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1                                              Gly is the only amino acid that has remained intolerant
2                                              Gly to Ser mutations within the two Gly residues in the
3                                              Gly-4941 replacement with Lys resulted in channels havin
4                                              Gly-MCA is a selective high-affinity FXR inhibitor that
5 ed only in active group (Bet v 1: P = 0.054, Gly m 4: P = 0.037), and no relevant changes occurred fo
6 sly at near-neutral and basic pH and Asn(16)-Gly(17) rather at basic pH.
7 sp at position 177, Gln/Glu at position 180, Gly/Arg at position 239, and Pro/Ser at position 280.
8 (241) alleles) and CELA3B ( approximately 2% Gly(241) alleles) points to individual variations in com
9        In addition, substitution of Gly-245, Gly-247, and Gly-250 affects the amount of PutP in the m
10 ted peptide (CabTRP Ia, Ala(1)-Pro(2)-Ser(3)-Gly(4)-Phe(5)-Leu(6)-Gly(7)-Met(8)-Arg(9)-NH2).
11 ntibody KD-247 targets the Gly(312)-Pro(313)-Gly(314)-Arg(315) arch of the third hypervariable (V3) l
12 ted interaction centered on residues Phe-36, Gly-37, Thr-58, Trp-59, and Lys-60.
13 enkephalin (Met-Enk), [d-Ala(2), N-MePhe(4), Gly-ol(5)]-enkephalin (DAMGO), endomorphin-2, and morphi
14 ioid receptor agonist [D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin produces paradoxical behavioural r
15 r the mu-selectivity of [D-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin (DAMGO)-related glycopeptides by al
16 n of a highly selective OXTR agonist [Thr(4),Gly(7)]-OXT to hippocampal slices resulted in an acute a
17 d phage-displayed peptide libraries Ser-[X]4-Gly-Gly-Gly, with Gly and Ser encoded using unique combi
18 nenzymatic deamidation, the sequence Asn(45)-Gly(46) being deamidated spontaneously at near-neutral a
19 a, Ala(1)-Pro(2)-Ser(3)-Gly(4)-Phe(5)-Leu(6)-Gly(7)-Met(8)-Arg(9)-NH2).
20                               Analogues 69 ([Gly(2),Nle(10),D-Thi(11),Phe(16)]hGLP-2-(1-30)-NH2), 72
21 ),D-Thi(11),Phe(16)]hGLP-2-(1-30)-NH2), 72 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-OH), 73 (
22 0),D-Phe(11),Leu(16)]hGLP-2-(1-33)-OH), 73 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-NH2), 81
23 ing residues from RasGRP1/3 (Thr(7), Tyr(8), Gly(19), and Leu(21), respectively) conferred potent bin
24 2)-Ser(3)-Lys(4)-Pro(5)-Asp(6)-Asn(7)-Pro(8)-Gly(9)-NH2) and a tachykinin-related peptide (CabTRP Ia,
25               The first new element (Gly-807-Gly-811) is short distance element on the C-terminal sid
26 ),D-Phe(11),Leu(16)]hGLP-2-(1-33)-NH2), 81 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-NHEt), an
27 he(11),Leu(16)]hGLP-2-(1-33)-NHEt), and 85 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-NH-((CH2)
28 ntains an RRM domain at the N terminus and a Gly-rich domain at the C terminus.
29              The consequences of replacing a Gly by Ser at each position in the required (Gly-Xaa-Yaa
30                             Analysis using a Gly-Phe-Cys-OMe model tripeptide revealed minimal epimer
31 t of mice with glycine-beta-muricholic acid (Gly-MCA) inhibits FXR signalling exclusively in intestin
32                 The nonessential amino acids Gly and Glu, and the essential amino acid Ile were more
33 -Ser, -Val and the three achiral amino acids Gly, beta-Ala, and GABA).
34 cids in all fractions were dominated by Ala, Gly, Glu and Ser.
35 minobutyric acid > Gln, Thr, Ser > Glu, Ala, Gly, Asn, Asp.
