ライフサイエンスコーパス: fMet

1 fMet-Leu-Phe triggered association of a cytosolic NADPH

2 responses to the neutrophil-activating agent fMet-Leu-Phe.

3 rophils were present, the neutrophil agonist fMet-Leu-Phe triggered calcium signaling in Fura-2-loade

4 ion in phorbol 12-myristate 13-acetate - and fMet-Leu-Phe-stimulated COS(phox) cells.

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 apid 50S subunit joining involves a GTP- and fMet-tRNA(fMet)-dependent "activation" of IF2, but a lac

8 e intensities of fluorophore-labeled IF2 and fMet-tRNA(f)(Met).

9 n intensities of fluorophore-labeled IF2 and fMet-tRNA(fMet) to determine the effects on both 30SIC f

10 ormational changes of ribosome-bound IF2 and fMet-tRNA(fMet), which are monitored by spectral changes

11 hanges of fluorescent derivatives of IF2 and fMet-tRNA(fMet).

12 tion of a binary complex between IF2(mt) and fMet-tRNA that may play an important role in mitochondri

13 contacts the 30S and 50S subunits as well as fMet-tRNA(fMet).

14 -tRNA whereas the fVal-tRNA bound as well as fMet-tRNA.

15 ndrial 28S subunits have the ability to bind fMet-tRNA in the absence of mRNA.

16 essenger via interaction with P-site binding fMet-tRNAfMet.

17 Activation of the respiratory burst by fMet-Leu-Phe was optimal at pH 7.2, but was significantl

18 oss-phosphorylated and cross-desensitized by fMet-Leu-Phe, C5a, and IL-8.

19 ch a single site, the P site, is occupied by fMet-tRNAfMet as directed by an AUG codon containing mRN

20 hese data indicate that activation of p38 by fMet-Leu-Phe and lipopolysaccharide involve different me

21 he release of leukotriene C(4) stimulated by fMet-Leu-Phe in IL-5-primed eosinophils.

22 ve inhibition of O-2 generation triggered by fMet-Leu-Phe, immune complexes, or phorbol myristate ace

23 g to programmed ribosomal complexes carrying fMet-tRNA in the P site.

24 trophils stimulated with the chemoattractant fMet-Leu-Phe (fMLP) are known to exhibit rapid activatio

25 L-selectin receptor, or the chemoattractant fMet-Leu-Phe (fMLP), platelet-activating factor, leukotr

26 The chemoattractant fMet-Leu-Phe and the phorbol ester phorbol myristate ace

27 We have reported that the chemoattractant, fMet-Leu-Phe (fMLP), induces the activation of NF-kappaB

28 NAs requires a SD sequence, the start codon, fMet-tRNA(fMet), and the GTP bound form of initiation fa

29 onyl-tRNA formyltransferase, lack detectable fMet-tRNAfMet but exhibit normal mitochondrial function

30 These are 1.8, 3.5, and 10.5 microM for fMet-tRNA, fVal-tRNA, and fGln-tRNA, respectively.

31 bosomes, exhibiting a 50-fold preference for fMet-tRNA over Met-tRNA in this assay.

32 initiator tRNAs that carry formylmethionine (fMet), formylglutamine (fGln), or formylvaline (fVal).

33 absence of the N-terminal formylmethionine (fMet), or conversion of the sulfur in this fMet to the s

34 odel of IF2 activation that reveals how GTP, fMet-tRNA(fMet), and specific structural elements of IF2

35 tor transfer RNA N-formyl-methionyl-tRNA(i) (fMet-tRNA(i)(fMet)) and a short piece of messenger RNA (

36 bosome in complex with the initiator tRNA(i)(fMet) and a short mRNA.

