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1 movement of peptidyl-tRNA from the A to the P site.
2 over the start codon of messenger RNA in the P site.
3 ning, and stable binding of Met-tRNAi to the P site.
4 stablishing tRNA(i)(Met):mRNA binding to the P site.
5 between RNAP and the ribosome active-center P site.
6 e the TLD is accommodated into the ribosomal P site.
7 and, under certain conditions, also from the P site.
8 quences along with key residues of the Glc-6-P site.
9 odon of mRNA are positioned in the ribosomal P site.
10 ity of the phosphodiester backbone at the 3'-P site.
11 ides 33.5, 34, and 35) pair with mRNA in the P site.
12 ing the tRNA into a novel orientation at the P site.
13 ite binding and translocation of tRNA to the P site.
14 end of a photoreactive tRNA at the ribosomal P site.
15 ed tRNA base U33 during translocation to the P site.
16 C pairs of tRNA(fMet) bound to the ribosomal P site.
17 -terminal mRNA nucleotides starting from the P site.
18 e been stalled with these sequences in their P site.
19 ansfer and a hitherto unexpected step at the P site.
20 act initiator tRNA base-paired to AUG in the P site.
21 residue that contacts the 25S rRNA near the P site.
22 from As(5+) and As(3+), respectively, at the P site.
23 he acceptor stem of the peptidyl-tRNA in the P site.
24 synthesis by directly binding the ribosomal P-site.
25 toring the occupancy status of the ribosomal P-site.
26 ead under Met-tRNA(i)(Met) reaching into the P-site.
27 for the binding of acetylthiocholine to the P-site.
28 ation of A-site-bound peptidyl-tRNA into the P-site.
29 mal binding of fMet-tRNA(fMet)(prf20) to the P-site.
30 et), eIF2, eIF3, and eIF5 and binds near the P-site.
31 perturbs fMet-tRNA(fMet) positioning in the P-site.
32 tRNA is base-paired to the AUG codon in the P-site.
33 m during translocation of tRNA(Pro) into the P-site.
34 50S subunit and displaces tRNA bound at the P-site.
35 ual binding of this inhibitor to both center P sites.
36 wing strong preference for RXRXXS/T over S/T,P sites.
37 mediates with PKI captured between the A and P sites.
38 nd initiator tRNA in the ribosomal peptidyl (P) site.
39 NA into the ribosomal peptidyl-tRNA binding (P) site.
40 Lys) in the ribosomal peptidyl-tRNA-binding (P) site.
41 xtaposition of tRNAs in the ribosomal A- and P-sites.
42 ector molecules to individual phosphorylated P-sites.
43 rylated the HBV CTD at the serine-proline (S-P) sites.
44 ALys and the slippery codons from the A- and P- sites.
45 the second slippage codon from the A- to the P- sites.
46 annealed AuPd(100) sample to form contiguous Pd sites.
47 surface with higher coverages of contiguous Pd sites.
48 res where TCE would be able to easily access Pd sites.
49 non-FRC users (mean difference in number of PD sites: 6.9, 5.6, and 5.6; P <0.05; mean difference in
50 llows the short CT domain sequence tethering P-site-992 to the PTK core to reach the catalytic site.