36 ated three mutant forms (I14X; X = Val, Ala, Gly) of the enzyme that have increased active site flexi
37 t the fourth position (ligand 3: H-Dmt-d-Ala-Gly-NMePhe-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) displays bin
38 t the fourth position (ligand 5: H-Dmt-d-Ala-Gly-Phe(4-F)-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) exhibits b
39 plasma with ligands 3, 5, and 7 (H-Tyr-d-Ala-Gly-Phe(4-F)-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) showed tha
40 Ile-Leu-Ala-Pro, Leu-Leu-Ala-Pro and Met-Ala-Gly-Val-Asp-His-Ile, with IC50 values in the range 43-15
41  I viral fusion proteins, including high Ala/Gly content, intermediate hydrophobicity, and few charge
42 ny dose level, sIgE/IgG4 against Bet v 1 and Gly m 4.
43                 The presence of Gln(180) and Gly(239), as in HLA-A2, led to higher cell surface expre
44 glucose homeostasis (GLUT-4, G6PDH, Hk-2 and Gly-Syn-1).
45 ition, substitution of Gly-245, Gly-247, and Gly-250 affects the amount of PutP in the membrane.
46 lix has two conserved glycines, Gly-4934 and Gly-4941, that facilitate RyR1 channel gating by providi
47 0), including a preference for Ser, Arg, and Gly at the +1 and a preference for Arg at the +7 positio
48                                Carnosine and Gly-His were the best substrates for all UPF0586 ortholo
49 helial lineage markers (CD45, CD31, CD14 and Gly-A) and the epithelial marker EpCAM.
50                        The role of GalT2 and Gly in the Fap1 glycosylation is unknown.
51 emonstrate abnormally elevated brain Glu and Gly levels in patients with first-episode psychosis by m
52                 Significantly higher Glu and Gly levels were found in both the anterior cingulate cor
53                                      Glu and Gly levels were measured in vivo in the anterior cingula
54                                      Glu and Gly levels were positively correlated in patients.
55           Peptides carrying multiple Pro and Gly (residues with lowest helical propensity) retain str
56 cosylation by adding a rhamnose residue, and Gly mediates the final glycosylation step by transferrin
57 cosylation by adding a rhamnose residue, and Gly mediates the final glycosylation step by transferrin
58 tagging") of LPXTG-containing substrates and Gly-terminated nucleophiles occurs in vitro as well as i
59 dons coding for Ser, Arg, Leu, Pro, Thr, and Gly.
60      Binding was attenuated by tirofiban and Gly-Pro-Arg-Pro amide, confirming a role for fibrin in a
61                                 Although Arg-Gly-Asp (RGD) integrin ligand and matrix softening confe
62  independently of IGF binding through an Arg-Gly-Asp (RGD) integrin-binding motif.
63                            C3 harbors an Arg-Gly-Asp (RGD) motif, which is the major integrin-binding
64 ocal stresses on the cell surface via an Arg-Gly-Asp-coated magnetic bead.
65 interactions are mediated through the Fn Arg-Gly-Asp (RGD) motif located within the tenth type III re
66 d lipid domains increased beta1-integrin-Arg-Gly-Asp-peptide affinity and valency, thus implicating L
67 elial cells, BA increased beta1-integrin-Arg-Gly-Asp-peptide affinity by 18% with a transition from s
68 ful intermediates for the preparation of Arg-Gly-Asp (RGD)-based cyclopentapeptides (cRGD) with nanom
69 th a higher affinity compared with other Arg-Gly-Asp binding integrins.
70  and two positively charged domains (Pro-Arg-Gly) at both N- and C-termini.
71 aving positively charged N-terminal (Pro-Arg-Gly)3 and negatively charged C-terminal (Glu-Hyp-Gly)3 t
72 cription was effectively blocked by RGD (Arg-Gly-Asp) peptide and neutralizing alphavbeta3 antibodies
73          We previously demonstrated that Arg-Gly-Asp (RGD)-containing ligand-mimetic inhibitors of in
74           Cyclic peptides containing the Arg-Gly-Asp (RGD) sequence have been shown to specifically b
75                  Peptides containing the Arg-Gly-Asp (RGD) sequence have high affinity for alphavbeta
76                                      The Arg-Gly-Gly repeats within the low-complexity region are req
77  migration by targeting integrins, using Arg-Gly-Asp (RGD) peptide-functionalized gold nanorods.
