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1 evidence of splice motifs in the sequence of L form.
2  to switch into a wall-free state called the L-form.
3 ific MSC inhibitor GsMTx4, in both the D and L forms.
4  and division mechanism of Bacillus subtilis L-forms.
5 proliferation of wall-less bacteria known as L-forms.
6 and the potential threat posed by pathogenic L-forms.
7 or studying the genetics and cell biology of L-forms.
8 the pentoses are better competitors than the l-forms.
9 iral life emerged using amino acids in their l-form?
10 nto a cell-wall-deficient state, called the "L-form" [1-3].
11 ing intramuscular immunisation, GBS67-CpGODN+L formed a vaccine depot at the injection site and induc
12                                        RNase L forms a crossed homodimer stabilized by ankyrin (ANK)
13 et cells are absent, the other subunit (CylL(L)'') forms a complex with CylL(S)'', blocking it from a
14  and gp120 than their respective native, all-l forms, although activity differences were modest, part
15  mutant strains indicated that exsD and pscB-L form an operon.
16                                       In the L-form analogues, the L-Tyr analogue has the highest ove
17 an MAIL protein detected was the 80 kDa MAIL-L form and human MAIL showed nuclear localization.
18 ere sufficient to support the import of both L-form and D-form conjugates in permeabilized cells.
19  investigated the functional significance of L-form and S-form C-CAM in rat prostate by examining the
20  define a molecular mechanism that regulates LD form and function to facilitate lipid utilization in
21  (Phaseolus vulgaris agglutinin; PHA; E- and L-forms) and snowdrop lectin (Galanthus nivalis agglutin
22  (2) RPA showed the 3' termini of both S and L forms, and there are putative polyadenylation signals
23 i to generate cell-wall-deficient, spherical L-forms, and found that they robustly reverted to a rod-
24 known for decades, the general properties of L-forms are poorly understood, largely due to the lack o
25                                              L-forms are variants of common bacteria that can grow an
26                                              L-forms are wall-deficient variants of common bacteria t
27 leucine, whereas their stereoisomers (d- and l-forms) are predicted to be significantly more challeng
28 dorferi, known variably as "cyst forms" and "L-forms," are responsible for the pathogenesis of chroni
29 ely competed only by cationic amino acids in L-form: arginine, lysine, ornithine, and 2,4-diamino-n-b
30 ation) and FNA (0.11 +/- 0.02 mg of HNO(2)-N/L, formed as a result of the increased NH(4)(+)-N concen
31  L', the all-trans photoproduct of wild-type L formed at 80 K.
32  regulate the nuclear accessibility of Pt(2) L form autolysosomes with photo-selectivity, which provi
33 es, in the life cycle of cell wall-deficient L-form bacteria.
34 nstrate the presence of cell-wall deficient (L-form) bacteria in fresh urine from 29 out of 30 older
35                                              L-forms become completely independent of the normally es
36                Subsequent reaction in CCl3Br(l) formed Br-terminated Ge(111), as shown by the disappe
37 the two isoforms, namely short (S) and long (L) forms by northern blot and RNAse protection assay (RP
38 e selectively engineered toward either d- or l-forms by changing the gelation conditions.
39  of the theoretical hydride complexes [H-[M]-L](+) formed by the protonation of pair of valence d ele
40 cent discovery that cell-wall-less bacteria (L-forms) can grow and divide independently of FtsZ(4,5),
41 cases, there were 82 S-form cases (37%), 121 L-form cases (55%), and 18 V-form cases (8%).
42 so, an increased percentage of S-form versus L-form cases had the M3 variant phenotype, 24% v 12% (P
43 There were no differences between S-form and L-form cases in either CR rate (79% v 69%; P = .14) or d
44                                              L-form cells may have an important role in chronic or re
45 ng the relative V(max)/K(m) values of D- and L-form dideoxy-CMP, we showed that this kinase lacked st
46 s membrane synthesis are sufficient to drive L-form division in Bacillus subtilis.
47                This reinforces the view that L-form division is driven by an excess accumulation of s
48                  We show that propagation of L-forms does not require the normal FtsZ-dependent divis
49  readily transition from the walled state to L-form during challenge with a cell wall targeting antib
50 ified an unexpected 'escape' step needed for L-form emergence from the rod.
51 with the 'R' form favoring S strand and the 'L' form favoring AS strand silencing.
52 tions act by facilitating the release of the L-form from its walled parent cell but that they act in
53 ecursor synthesis promotes the generation of L-forms from both Gram-positive and Gram-negative bacter
54                             We show that the L-forms generated have in common a mechanism of prolifer
55 l descriptions of the optimal conditions for L-form growth and non-lytic killing by beta-lactam antib
56  gluconeogenesis or depleting oxygen enables L-form growth in Bacillus subtilis, Listeria monocytogen
57 ic culture conditions also worked to promote L-form growth without the class 2 mutations in both Gram
58 s from the respiratory chain, which prevents L-form growth.