37 s the proper positioning of the fMet-tRNA(i)(fMet) for the formation of the first peptide bond during

38 RNA N-formyl-methionyl-tRNA(i) (fMet-tRNA(i)(fMet)) and a short piece of messenger RNA (mRNA) at a re

39 involved in neutrophil activation, including fMet-Leu-Phe (fMLP), platelet-activating factor (PAF), g

40 of eosinophils, chemotactic agents including fMet-Leu-Phe, IL-8, and RANTES, promote vigorous transie

41 by interfering with the binding of initiator fMet-tRNA(i)(Met) to the ribosomal peptidyltransferase P

42 ed Phe-tRNA(Phe), an analog of the initiator fMet-tRNA(Met), enhanced the population of complexes tha

43 that oxazolidinones interfere with initiator fMet-tRNA binding to the P-site of the ribosomal peptidy

44 mammalian IF2(mt) in complex with initiator fMet-tRNA(iMet) and the eubacterial ribosome.

45 the presence of an aminoacylated initiator, fMet-tRNA(fMet), and IF2 in the GTP-bound state.

46 show that the N terminus of S105 retains its fMet residue but that the N terminus of S107 is fully de

47 replace yeast IF-2(mt) in strains that lack fMet-tRNA which suggests that this paradigm may extend t

48 Chemoattractants like fMet-Leu-Phe (fMLP) induce neutrophils to polarize with

49 same as seen earlier in the initiation-like fMet-tRNA(f)(Met)-ribosome complex, where it was visuali

50 d on its deletion, proper N-formyl-methionyl(fMet)-tRNA(fMet) positioning and efficient transpeptidat

51 ity of bovine IF-2(mt) to bind mitochondrial fMet-tRNA.

52 a 25-fold greater affinity for mitochondrial fMet-tRNA than Met-tRNA, using either the native mitocho

53 al 55S ribosomes in the presence of IF2(mt), fMet-tRNA and poly(A,U,G).

54 ramework of the crystal structure of the MTF.fMet-tRNA complex published recently.

55 as seen in the crystal structure of the MTF.fMet-tRNA(fMet) complex.

56 38 in response to lipopolysaccharide but not fMet-Leu-Phe.

57 In spite of the absence of fMet-tRNA(fMet), the mutant strains exhibited normal mit

58 oop of 16S rRNA or the extended anticodon of fMet-tRNA.

59 dissociation and in promoting the binding of fMet-tRNA to E. coli ribosomes.

60 Full-length IF3(mt) reduces the binding of fMet-tRNA to the 28S subunit in the absence of mRNA.

61 nit association, recruitment, and binding of fMet-tRNA to the ribosomal P-site and initiation dipepti

62 of IF3(mt) to reduce the level of binding of fMet-tRNA to the ribosome in the absence of mRNA.

63 70 S formation, but allows normal binding of fMet-tRNA(fMet)(prf20) to the P-site.

64 of translation, inducing the dissociation of fMet-tRNA(fMet) from the 30 S initiation complexes (30SI

65 of EF-P to enhance the rate of formation of fMet-Lys or fMet-Phe, indicating that the role of EF-P i

66 errin release from the secondary granules of fMet-Leu-Phe-activated PMNs was significantly lower at p

67 28S subunits also bind mRNA independently of fMet-tRNA or added initiation factors.

68 IF2 binds to the single-stranded portion of fMet-tRNA(fMet), thereby forcing the tRNA into a novel o

69 f the 5'-AUG is dependent on the presence of fMet-tRNA and is enhanced by the presence of the mitocho

70 In addition to the removal of fMet, removal of the next two amino acids also resulted

71 n the buffer condition used, whereas that of fMet-tRNAfMet remains the same in both buffer conditions

72 suppresses the respiratory burst of not only fMet-Leu-Phe but also phorbol 12-myristate 13-acetate-st

73 in response to phorbol myristate acetate or fMet-Leu-Phe was reduced in beta-PKC-depleted cells.

74 tion with phorbol 12-myristate 13-acetate or fMet-Leu-Phe, p40(phox) translocated to plasma membrane

75 enhance the rate of formation of fMet-Lys or fMet-Phe, indicating that the role of EF-P is not to spe

76 In contrast, the binding of fVal-tRNA or fMet-tRNA was not affected much by the addition of IF2.

77 Either deacylated tRNAfMet or fMet-tRNAfMet were bound to the 70 S ribosomes, which we

78 Peak fMet-Leu-Phe-induced Ca2+ levels were significantly high

79 here that the prototypic chemotactic peptide fMet-Leu-Phe (fMLF) stimulates the activation of nuclear

80 of receptors include the chemotactic peptide fMet-Leu-Phe, lipoxin A(4), serum amyloid A and beta-amy

81 e cells are treated with chemotactic peptide fMet-Leu-Phe.

