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1 fMet-Leu-Phe triggered association of a cytosolic NADPH
3 rophils were present, the neutrophil agonist fMet-Leu-Phe triggered calcium signaling in Fura-2-loade
5 l transduction pathways that mediate C5a and fMet-Leu-Phe (fMLP)-induced pertussis toxin (PTx)-sensit
6 ic HL-60 cells, T leukemic MOLT-4 cells, and fMet-Leu-Phe-activated, but not resting, human neutrophi
7 joining, initiation factor dissociation and fMet-tRNA(fMet) positioning during formation of the 70S
8 ed that the ribosome, initiation factors and fMet-tRNA(fMet) can acquire different conformations in t
9 ents to the ribosome, initiation factors and fMet-tRNA(fMet) that occur during maturation of a 70S in
10 apid 50S subunit joining involves a GTP- and fMet-tRNA(fMet)-dependent "activation" of IF2, but a lac
12 n intensities of fluorophore-labeled IF2 and fMet-tRNA(fMet) to determine the effects on both 30SIC f
13 ormational changes of ribosome-bound IF2 and fMet-tRNA(fMet), which are monitored by spectral changes
16 tion of a binary complex between IF2(mt) and fMet-tRNA that may play an important role in mitochondri
19 at there was significant competition between fMet-ethyl ester formation and release in all three rele
24 ch a single site, the P site, is occupied by fMet-tRNAfMet as directed by an AUG codon containing mRN
25 hese data indicate that activation of p38 by fMet-Leu-Phe and lipopolysaccharide involve different me
26 N-terminal part of PSMalpha2 was replaced by fMet-Ile-Phe-Leu (an FPR1-selective peptide agonist) pot
28 ve inhibition of O-2 generation triggered by fMet-Leu-Phe, immune complexes, or phorbol myristate ace
30 trophils stimulated with the chemoattractant fMet-Leu-Phe (fMLP) are known to exhibit rapid activatio
31 L-selectin receptor, or the chemoattractant fMet-Leu-Phe (fMLP), platelet-activating factor, leukotr
33 We have reported that the chemoattractant, fMet-Leu-Phe (fMLP), induces the activation of NF-kappaB
34 NAs requires a SD sequence, the start codon, fMet-tRNA(fMet), and the GTP bound form of initiation fa
35 onyl-tRNA formyltransferase, lack detectable fMet-tRNAfMet but exhibit normal mitochondrial function
36 ) release, changes conformation facilitating fMet-tRNA(i)(fMet) accommodation into the P site and tra
40 initiator tRNAs that carry formylmethionine (fMet), formylglutamine (fGln), or formylvaline (fVal).
41 the level of circulating N-formylmethionine (fMet), which initiates mitochondrial protein translation
42 absence of the N-terminal formylmethionine (fMet), or conversion of the sulfur in this fMet to the s
43 odel of IF2 activation that reveals how GTP, fMet-tRNA(fMet), and specific structural elements of IF2
44 tor transfer RNA N-formyl-methionyl-tRNA(i) (fMet-tRNA(i)(fMet)) and a short piece of messenger RNA (
45 anges conformation facilitating fMet-tRNA(i)(fMet) accommodation into the P site and transition of th
48 s the proper positioning of the fMet-tRNA(i)(fMet) for the formation of the first peptide bond during
49 RNA N-formyl-methionyl-tRNA(i) (fMet-tRNA(i)(fMet)) and a short piece of messenger RNA (mRNA) at a re
50 ) holds initiator transfer RNA (fMet-tRNA(i)(fMet)) in a specific orientation in the peptidyl (P) sit
51 involved in neutrophil activation, including fMet-Leu-Phe (fMLP), platelet-activating factor (PAF), g
52 of eosinophils, chemotactic agents including fMet-Leu-Phe, IL-8, and RANTES, promote vigorous transie
54 nitiation factors, and a dedicated initiator fMet-tRNA(fMet) bind the small (30S) ribosomal subunit.