59 ving two stereoisomers d and l, but only the l form has a biological positive effect, thus chiral rec
60 ted a progressive transition from a B- to an L-form helix as DNA is gently stretched and progressivel
61 ved peptides exist as the nonisomerized, all-l forms in individual neuron cell bodies.
62 idual ammonium concentration (0.02-0.52 mg N/L) formed in the high-DO MBBR.
63 veloped a controllable system for generating L-forms in the highly tractable model bacterium Bacillus
64 ly due to the lack of systematic analysis of L-forms in the molecular biology era.
65 tates (sulfide, sulfoxide and sulfone) as D-/L- forms into histone eH3.1 at site 4 (a relevant lysine
66                 Our results suggest that the L-form mode of proliferation is conserved across the bac
67              This indicates that both D- and L-form NLS peptides use the same import machinery.
68                                     The D or L form of 2-hydroxyglutarate (2HG) accumulates in certai
69                                          The L form of HBsAg was both necessary and sufficient for vi
70 was superseded by levothyroxine, a synthetic L form of tetraiodothyronine.
71  The transcriptional activities of the J and L forms of PTF1 are independent of Notch signaling, beca
72                Chemically synthesized D- and L- forms of the protein ligand showed reciprocal chiral
73 e all possible dipeptide combinations of the L-form of alanine, valine, and leucine and the achiral a
74 e all possible dipeptide combinations of the L-form of alanine, valine, leucine, and the achiral amin
75                             For example, the l-form of small cardioactive peptide B was detected at h
76 ouble mutant R104M-D133A in complex with the L-form of thymidine supplies a structural explanation fo
77 riers, exhibiting greater preference for the l-forms of arginine, lysine and ornithine.
78               In order to measure the d- and l-forms of aspartate and glutamate, we developed and app
79 yme that catalyzes the degradation of d- and l-forms of DAP to pyruvate and ammonia.
80 n assessed for their ability to identify non-LS forms of inherited risk.
81 motif [CS][CS]-x(0,2)-G-x(1)-C-x(2,3)-S-x(3)-L formed part of an endosome targeting signal for GPI-PL
82                             In addition, the LES formed pathogenic partnerships with AGS in the G. me
83 Bcl-x(L) and DeltaN76Bcl-x(L), but not Bcl-x(L), formed pores large enough to release cytochrome c an
84                         Moreover, the D- and L-forms preferentially bound spleen-derived T-cells over
85 ell wall synthesis is blocked is crucial for L-form proliferation in a wide range of bacteria and als
86                                     Instead, L-form proliferation is driven by a simple biophysical p
87                                              L-form proliferation is remarkable in being independent
88 m Bacillus subtilis and thus how to generate L-forms reliably and reproducibly.
89 e capable of switching into a wall-deficient L-form state in which they are resistant to antibiotics
90 thways involved in switching to and from the L-form state remain poorly understood.
91 uantitatively convert from the walled to the L-form state.
92 ave the ability to switch to a wall-free or 'L-form' state.
93          E. coli switches between walled and L-form states in a zebrafish larva infection model.
94                                              L-form strains are wall-deficient derivatives of common
95                                C-CAM1 (long (L)-form) strongly suppresses the tumorigenicity of human
96 ntrolling lipid droplet (LD) assembly at the LD-forming subdomain of the endoplasmic reticulum (ER).
97                     The results suggest that L-form switching is a physiologically relevant phenomeno
98                                Using the new L-form system, we show here that we can delete essential
99 because of the higher solubility of the pure L form than of the more stable DL racemic compound cryst
100 acteria can form wall-deficient variants, or L-forms, that divide by a simple mechanism that does not
101  only two genetic changes are needed for the L-form transition in Bacillus subtilis [7].
102 ecently determined the genetic basis for the L-form transition in the rod-shaped bacterium Bacillus s
103 e promoters, 11 common SNPs are in extensive LD, forming two 48-kb haplotypes of equal frequency, in
104 m type, PML exon 3 RAR alpha exon 3; a long (L)-form type, PML exon 6 RAR alpha exon 3; or a variable
105 but that the identification of the S-form or L-form type of PML-RAR alpha mRNA, per se, does not pred
106  therapy, the S-form type, compared with the L-form type, was associated with higher values for the w
107 with the second residue (W) in the D- versus L-form was 90 +/- 10%.
108 AEFLa in Aplysia was detected only in an all L-form, we found that both GFFD and GdFFD were present i
109                           The D-form and the L-form were equally effective.
110 re proteolytically resistant in cytosol, the L-forms were rapidly degraded.
111 a protein transduction domain (PTD1) and its L-form with the double substitution A6L and I8A (PTD4),

 
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