78 g/Arg vs 0.85 [95% CI, 0.63 to 1.15] for Arg/Gly or Gly/Gly, P = .97).
79 around Gly(3)-Phe(4) and a gamma-turn around Gly(2), providing spectroscopic evidence for the formati
80 characterized by a type II' beta-turn around Gly(3)-Phe(4) and a gamma-turn around Gly(2), providing
81 in sequences revealed the presence of an Asp-Gly-Glu (DGE) alpha2beta1 integrin-binding motif in the
82 e O-acetyltransferase uses a similar Gly-Asp-Gly-Ile motif to form the "cysteine synthase" complex wi
83 both the hemiaminal and imine formed between Gly and an aldehyde.
84  The high-affinity FXR agonist GW4064 blocks Gly-MCA action in the gut, and intestine-specific Fxr-nu
85 ed through multiple amino acid residues, but Gly-171 and Leu-175 of P2 were more critical.
86 al exchange of Gln/Glu at position 180 or by Gly/Arg at position 239.
87 major C3S (Arg(102)) and disease-linked C3F (Gly(102)) allotypes of C3b were experimentally explained
88                                          CAP-Gly domain of dynactin, a microtubule-associated activat
89 lasmic linker protein 170 (CLIP170) is a CAP-Gly domain-containing protein that is associated with th
90 ecording direct dipolar contacts between CAP-Gly and tubulin using double rotational echo double reso
91 s indicate that the structure adopted by CAP-Gly varies, particularly around its loop regions, permit
92                         On the contrary, CAP-Gly bound to EB1 is significantly more rigid.
93 onal plasticity and internal dynamics in CAP-Gly, which is essential for the biological functions of
94 ssential for the biological functions of CAP-Gly and its ability to bind to polymeric microtubules an
95 rigin, we addressed internal dynamics of CAP-Gly assembled on polymeric microtubules, bound to end-bi
96 analysis of residue-specific dynamics of CAP-Gly on time scales spanning nano- through milliseconds r
97  present the intermolecular interface of CAP-Gly with microtubules, derived by recording direct dipol
98 l plasticity is an intrinsic property of CAP-Gly.
99 keleton-associated protein glycine-rich (CAP-Gly) domain of dynactin motor on polymeric microtubules,
100 e is due to low plus end affinity of the CAP-Gly domain-containing N-terminus and intramolecular inhi
101 lanine substitution of the conserved central Gly(6)-Gln(7) residues or by random sequence scrambling
102 e tetrapeptide substrates acetyl-Lys-Lys-Cha-Gly-AFC (Ac-KKChaG-AFC) and acetyl-Lys-Thr-Cha-Gly-AFC (
103 y-AFC (Ac-KKChaG-AFC) and acetyl-Lys-Thr-Cha-Gly-AFC (Ac-KTChaG-AFC).
104      Moreover, DTD's activity on non-cognate Gly-tRNA(Ala) is conserved across all bacteria and eukar
105  the GG motif constituted of two consecutive Gly at the C-terminus.
106                               The consequent Gly-tRNA(Gly) 'misediting paradox' is resolved by EF-Tu
107       Moreover, substitutions of a conserved Gly(717) residue, which alter intrinsic enzyme sensitivi
108                      An absolutely conserved Gly in the middle of the alpha1-helix of betaI helps mai
109 cAtg4.2, including mutation of the conserved Gly-244 residue in the hinge region enabling flexibility
110 is highly preferred for binding to conserved Gly:Asp:Asn residues.
111 tics, a series of GLP-2 analogues containing Gly substitution at position 2, norleucine in position 1
112                                 In contrast, Gly replacements N-terminal to the GFPGER sequence, up t
113  whereas a low response of the corresponding Gly-4934 variants suggested loss of function.