55 by interfering with the binding of initiator fMet-tRNA(i)(Met) to the ribosomal peptidyltransferase P
56 ed Phe-tRNA(Phe), an analog of the initiator fMet-tRNA(Met), enhanced the population of complexes tha
57 that oxazolidinones interfere with initiator fMet-tRNA binding to the P-site of the ribosomal peptidy
60 show that the N terminus of S105 retains its fMet residue but that the N terminus of S107 is fully de
61 replace yeast IF-2(mt) in strains that lack fMet-tRNA which suggests that this paradigm may extend t
63 same as seen earlier in the initiation-like fMet-tRNA(f)(Met)-ribosome complex, where it was visuali
64 In human cytoplasmic hybrid (cybrid) lines, fMet modulated both mitochondrial and cytosolic proteins
65 rt peptides bearing N-formylated methionine (fMet) that are characteristic of protein synthesis in ba
66 d on its deletion, proper N-formyl-methionyl(fMet)-tRNA(fMet) positioning and efficient transpeptidat
68 a 25-fold greater affinity for mitochondrial fMet-tRNA than Met-tRNA, using either the native mitocho
72 critical roles of the first 3 aa linked to N-fMet as well as the C terminus of PSMalpha2 in promoting
78 nit association, recruitment, and binding of fMet-tRNA to the ribosomal P-site and initiation dipepti
82 of translation, inducing the dissociation of fMet-tRNA(fMet) from the 30 S initiation complexes (30SI
83 of EF-P to enhance the rate of formation of fMet-Lys or fMet-Phe, indicating that the role of EF-P i
84 errin release from the secondary granules of fMet-Leu-Phe-activated PMNs was significantly lower at p
86 IF2 binds to the single-stranded portion of fMet-tRNA(fMet), thereby forcing the tRNA into a novel o
87 f the 5'-AUG is dependent on the presence of fMet-tRNA and is enhanced by the presence of the mitocho
89 n the buffer condition used, whereas that of fMet-tRNAfMet remains the same in both buffer conditions
90 suppresses the respiratory burst of not only fMet-Leu-Phe but also phorbol 12-myristate 13-acetate-st
92 tion with phorbol 12-myristate 13-acetate or fMet-Leu-Phe, p40(phox) translocated to plasma membrane
93 enhance the rate of formation of fMet-Lys or fMet-Phe, indicating that the role of EF-P is not to spe
97 here that the prototypic chemotactic peptide fMet-Leu-Phe (fMLF) stimulates the activation of nuclear
98 of receptors include the chemotactic peptide fMet-Leu-Phe, lipoxin A(4), serum amyloid A and beta-amy
100 n complex bound to S. aureus-derived peptide fMet-Ile-Phe-Leu (fMIFL) and E. coli-derived peptide fMe
102 d not migrate toward the formylated peptide (fMet-Leu-Phe; fMLF), and chemotaxis toward the C. albica
104 osomal subunit to an initiator transfer RNA (fMet-tRNA(fMet))-containing 30S ribosomal initiation com
105 factor 2 (IF2) holds initiator transfer RNA (fMet-tRNA(i)(fMet)) in a specific orientation in the pep
106 ndrial initiation factor 2 (IF2(mt)), [(35)S]fMet-tRNA, and either poly(A,U,G) or an in vitro transcr
107 el electrophoresis systems that can separate fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows th
108 kely forwarded from IF2-G2 to the C-terminal fMet-tRNA binding domain (IF2-C2) because the connected
112 coli 70S initiation complexes containing the fMet-tRNA(fMet) M1 variant paired to the noncanonical CU
113 P) site is mediated by the inspection of the fMet moiety by initiation factor IF2 and of three conser
115 ven slight changes to the recognition of the fMet-tRNA(fMet) anticodon stem by the ribosome can impac
116 -P facilitates the proper positioning of the fMet-tRNA(i)(fMet) for the formation of the first peptid
117 egron pathway, the Pro/N-degron pathway, the fMet/N-degron pathway, and the newly named, in this pers
118 d extended base pairing interaction with the fMet-tRNA anticodon loop, suggesting that this interacti
119 (fMet), or conversion of the sulfur in this fMet to the sulfoxide, resulted in a decrease in LH1 for
120 igration in response to these agonists or to fMet-Leu-Phe occurs only after exposure to differentiati
123 e accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recogni
127 quire a formylated initiator methionyl-tRNA (fMet-tRNAfMet) in a process involving initiation factor
128 vealed that in vitro formation of a 30S-tRNA(fMet)-mRNA ternary complex was inhibited unless a 5' del