51 We discovered that the in cis interaction of P-site-992 with the catalytic site was facilitated by a
52 ion was the case of the most kinase-proximal P-site-992, the catalytic site binding of which occurred
55 cture studies have placed this loop near the P site and have shown it to be involved in the decoding
56 where they contact the peptidyl-tRNA in the P site and play a critical role in promoting the synthes
57 destabilizes codon-anticodon pairing in the P site and promotes slippage of the mRNA in the 5' direc
58 the initiation codon occupies the ribosomal P site and that an elongator tRNA initiates translation
60 aled multiple contacts between the ribosomal P site and tRNA, but how these contacts contribute to P-
61 resolved, one that prevents access to the Q(p) site and another that permits it, supporting a gating
65 ing site, ejection of the eIF1A-CTT from the P-site and rearrangement to a closed conformation of the
68 anner, thus limiting the number of available Pd sites and decreasing the TCE degradation reaction rat
69 potential of a small pore between the E and PS sites and elimination of several structural interacti
71 the tRNA at the peptidyl-tRNA binding site (P site) and with mRNA shed light on the role of these el
72 ite, termed the proximal polyadenylation (pA)p site, and by facilitating splicing of an upstream adja
74 slocation of the A-site tRNA 3' end into the P site, and we estimated the magnitude of rotation angle
75 -site, rearrangement of peptidyl-tRNA in the P-site, and availability of cognate aa-tRNA correspondin
76 ee main pockets in the binding site (D-site, P-site, and the rim of the S1-site) leads to higher affi
77 d to an E site, rotate into a pre-insertion (PS) site, and ultimately align in the catalytic (A) site
78 hannel blocker, or 2',5'-dideoxyadenosine, a P-site antagonist of transmembrane adenylate cyclases.
82 onstants for the binding of carbachol to the P-site are about an order of magnitude larger (i.e., ind
83 RNA and binding of the tRNA to the ribosomal P-site - are as important for re-initiation as for de no
84 the translocation of tRNA from the A to the P site as the small ribosome subunit spontaneously rotat
85 sed affinities for tRNA binding to the A and P sites as well as the cricket paralysis virus internal
86 places the initiation codon directly in the P site, as on HCV-like IRESs and, as we show here, SV 26
87 rombin can make stronger interactions in the P-site, as a result of its exclusive 60-loop, makes of t
88 yl-tRNAs and tRNA(fMet) dissociated from the P site at a similar low rate, even in the presence of va
89 tronic heterogeneity and the distribution of Pd sites at the NP surface, with these two factors playi
94 we solved the crystal structures of proposed P site binding domains from two intergenic region IRES R
96 py a different site in the ribosome than the P-site-binding TCV TSS, suggesting that these two TSS em
97 cating that approximately half of the center P sites bound stigmatellin more slowly and in a differen
99 and molecular dynamics simulations show that P site-bound peptidyl-D-aa-tRNA can trap the ribosomal p
100 binding of the tRNAs to the ribosomal A and P sites, but prevents correct positioning of their CCA-e
101 coarse-grained molecular simulations of the P-site/catalytic site binding reactions that precede EGF
103 es corresponding to direct contacts with the P-site codon or tRNA in bacterial 70S complexes confer G
104 th of the spacer between the SD sequence and P-site codon strongly affects the rate of ribosome trans
106 tion, the spacer between the SD sequence and P-site codon undergoes structural rearrangements, which
108 second intron and polyadenylation at the (pA)p site compete during processing of the B19V pre-mRNA.
109 conserved 18S rRNA residues corresponding to P-site contacts in bacterial ribosomes, are critical for
111 Cy3-labeled ribosomal protein L11 and A- or P-site Cy5-labeled tRNA or Cy3- and Cy5-labeled tRNAs.
112 After translational termination, mRNA and P site deacylated tRNA remain associated with ribosomes
113 c 80S ribosomes remain associated with mRNA, P-site deacylated tRNA, and release factor eRF1 and must
116 ial in their direct binding to the ribosomal P-site due to the hallmark occurrence of the three conse
121 P-tRNA is contacted by domain IV of EF-G and P-site elements within the 30S subunit body, whereas the
126 to the A-site whenever it is vacant and the P-site has peptidyl-tRNA; and association of the EF-Tu t
127 eciprocal crosstalk does not occur at PX(S/T)P sites, i.e., at sites phosphorylated by proline-direct
128 ositioning of mRNA upstream of the ribosomal P site in 48S complexes formed on AUG codons following i
130 tional change is transmitted from one center P site in the dimer to the other upon stigmatellin bindi
131 valent dopants were considered on both V and P sites in order to form Li vacancies needed for Li diff
132 oduced kinase-activating mutations after Lox-P sites in the mouse Stk39 gene, which encodes the termi
133 porter gene constructs in vivo, we show that P sites in these modules mediate activation by proneural
135 obtained for carbachol binding to the A- and P-sites in E and of 2 and 32 mM for carbachol binding to
138 ny of eight candidate phosphorylation sites (P-sites) in either of the two C-terminal (CT) domains.