114 d displaying a terminal carboxylic acid (DBS-Gly).
115 iggers assembly of DBS-CO2H, followed by DBS-Gly; a good degree of kinetic self-sorting is achieved.
116 re formed, in which the network based on DBS-Gly is positively patterned into a pre-existing network
117 N-unsubstituted alpha-amino acids, dipeptide Gly-Gly, and also benzylamine were used as the amine com
118 ncorporated species included two dipeptides (Gly-Phe (2) and Phe-Gly (3)), as well as a thiolated dip
119 ir triple-helical structures and distinctive Gly-Xaa-Yaa repeating sequence, where Xaa is often proli
120                       The first new element (Gly-807-Gly-811) is short distance element on the C-term
121 irulence peptide 1 (vp1), a highly expressed Gly-Gly peptide-encoding gene in chinchilla middle ear e
122 e RetGC1 binding site, insertion of an extra Gly residue between Ser-173 and Leu-174 as well as delet
123              A linker encompassing six extra Gly residues relative to wild-type EmrE failed to give r
124 hemiaminal/imine in the observed facilitated Gly transport.
125 mbrane and coiled coil regions by a flexible Gly-rich linker.
126 no acid residues in the P2 position, and for Gly in the P1 position, which is absolutely conserved in
127 Ala, Asp, Ser, and Thr at high rates and for Gly, Lys, Phe, Tyr, and Val at moderate or low rates, re
128 rmyl-protected glycine as the ligand (Formyl-Gly-OH) was crucial for the development of this reaction
129 ly (FnIII9(2G)10) insertion, and (iv) a four-Gly (FNIII9(4G)10) insertion in the interdomain linker r
130 in alpha3beta1 binding 17-fold, and the four-Gly insertion decreased binding 39-fold compared with Fn
131 the dynamics of the major amino acids, e.g., Gly, remained unaltered with respect to parity.
132     All fractions were rich in Lys, Glu/Gln, Gly, Pro, Ala, Asp/Asn, and Arg.
133 due in the small subunit with Ser, Val, Gln, Gly, or Asp, and we analyzed the effects of these mutati
134 n-473 is positioned on a short loop (Asn-Gln-Gly-Glu-Pro) instead of an alpha-helix and forms hydroge
135  (TTLL5) glutamylates RPGR(ORF15) in its Glu-Gly-rich repetitive region containing motifs homologous
136 of RPGR (RPGR(ORF15)), carrying multiple Glu-Gly tandem repeats and a C-terminal basic domain of unkn
137 displayed peptide libraries Ser-[X]4-Gly-Gly-Gly, with Gly and Ser encoded using unique combinations
138 uantify in vivo glutamate (Glu) and glycine (Gly) levels in patients with first-episode psychosis as
139 med via adsorption of zwitter-ionic glycine (Gly-zw) onto the surface of sodium montmorillonite (Na-M
140 we demonstrate that substitution of glycine (Gly) with aza-glycine in collagen may increase the numbe
141 ergistically transport highly polar glycine (Gly) across vesicle membranes.
142                               Using glycine (Gly) as an example, we demonstrate a novel method to acc
143 ore-lining helix has two conserved glycines, Gly-4934 and Gly-4941, that facilitate RyR1 channel gati
144  8 > Pru p 1 > Aln g 1 > Api g 1 > Act d 8 > Gly m 4.
145            Among the small peptides 2-31, (H)Gly-Gly-Phe-Leu(OMe) (30) reduced prostaglandin producti
146 work (MOF) based on the tripeptide Gly-l-His-Gly (GHG) for the enantioselective separation of metamph
147 rmining factor; if it is turned away from HN(Gly), the chemostability increases.
148 omprising a formamidinylated, N-hydroxylated Gly-Gln dipeptide conjugated to 6'-amino-pseudouridine.
149 3 and negatively charged C-terminal (Glu-Hyp-Gly)3 triad extensions, respectively.