82 d not migrate toward the formylated peptide (fMet-Leu-Phe; fMLF), and chemotaxis toward the C. albica

83 t affect stable 70 S formation, but perturbs fMet-tRNA(fMet) positioning in the P-site.

84 ndrial initiation factor 2 (IF2(mt)), [(35)S]fMet-tRNA, and either poly(A,U,G) or an in vitro transcr

85 el electrophoresis systems that can separate fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows th

86 kely forwarded from IF2-G2 to the C-terminal fMet-tRNA binding domain (IF2-C2) because the connected

87 The fGln-tRNA bound less well than fMet-tRNA whereas the fVal-tRNA bound as well as fMet-tR

88 We previously demonstrated that fMet-Leu-Phe (fMLP) stimulates NF-kappaB activation, and

89 IF3(mt) promotes the dissociation of the fMet-tRNA bound in the absence of mRNA.

90 -P facilitates the proper positioning of the fMet-tRNA(i)(fMet) for the formation of the first peptid

91 d extended base pairing interaction with the fMet-tRNA anticodon loop, suggesting that this interacti

92 (fMet), or conversion of the sulfur in this fMet to the sulfoxide, resulted in a decrease in LH1 for

93 igration in response to these agonists or to fMet-Leu-Phe occurs only after exposure to differentiati

94 ed equivalent amounts of O(2) in response to fMet-Leu-Phe and phorbol myristate acetate.

95 Boyden chamber, the chemotactic response to fMet-Leu-Phe was maximal at pH 7.2.

96 e accommodation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recogni

97 quire a formylated initiator methionyl tRNA (fMet-tRNA(fMet)) for initiation.

98 uses a formylated initiator methionyl-tRNA (fMet-tRNA(f)(Met)).

99 (ICs) that carry an N-formyl-methionyl-tRNA (fMet-tRNA(fMet)).

100 quire a formylated initiator methionyl-tRNA (fMet-tRNAfMet) in a process involving initiation factor

101 vealed that in vitro formation of a 30S-tRNA(fMet)-mRNA ternary complex was inhibited unless a 5' del

102 tor tRNAs, N-acetyl-aminoacyl-tRNAs and tRNA(fMet) dissociated from the P site at a similar low rate,

103 te fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows that there is no formylation in vivo of the

104 position 37 of an ectopically expressed tRNA(fMet).

105 letion, proper N-formyl-methionyl(fMet)-tRNA(fMet) positioning and efficient transpeptidation are aff

106 n the crystal structure of the MTF.fMet-tRNA(fMet) complex.

107 tion, inducing the dissociation of fMet-tRNA(fMet) from the 30 S initiation complexes (30SIC) contain

108 table 70 S formation, but perturbs fMet-tRNA(fMet) positioning in the P-site.

109 ies of fluorophore-labeled IF2 and fMet-tRNA(fMet) to determine the effects on both 30SIC formation a

110 tion, but allows normal binding of fMet-tRNA(fMet)(prf20) to the P-site.

111 rmylated initiator methionyl tRNA (fMet-tRNA(fMet)) for initiation.

112 ation of the formylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.

113 carry an N-formyl-methionyl-tRNA (fMet-tRNA(fMet)).

114 nce of an aminoacylated initiator, fMet-tRNA(fMet), and IF2 in the GTP-bound state.

