tau was present in the sarkosyl-insoluble fraction, and composed of three- and
25 olubility in various reagents, including the sarkosyl-insoluble fraction.
26 ses, and the amount of phosphorylated tau in sarkosyl-insoluble fractions is inversely proportional t
27 sary for the evolution of tau oligomers into Sarkosyl-insoluble inclusions even though it is not exte
28 of active GSK3beta leads to the formation of Sarkosyl-insoluble inclusions.
29  neither Tau-D421 nor full-length tau formed Sarkosyl-insoluble inclusions.
30                             We have purified sarkosyl-insoluble NFTs and performed liquid chromatogra
31           Subchronic MPTP exposure increased sarkosyl-insoluble p-Tau in striatum of WT but not alpha
32                                     However, sarkosyl-insoluble phosphorylated tau levels and ubiquit
33    In Nrf2-knockout mice, phosphorylated and sarkosyl-insoluble tau accumulates in the brains concurr
34 ectants, R406W had the highest proportion of sarkosyl-insoluble tau by day 7.
35 In addition, fisetin decreased the levels of sarkosyl-insoluble tau in an active GSK-3beta-induced ta
36             In contrast, formation of either sarkosyl-insoluble tau or paired helical filaments was n
37 ikely accounts for our previous finding that sarkosyl-insoluble tau protein extracted from the filame
38                Low levels of phosphorylated, sarkosyl-insoluble tau were detected at 2 months, with a
39                  Treatment nearly eliminated Sarkosyl-insoluble Tau with the most prominent effect on
40                  Furthermore, the content of Sarkosyl-insoluble tau, a measure of abnormal tau aggreg
41 cord, where it had no impact on the level of sarkosyl-insoluble tau.
42 ically relevant epitopes and accumulation of sarkosyl-insoluble tau.
43    By immunoblotting, it was not detected in sarkosyl-insoluble tau.
44 ontrol brain or recombinant U1-70K to become Sarkosyl-insoluble.
45 merase will initially resume elongation when Sarkosyl is added but loses this capacity within minutes
46 cription in isolated nuclei is stimulated by sarkosyl or high salt.
47                    Complexes treated with 1% Sarkosyl remain elongation-competent but demonstrate a 5
48 ue to increased efficiency of formation of a Sarkosyl-resistant pre-initiation complex.
49 n the other hand, purifying the PFs by using Sarkosyl resulted in no FlaA in the isolated PFs.
50 n, where transcriptional activity acquires a sarkosyl sensitive component in the adult.
51 ied a novel Ets-1 site (at -50), and a novel Sarkosyl-sensitive DNase I-hypersensitive site generated
52 ed DNA and does not require ATP-dependent or Sarkosyl-sensitive factors.
53 tions in the initiator element increased the sarkosyl sensitivity of the rate of elongation and decre
54 n of M. xanthus membranes with the detergent sarkosyl showed that CarR was associated with the inner
55 ranscription experiments using the detergent Sarkosyl showed that this stimulation is due to increase
56  electrophoretic mobility, immunoreactivity, Sarkosyl solubility, and, as a novel approach, resistanc
57  transition of accumulating tau species from Sarkosyl soluble 55 kDa to insoluble hyperphosphorylated
58 phorylated tau aggregates were predominantly sarkosyl soluble and migrated in the light sucrose densi
59 ast, proteinase K-treated AD homogenates and Sarkosyl-soluble AD fractions were unable to induce U1-7
60  trachomatis serovar L2 434/Bu EB, COMC, and Sarkosyl-soluble EB fractions to identify proteins enric
61  studies showed that p76 predominated in the Sarkosyl-soluble fraction of the bacterial cell pellet.
62 he HMW IgBPs were found predominantly in the Sarkosyl-soluble fraction of the culture supernatant.
63 evious studies were strongly enriched in the Sarkosyl-soluble fraction, suggesting that these protein
64 lated tau profiles, with markedly suppressed sarkosyl-soluble phosphorylated tau isoforms.
65 II appear to be paused, in that they display sarkosyl-stimulated trancription in a nuclear run-on tra
66 owing exposure to guanidine hydrochloride or Sarkosyl than was RML PrP27-30.
67 t dodecylmaltoside and the anionic detergent sarkosyl that a linear relationship between detergent qu
68                    Addition of the detergent Sarkosyl to cell lysates solubilized PrPSc106, which ret
69  low concentrations of the anionic detergent Sarkosyl to limit cell-free transcription to a single ro
70                                        Using Sarkosyl to limit transcription to a single-round, we co
71  sensitivity of RNAP IIO in both control and Sarkosyl-treated elongation complexes is dependent on th
72                            The incubation of Sarkosyl-treated elongation complexes with nuclear extra
73  resistant to low (0.015%) concentrations of Sarkosyl was accelerated on templates containing either
74                  Sodium lauroyl sarcosinate (sarkosyl) was applied to enhance the dead bacterial perm
75 er, addition of recombinant Xenopus TFIIS to Sarkosyl-washed pol I elongation complexes had no effect
76                  Subsequent elongation by 1% Sarkosyl-washed U(14)/G(16) complexes is unaffected by p
77 sed particles are unstable in the detergent, sarkosyl, which does not disrupt wild-type phage.

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