150 ing in collagen peptides composed of Pro-Hyp-Gly triplet repeats, allowing for truncation to the smal
151 sequence comprising a central block (Pro-Hyp-Gly) and two positively charged domains (Pro-Arg-Gly) at
152 Ga-P03034 ((68)Ga-DOTA-dPEG2-Lys-Arg-Pro-Hyp-Gly-Cha-Ser-Pro-Leu) in B1R-positive (B1R+) HEK293T::hB1
153 02090 ((68)Ga-DOTA-dPEG2-Lys-Lys-Arg-Pro-Hyp-Gly-Cpg-Ser-D-Tic-Cpg) derived from 2 potent B1R antagon
154 04158 ((68)Ga-DOTA-dPEG2-Lys-Lys-Arg-Pro-Hyp-Gly-Igl-Ser-D-Igl-Oic) and Z02090 ((68)Ga-DOTA-dPEG2-Lys
155  Systematic mutation of tyrosine residues in Gly/Ser-Tyr-Gly/Ser motifs of the IDR reduced this effec
156 h 18 of the 20 common amino acids, including Gly, Ala, Ser, Thr, Asp, and Glu, which are relatively s
157  the highest sensitivity and selectivity Leu-Gly-Arg-Met-Gly-Leu-Pro-Gly-Lys was selected to construc
158                            We identify a Lys-Gly-Glu (KGE) integrin-binding motif in the FVIIa protea
159 ed fluorescence assay suitable for measuring Gly influx, and other fluorescence assays for leakage an
160           Intra-PFC DAMGO (D-[Ala2,N-MePhe4, Gly-ol]-enkephalin; a mu-opioid agonist) and d-amphetami
161 o the effects of the agonist d-Ala2-N-MePhe4-Gly-ol enkephalin (DAMGO).
162  sensitivity and selectivity Leu-Gly-Arg-Met-Gly-Leu-Pro-Gly-Lys was selected to construct calibratio
163 mming included a higher rate of metabolizing Gly, which provides additional evidence that the metabol
164 architecture can efficiently edit mischarged Gly-tRNA(Ala) species four orders of magnitude more effi
165 lactose permease (the LacY double-Trp mutant Gly-46-->Trp/Gly-262-->Trp) with bound p-nitrophenyl-alp
166 he catalytic properties of the [Ni(P(Cy) 2 N(Gly) 2 )2 ](2+) complex with the [NiFe]-hydrogenase from
167 tability and structural measures, such as NH(Gly)-CO(Asn-sc) distances.
168 examined by measuring its inhibition of NMDA/Gly-mediated current through NMDAR ion channels in mouse
169  bands from PAGE gels reveal an abundance of Gly/Ala/Ser/Thr repeats exemplified by a prominent, prev
170 y, ceramide treatment reverses the action of Gly-MCA in high-fat diet-induced obese mice.
171          We suggest that the complexation of Gly-zw on the Na-MMT surface accelerates CO2 hydrate nuc
172  was also partially rescued upon deletion of Gly-457.
173                                  Deletion of Gly-720 and Tyr-721 from a highly conserved GYxxO traffi
174                          Here, the effect of Gly replacements within and nearby the integrin binding
175          We critically examine the effect of Gly-to-d-Ala substitutions on protein stability using ex
176 re unresponsive to the beneficial effects of Gly-MCA.
177 atic attraction between the -NH3(+) group of Gly-zw, and the negatively charged Na-MMT surface, provi
178 e by coordinating with the -COO(-) groups of Gly-zw.
179                   However, the importance of Gly-221 for HABP2 activity is unclear.
180 he presence of the proximal l-Ala instead of Gly in the common configuration of the peptide side chai
181 mpact of deletion and replacement mutants of Gly-457 and its two adjacent residues in GAT-1.
182 neral surface (regardless of the presence of Gly-zw) becomes greater than that of bulk phase.
183                               Replacement of Gly residues C-terminal to GFPGER did not affect integri
184 21A, and G221S mutants to assess the role of Gly-221 in HABP2 catalysis.
185 ined by deleting positions on either side of Gly-457.
186 null effect observed for the small subset of Gly-to-d-Ala substitutions which are not stabilizing.