140 or at the ends of RNA helix 34, in the tRNA P-site, in the distal end of helix 28 and in the helix 1
141 e-quarters of the frameshift sequence in the P site, indicating that the 5' bases of the expanded ant
142 nly the adduct in the minor groove at the 3'-P site inhibited 3'-P, suggesting the importance of the
144 1)), stabilized with the quinol oxidation (Q(P)) site inhibitor stigmatellin alone or in combination
146 phosphorylation at the phosphorylation site (P-site) inhibits holoenzyme reassociation with the catal
147 voking a closed conformation and more stable P site interaction of Met-tRNAi; however, physical evide
148 ction between the initiator tRNA and the 30S P site is tuned to balance efficiency and accuracy durin
154 Selective adsorption of CO at these atomic Pd sites is shown to either prevent the uptake of hydrog
158 on of wild-type ribosome shows that that the P-site loop is inherently flexible, i.e. it is extended
160 mational switch in Nmd3 that allows the uL16 P-site loop to fully accommodate into the PTC where it c
165 s that decrease fidelity, we found that many P-site mutations increase the stringency of start codon
168 w mechanism when tRNA(Pro) is stalled in the P-site next to an empty A-site and a fast mechanism duri
174 most likely accommodation of tRNA(i) in the P site of the 40 S subunit driven by base pairing betwee
176 find that BlaS enhances tRNA binding to the P site of the large ribosomal subunit and slows down spo
178 stabilize interactions of tRNA(Pro) with the P site of the ribosome, causing large conformational cha
181 termediates wherein peptidyl-tRNA enters the P site of the small ribosomal subunit via reversible, sw
183 phosphorylates the functionally critical S/T-P sites of the hepadnavirus core CTD and is incorporated
184 the anticodon stem loops reside in the A and P sites of the small subunit, while the acceptor ends in
186 T is strongly enhanced when it binds to the P-site of AChE, and this fluorescence is partially quenc
191 r with a similar efficiency in cis, with the P-sites of both receptor monomers being phosphorylated t
193 Adjacent transfer RNAs (tRNAs) in the A- and P-sites of the ribosome are in dynamic equilibrium betwe
194 n when these pairs are present in the A- and P-sites of the ribosome independent of other factors kno
196 Due to the geometrical separation of the Pd sites on the surfaces, the steric approach of the rea
198 bound in various combinations to the A-site, P-site, or E-site of ribosomes, and their effect on conf
199 ome is able to accept an electrophile in the P site other than the carboxyl group during elongation.
201 , however, we find that ribosomes carrying a P-site peptidyl-D-aa-tRNA partition into subpopulations
202 sphorylation reaction lead to selectivity in P-site phosphorylation, we performed coarse-grained mole
203 reduced by accommodation of Met-tRNAi in the P site (PIN state) and by their interactions with the an
205 bound in a state not fully engaged with the P site ("POUT") to a closed, arrested conformation with
206 tionally important rRNA helices in the A and P-sites, prior to the completion of the maturation proce
209 ike structure in the A site, whereas the 40S P site remains unoccupied during this initial step.
211 A within the second intron (in which the (pA)p site resides) interfered with the polyadenylation, lea
212 u sites with increased reactivity, while the Pd sites responsible for unselective decarbonylation pat
213 responding codon move spontaneously into the P site, resulting in a complex with a 3 nt longer spacer
214 anslocation of the expanded anticodon to the P site results in movement of mRNA by four nucleotides,
215 rearrange to hand off the A-site tRNA to the P site, revealing an active role for ribosomal RNA in th
216 within the first intron (upstream of the (pA)p site) stimulated the polyadenylation; in contrast, spl
219 talyze the covalent linkage of an A-site and P-site substrate; however, the product did not contain a
221 e of insertion of a NeoR gene flanked by lox P sites targeted to the first intron of the Th gene.