115 2 activation that reveals how GTP, fMet-tRNA(fMet), and specific structural elements of IF2 drive and

116 es a SD sequence, the start codon, fMet-tRNA(fMet), and the GTP bound form of initiation factor 2 bou

117 The 70SIC contains initiator tRNA, fMet-tRNA(fMet), bound in the P (peptidyl)-site in response to the

118 phoresis systems that can separate fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows that there i

119 In spite of the absence of fMet-tRNA(fMet), the mutant strains exhibited normal mitochondrial

120 to the single-stranded portion of fMet-tRNA(fMet), thereby forcing the tRNA into a novel orientation

121 changes of ribosome-bound IF2 and fMet-tRNA(fMet), which are monitored by spectral changes of fluore

122 ubunit joining involves a GTP- and fMet-tRNA(fMet)-dependent "activation" of IF2, but a lack of data

123 fluorescent derivatives of IF2 and fMet-tRNA(fMet).

124 he 30S and 50S subunits as well as fMet-tRNA(fMet).

125 that these interactions play a role in tRNA(fMet) discrimination by IF3.

126 for the vital need of the 3GC pairs in tRNA(fMet) for its function in Escherichia coli.

127 t the 3GC pairs play a critical role in tRNA(fMet) retention in ribosome during the conformational ch

128 n is less dependent on the 3GC pairs in tRNA(fMet).

129 ond, the models reconcile how initiator tRNA(fMet) interacts less strongly with the L1 stalk compared

130 I cleaves each strand of the intronless tRNA(fMet) gene adjacent to the anticodon triplet leaving 3 b

131 study the interactions between the Met-tRNA(fMet) and MTF in solution.

132 on of the initiator methionyl-tRNA (Met-tRNA(fMet)).

133 that can separate fMet-tRNA(fMet), Met-tRNA(fMet), and tRNA(fMet) shows that there is no formylation

134 ive promoter (FP1) located 5' to the mt tRNA(fMet)-RNase P RNA-tRNA(Pro) gene cluster, so that the mi

135 In vivo, the 3GC mutant tRNA(fMet) occurred less abundantly in 70S ribosomes but norm

136 enhanced initiation with the 3GC mutant tRNA(fMet), suggesting that the 70S mode of initiation is les

137 AspRS, was found to bind to noncognate tRNA(fMet) in the presence of Mg(2+).

138 de the sole contact to the G-C pairs of tRNA(fMet) bound to the ribosomal P site.

139 The binding of tRNA(fMet) to amino-terminal peptides was also observed using

140 A-3' terminus and the anticodon loop of tRNA(fMet), and its tRNA specificity is controlled by these i

141 ranslation by site-specific cleavage of tRNA(fMet).

142 -tRNA binding and suggest that ribosome-tRNA(fMet) interactions are uniquely tuned for tight binding.

143 omoter (SP)which is located between the tRNA(fMet) and RPM1 genes.

144 at least one additional feature of the tRNA(fMet) anticodon stem loop.

145 oup I intron has also been found in the tRNA(fMet) gene of some cyanobacteria but not in plastids, su

146 A self-splicing intron in the tRNA(fMet) gene of Synechocystis PCC 6803, which has been pro

147 e entire anticodon stem and loop of the tRNA(fMet) gene.

148 Conversely, the tRNA(fMet) intron has a sporadic distribution, implying that

149 no-terminal peptides bound similarly to tRNA(fMet), whereas little or no binding of polynucleotides,

150 uridine (D) stem of the initiator tRNA (tRNA(fMet)).

151 coupled from the expression of upstream tRNA(fMet) gene, and that RPM1 might be independently transcr

152 The 70SIC contains initiator tRNA, fMet-tRNA(fMet), bound in the P (peptidyl)-site in respo

153 of binding affinities of various fAA-tRNAs (fMet-, fGln-, fVal-, fIle-, and fPhe-tRNAs) to IF2 using

154 to mount a rise in Ca2+ when challenged with fMet-Leu-Phe, they increase Ca2+ in response to P2U agon

155 th the fluorophore-Met-tRNA(f) compared with fMet-tRNA(f) with pyrene having the least and eosin the

156 F-2(mt) responsible for the interaction with fMet-tRNA was mapped to the C2 sub-domain of domain VI o

157 The ribosomal reaction of puromycin with fMet-tRNA proceeds 3 x 107-fold more rapidly, with a sec