187                 In addition, substitution of Gly-245, Gly-247, and Gly-250 affects the amount of PutP
188         Here, we report that substitution of Gly-4941 with Asp or Lys results in functional channels
189  hexapeptide and several regions upstream of Gly(215) that comprise residues of the interface surface
190                       The replacement of one Gly in the essential repeating tripeptide sequence of th
191                 Mutation of Glu-87 to Ala or Gly rendered the protein constitutively active as a kina
192 s 0.85 [95% CI, 0.63 to 1.15] for Arg/Gly or Gly/Gly, P = .97).
193 abolism (2-hydroxybutanoic acid, oxoproline, Gly, and Glu) were altered in UCP3 Tg mice across all tr
194 lu(1066)), P2 (Asp(1090)-Cys(1104)), and P3 (Gly(1127)-Cys(1140))).
195 very different distributions of FAA- and PAA-Gly.
196                             We found that PB-Gly-Taxol bound the target protein beta-tubulin with bot
197  }(Ac) wheel with glycolate ligands, {Pd84 }(Gly) , and the next in a magic number series for this cl
198               To our knowledge, the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been prev
199 tivation and coupling of C-terminal peptidyl Gly thioacids with the N-terminus of an unprotected pept
200 ergoes self-cleavage between the periplasmic Gly-191 and Thr-192 residues independent of the percepti
201 included two dipeptides (Gly-Phe (2) and Phe-Gly (3)), as well as a thiolated dipeptide analogue (4)
202 trinsically disordered proteins, such as Phe-Gly repeat domains, alters drastically when they are con
203 rgo rearrangements of the N-terminal Asp-Phe-Gly (DFG) motif of the activation loop, with some, inclu
204    N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-
205    N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala along with thei
206 N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala were identified
207 e in water over 10 days except N,N-di-Cl-Phe-Gly.
208  the small hydrophobic peptide Z-d-Phe-l-Phe-Gly (FIP) was shown to block MeV infections and syncytiu
209  The inhibitors carbobenzoxy (Z)-d-Phe-l-Phe-Gly (fusion inhibitor peptide [FIP]) and 4-nitro-2-pheny
210 ine and M is a given monosaccharide), [l-Phe-Gly + M + H](+) (where l-Phe-Gly is l-phenylalanine-glyc
211 phenylalanine-glycine), and [Mn(II) + (l-Phe-Gly - H) + M](+) complex ions are used to determine coll
212 haride), [l-Phe-Gly + M + H](+) (where l-Phe-Gly is l-phenylalanine-glycine), and [Mn(II) + (l-Phe-Gl
213 t to the inhibitory effects of Z-d-Phe-l-Phe-Gly.
214 f either Nup214 or Nup358, the two major Phe-Gly (FG) repeat nucleoporins localized on the cytoplasmi
215 nine (Tyr-Ala), and phenylalanylglycine (Phe-Gly), reacted with sodium hypochlorite, and these reacti
216                    Since only subsets of Phe/Gly motifs, particularly those within Nup62, Nup98, and
217 ing infection, including the cleavage of Phe/Gly-containing nucleoporin proteins (Nups) within nuclea
218 ns of poly(Gly-Pro), poly(Gly-Ala), and poly(Gly-Arg) dipeptide repeat proteins, as well as TDP-43 pa
219 ntained nuclear RNA foci, inclusions of poly(Gly-Pro), poly(Gly-Ala), and poly(Gly-Arg) dipeptide rep
220  RNA foci, inclusions of poly(Gly-Pro), poly(Gly-Ala), and poly(Gly-Arg) dipeptide repeat proteins, a
221 fied that calpain-1 cleaves hERG at position Gly-603 in the S5-pore linker of hERG.