223 king a peptidyl group is translocated to the P site, the mRNA slips to allow re-pairing of the tRNA w
225 ricts the mRNA entry channel and narrows the P site to enclose tRNAi, thus elucidating key events in
227 ly delivered initiator aminoacyl-tRNA at the P site to the distant GTPase center through interdomain
230 esults identify molecular signaling from the P-site to Tif6 via Efl1, suggesting that the integrity o
232 ite, termed the proximal polyadenylation (pA)p site, to allow accumulation of RNAs that extend into t
233 show that a loop of Rpl10 that embraces the P-site transfer ribonucleic acid was required for releas
238 ns formed between EF4, the ribosome, and the P site tRNA and illuminate the GTPase activation mechani
240 base-pair formation between G2252 and C74 of P site tRNA was disrupted, indicating that this conserve
246 the pre-translocation ribosome in which the P-site tRNA adopts the P/E hybrid state, the L1 stalk do
247 rangements in the intact ribosome that clamp P-site tRNA and mRNA on the small ribosomal subunit.
248 ce that four base-pairs can form between the P-site tRNA and mRNA, and the fourth base-pair involves
251 lization of the deformed conformation of the P-site tRNA by BlaS strongly inhibits peptidyl-tRNA hydr
253 inetic mechanisms, where the identity of the P-site tRNA dictates the kinetic route that is taken.
258 IRES) utilizes a unique mechanism, involving P-site tRNA mimicry, to directly assemble 80S ribosomes
259 irical testing allowed the rate constant for P-site tRNA slippage (k(s)) to be estimated as k(s) appr
261 g broken, in such a manner as to release the P-site tRNA so that it may exit as a free molecule and b
262 not participate in hydrogen-bonding with the P-site tRNA that is required for the efficient proton tr
264 mechanism by bending the 3' terminus of the P-site tRNA toward the A site of the large ribosomal sub
265 93U, changing the h31 loop located below the P-site tRNA(i)(Met), show phenotypes indicating defectiv
266 ose proximity of the SD clearly destabilizes P-site tRNA, RF2-dependent termination and EF-Tu-depende
267 ast, eIF1A-CTT appears to interfere with the P-site tRNA-head interaction in the 'closed' complex and
277 n overlapping the binding sites of the A and P site tRNAs, and RbfA's functionally important C termin
279 al subunit, and interactions with A-site and P-site tRNAs, mRNA, and the antibiotic paromomycin.
283 ctive engagement of peptidyl-tRNA within the P site, we now show that base-pairing mismatches between
284 l phylogenetic conservation of the ribosomal P site, we solved the crystal structures of proposed P s
286 at a reference (R-site) and a polluted site (P-site), were assessed to confirm the findings of a form
287 ible, i.e. it is extended into the ribosomal P-site when this is unoccupied by tRNA, while it is retr
288 , which places the initiation codon into the P site, where it directly base-pairs with eIF2-bound ini
289 le for inhibiting polyadenylation at the (pA)p site, whereas actual splicing, and perhaps assembly of
290 centrations were significantly higher at the P-site, whereas TBT concentrations were in the same rang
291 A that demarcates the boundary between A and P sites, which is potentially important to prevent slipp
292 number of mRNA nucleotides downstream of the P-site, which suggests that ABCE1/Pelota/Hbs1 would disa
293 producing energetic electrons at the surface Pd sites, which enhances the sites' intrinsic catalytic
294 RNA is captured in transition toward the 30S P site, while its 3' acceptor end contacts both the A an
295 ter carbon of the peptidyl-tRNA bound to the P site, while preventing the nucleophilic attack of wate
296 eral conserved serine/threonine-proline (S/T-P) sites whose phosphorylation state is known to regulat
297 nd structurally characterized to bind to the P-site with demonstrated selectivity for the inhibition
299 MRK preferentially phosphorylates R-P-X-S/T-P sites, with the preference for arginine at position -3
300 that Pin1 binds c-Fos through specific pS/T-P sites within the c-Fos TAD, and that this interaction