129 tor tRNAs, N-acetyl-aminoacyl-tRNAs and tRNA(fMet) dissociated from the P site at a similar low rate,
130 te fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows that there is no formylation in vivo of the
131 on weakens A-minor interactions between tRNA(fMet) and 16S nucleotides A1339 and G1338, with IF2 stre
132 C40 pair of tRNA(fMet) with C-G (called tRNA(fMet) M1) reduces discrimination against the noncanonica
133 planting identity elements into E. coli tRNA(fMet) , we have engineered an orthogonal initiator tRNA
135 letion, proper N-formyl-methionyl(fMet)-tRNA(fMet) positioning and efficient transpeptidation are aff
136 changes to the recognition of the fMet-tRNA(fMet) anticodon stem by the ribosome can impact the star
138 e ribosome, initiation factors and fMet-tRNA(fMet) can acquire different conformations in these compl
140 tion, inducing the dissociation of fMet-tRNA(fMet) from the 30 S initiation complexes (30SIC) contain
142 nitiation complexes containing the fMet-tRNA(fMet) M1 variant paired to the noncanonical CUG start co
143 initiation factor dissociation and fMet-tRNA(fMet) positioning during formation of the 70S elongation
145 e ribosome, initiation factors and fMet-tRNA(fMet) that occur during maturation of a 70S initiation c
146 ies of fluorophore-labeled IF2 and fMet-tRNA(fMet) to determine the effects on both 30SIC formation a
149 ation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.
150 unit to an initiator transfer RNA (fMet-tRNA(fMet))-containing 30S ribosomal initiation complex to fo
153 2 activation that reveals how GTP, fMet-tRNA(fMet), and specific structural elements of IF2 drive and
154 es a SD sequence, the start codon, fMet-tRNA(fMet), and the GTP bound form of initiation factor 2 bou
155 The 70SIC contains initiator tRNA, fMet-tRNA(fMet), bound in the P (peptidyl)-site in response to the
156 phoresis systems that can separate fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows that there i
158 to the single-stranded portion of fMet-tRNA(fMet), thereby forcing the tRNA into a novel orientation
159 changes of ribosome-bound IF2 and fMet-tRNA(fMet), which are monitored by spectral changes of fluore
160 ubunit joining involves a GTP- and fMet-tRNA(fMet)-dependent "activation" of IF2, but a lack of data
166 t the 3GC pairs play a critical role in tRNA(fMet) retention in ribosome during the conformational ch
168 ond, the models reconcile how initiator tRNA(fMet) interacts less strongly with the L1 stalk compared
169 I cleaves each strand of the intronless tRNA(fMet) gene adjacent to the anticodon triplet leaving 3 b
172 that can separate fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows that there is no formylation
173 ive promoter (FP1) located 5' to the mt tRNA(fMet)-RNase P RNA-tRNA(Pro) gene cluster, so that the mi
175 enhanced initiation with the 3GC mutant tRNA(fMet), suggesting that the 70S mode of initiation is les
178 ow yields, deleting redundant copies of tRNA(fMet) from the genome afforded an E. coli strain in whic
181 A-3' terminus and the anticodon loop of tRNA(fMet), and its tRNA specificity is controlled by these i
183 -tRNA binding and suggest that ribosome-tRNA(fMet) interactions are uniquely tuned for tight binding.
186 oup I intron has also been found in the tRNA(fMet) gene of some cyanobacteria but not in plastids, su
190 0S initiation complexes containing this tRNA(fMet) variant paired to the canonical bacterial start co
191 no-terminal peptides bound similarly to tRNA(fMet), whereas little or no binding of polynucleotides,
193 coupled from the expression of upstream tRNA(fMet) gene, and that RPM1 might be independently transcr
195 of binding affinities of various fAA-tRNAs (fMet-, fGln-, fVal-, fIle-, and fPhe-tRNAs) to IF2 using
196 d formation with the N-formyl group and with fMet, a model supported by MD simulation and functional
197 to mount a rise in Ca2+ when challenged with fMet-Leu-Phe, they increase Ca2+ in response to P2U agon
198 th the fluorophore-Met-tRNA(f) compared with fMet-tRNA(f) with pyrene having the least and eosin the
199 F-2(mt) responsible for the interaction with fMet-tRNA was mapped to the C2 sub-domain of domain VI o
200 The ribosomal reaction of puromycin with fMet-tRNA proceeds 3 x 107-fold more rapidly, with a sec