222 e is required for an attack on the preceding Gly-191, after which the resulting ester bond is likely
223 e key amino acid substitutions (Trp --> Pro, Gly --> Ser and Arg --> Leu) are responsible for the evo
224  we report that the matrikine acetylated Pro-Gly-Pro (PGP) stimulates vascular inflammation through a
225 degrading the neutrophil chemoattractant Pro-Gly-Pro (PGP) and rationalized that the failure of conve
226 e traditional beta-turn motifs such as d-Pro-Gly, both the 2-Abz and d-Phe rings may be further funct
227             These reactions build up H2N-Pro-Gly-Ala-CONHL and H2N-Cys-His-Asp-CONHL (where L = organ
228  and selectivity Leu-Gly-Arg-Met-Gly-Leu-Pro-Gly-Lys was selected to construct calibration curves.
229 d inactivates the chemotactic tripeptide Pro-Gly-Pro.
230 Gly by Ser at each position in the required (Gly-Xaa-Yaa)6 Fn-binding sequence are probed here, using
231 g site is located in the vicinity of residue Gly(33), a residue involved in Met(35) oxidation.
232 O prosthetic group created from (189)Ala-Ser-Gly(191) residues and the bound l-phenylalanine and l-ty
233 li serine O-acetyltransferase uses a similar Gly-Asp-Gly-Ile motif to form the "cysteine synthase" co
234 triple helix conformation and stabilisation (Gly, Pro, Hyp and Hyl), whilst the Lys content was great
235 modeling showed that the stretch surrounding Gly-457 is likely to form a pi-helix.
236 n which the residue preceding the C-terminal Gly-Gly (diGly) is replaced with a lysine (SUMO(KGG)).
237  from Gram-positive bacteria lack C-terminal Gly-Tyr-Gly-Ile motifs, suggesting that they do not inte
238 EC536) CdiA-CT(EC536) inserts its C-terminal Gly-Tyr-Gly-Ile peptide tail into the active-site cleft
239                               The N-terminal Gly-rich fragment of rSp0032 and the C-terminal His-rich
240 ond and ligates protein-LPXT to the terminal Gly residue of the nascent cross-bridge of peptidoglycan
241  (i) the critical spacer length (longer than Gly) and (ii) the presence of Ca(2+) and Mg(2+) in all i
242 zation and solid-state assays indicated that Gly replacements at four sites within the Fn-binding seq
243         Whereas previous studies showed that Gly to Ser mutations within an integrin-binding site cau
244                      These data suggest that Gly-MCA may be a candidate for the treatment of metaboli
245                                          The Gly-to-Arg substitution at the 16 position (rs1042713) i
246 ain, which is defined by the presence of the Gly-X-Y triplet repeats, is amongst the most versatile a
247 hin the GS(S/T) motif found in all PSDs, the Gly-307 residue is also essential, but the Ser/Thr-309 i
248 nized monoclonal antibody KD-247 targets the Gly(312)-Pro(313)-Gly(314)-Arg(315) arch of the third hy
249 ve the turn where it can form H-bonds to the Gly(3) and C-terminus C horizontal lineO groups.
250 the self-assembly of type I collagen via the Gly-X-Y motif, the molecular mechanism by which enamel m
251 s the editing activity of ORRM4, whereas the Gly-rich domain is required for its interaction with ORR
252 avin N5 and strong H-bond formation with the Gly-141 carbonyl.
253 lation with norepinephrine compared with the Gly-389 variant.
254  Molecular dynamics simulations showed these Gly replacements interfered with the interaction of a co
255            Strict L-chiral rejection through Gly-cisPro motif during chiral proofreading underlies th
256  via interactions with residues within TMS1 (Gly(56), Thr(57)), TMS3 (Glu(138)), and TMS6 (Phe(248)),
257                           Immunoglobulins to Gly m 4, Vig r 1 and Api g 1.01 were detected in <65% of
258                    ImAP41 contains an Asp-to-Gly substitution in helix III and our structures show th
259 anic framework (MOF) based on the tripeptide Gly-l-His-Gly (GHG) for the enantioselective separation
260 slowdown is not attributable to altered tRNA(Gly) aminoacylation, and cannot be rescued by Drosophila
261 er Sequence of the glyQS leader RNA and tRNA(Gly) anticodon to test the effect of all possible pairin
262 tRFs derived from tRNA(Glu), tRNA(Asp), tRNA(Gly), and tRNA(Tyr) that, upon induction, suppress the s
263                      The consequent Gly-tRNA(Gly) 'misediting paradox' is resolved by EF-Tu in the ce
264 unterpart in charging the mitochondrial tRNA(Gly) isoacceptor, which carries a defective TpsiC hairpi
265 m specific tRNA loci (e.g., the nuclear tRNA(Gly) and tRNA(Leu), the mitochondrial tRNA(Val) and tRNA
266 RS efficiently charged the cytoplasmic tRNAs(Gly) of C. elegans, the mitochondrial form was much more
267 rminal catalytic domain (CAT), a central Trp-Gly-Arg (WGR) domain and an N-terminal region (NTR).
268 ase (the LacY double-Trp mutant Gly-46-->Trp/Gly-262-->Trp) with bound p-nitrophenyl-alpha-d-galactop
269  [BrPhe(22)]sCT(8-32) adopts a type II turn (Gly(28)-Thr(31)), whereas CGRP and AM adopt type I turns
270          Gly to Ser mutations within the two Gly residues in the essential GFPGER sequence prevented
271 te mutation (FnIII9(R)-->(A)10), (iii) a two-Gly (FnIII9(2G)10) insertion, and (iv) a four-Gly (FNIII
272  polar mixture composed of Leu-Val, Leu-Tyr, Gly-Tyr, and Ala-Tyr dissolved in DMSO-d6/GL (8:2, v/v)
273                                     N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly,
274                                     N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and
275                  N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and
276                  N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala a
277 am-positive bacteria lack C-terminal Gly-Tyr-Gly-Ile motifs, suggesting that they do not interact wit
278 diA-CT(EC536) inserts its C-terminal Gly-Tyr-Gly-Ile peptide tail into the active-site cleft of CysK
279 which recognizes the pan-opioid sequence Tyr-Gly-Gly-Phe at the N terminus of most endogenous opioid
280 mutation of tyrosine residues in Gly/Ser-Tyr-Gly/Ser motifs of the IDR reduced this effect, depending
281  three model dipeptides, tyrosylglycine (Tyr-Gly), tyrosylalanine (Tyr-Ala), and phenylalanylglycine
282 ceptor ligand, analogs H-Tyr-c[D-Lys-Xxx-Tyr-Gly] were synthesized and their biological activity was
283  largely undetectable in the effluent unless Gly-Pro-Arg-Pro (GPRP) was added to block fibrin polymer
284 endent on stretches of rare codons, Leu(UUA)-Gly(GGU)-Val(GUA).
285 nyl)alanine at positions 92 and 96; Z = Val, Gly, or Asn at position 95)).
286 aniline-diglycolic acid-DPhe-Gln-Trp-Ala-Val-Gly-His-Leu-NHEt), showing excellent tumor localizing ef
287 rboxymethyl-piperidine-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bombesin
288 rboxymethyl-piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bombesin
289 arboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 (RM2, 1; DOTA:1,4,7,10-tetraazacyclo
290 entified as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and Glu-Lys-Ser-Tyr-Glu-Leu-Pro.
291 he evolutionary replacement of Ala(241) with Gly.
292                              Constructs with Gly to Ser substitutions within and nearby the inserted
293 peptide libraries Ser-[X]4-Gly-Gly-Gly, with Gly and Ser encoded using unique combinations of codons
294 in cleavage site between gp120 and gp41 with Gly-Ser linkers of various lengths.
295 anistically, the metabolic improvements with Gly-MCA depend on reduced biosynthesis of intestinal-der
296 rmed the new hydrogen bond interactions with Gly 48 in the flap of the enzyme.
297 ment of the central hydrophobic residue with Gly (L83G) also conferred no ethidium resistance phenoty
298 died peptides of the sequence EGAAXAASS (X = Gly, Ile, Tyr, Trp) through comparison of molecular dyna
299 protocols for the preparation of various Xaa-Gly dipeptide surrogates in the form of Xaa-psi[triazole
300                % MS SI restoration for the Z-Gly-Gly-Val and bradykinin peptides were 75-83% while %

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