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1 he mRNA in the ribosomal peptidyl-tRNA site (P site).
2 minoacyl site (A site) to the peptidyl site (P site).
3 e the TLD is accommodated into the ribosomal P site.
4 and, under certain conditions, also from the P site.
5 quences along with key residues of the Glc-6-P site.
6 odon of mRNA are positioned in the ribosomal P site.
7 ity of the phosphodiester backbone at the 3'-P site.
8 e been stalled with these sequences in their P site.
9 ansfer and a hitherto unexpected step at the P site.
10 ides 33.5, 34, and 35) pair with mRNA in the P site.
11 ing the tRNA into a novel orientation at the P site.
12 ite binding and translocation of tRNA to the P site.
13 end of a photoreactive tRNA at the ribosomal P site.
14 ed tRNA base U33 during translocation to the P site.
15 C pairs of tRNA(fMet) bound to the ribosomal P site.
16 act initiator tRNA base-paired to AUG in the P site.
17  residue that contacts the 25S rRNA near the P site.
18 from As(5+) and As(3+), respectively, at the P site.
19 he acceptor stem of the peptidyl-tRNA in the P site.
20  movement of peptidyl-tRNA from the A to the P site.
21 over the start codon of messenger RNA in the P site.
22 ning, and stable binding of Met-tRNAi to the P site.
23 stablishing tRNA(i)(Met):mRNA binding to 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 m during translocation of tRNA(Pro) into the P-site.
33 cts with the ribosomal A-site but not in 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 mediates with PKI captured between the A and P sites.
37 wing strong preference for RXRXXS/T over S/T,P sites.
38 NA into the ribosomal peptidyl-tRNA binding (P) site.
39 Lys) in the ribosomal peptidyl-tRNA-binding (P) site.
40 nd initiator tRNA in the ribosomal peptidyl (P) site.
41 xtaposition of tRNAs in the ribosomal A- and P-sites.
42 NA and peptidyl tRNA to the ribosomal E- and P-sites.
43 ector molecules to individual phosphorylated P-sites.
44 rylated the HBV CTD at the serine-proline (S-P) sites.
45 ALys and the slippery codons from the A- and P- sites.
46 the second slippage codon from the A- to the P- sites.
47 annealed AuPd(100) sample to form contiguous Pd sites.
48  surface with higher coverages of contiguous Pd sites.
49 res where TCE would be able to easily access Pd sites.
50 the transition state, including the critical P-site 2'-OH.
51  non-FRC users (mean difference in number of PD sites: 6.9, 5.6, and 5.6; P <0.05; mean difference in
52 llows the short CT domain sequence tethering P-site-992 to the PTK core to reach the catalytic site.
53 We discovered that the in cis interaction of P-site-992 with the catalytic site was facilitated by a
54 ion was the case of the most kinase-proximal P-site-992, the catalytic site binding of which occurred
55            This new slow step, which we term P-site accommodation, has implications for the activatio
56 has no effect on the affinity of tRNA to the P-site, an esterified pheylalanine stabilizes binding to
57                Additional domains occupy the P site and extend toward the sarcin-ricin loop to intera
58 cture studies have placed this loop near the P site and have shown it to be involved in the decoding
59  where they contact the peptidyl-tRNA in the P site and play a critical role in promoting the synthes
60  destabilizes codon-anticodon pairing in the P site and promotes slippage of the mRNA in the 5' direc
61  the initiation codon occupies the ribosomal P site and that an elongator tRNA initiates translation
62 ribosome when its TLD moves to the ribosomal P site and translation resumes on its ORF.
63 aled multiple contacts between the ribosomal P site and tRNA, but how these contacts contribute to P-
64                                     From the P-site and A-site effects on bypassing, we estimated the
65 t, and binding of fMet-tRNA to the ribosomal P-site and initiation dipeptide formation.
66 n peptidyl-tRNA moves from the A-site to the P-site and mRNA is displaced by three nucleotides in the
67 by organophosphates as they pass through the P-site and phosphorylate the catalytic serine in the A-s
68 ing site, ejection of the eIF1A-CTT from the P-site and rearrangement to a closed conformation of the
69               Following translocation to the P-site and transfer of the formed peptidyl moiety, the d
70 anner, thus limiting the number of available Pd sites and decreasing the TCE degradation reaction rat
71  potential of a small pore between the E and PS sites and elimination of several structural interacti
72 ween the binding site for the peptidyl tRNA (P site) and the exiting tRNA (E site).
73  the tRNA at the peptidyl-tRNA binding site (P site) and with mRNA shed light on the role of these el
74 A by four nucleotides from the A site to the P site, and from the P site to the E site.
75 slocation of the A-site tRNA 3' end into the P site, and we estimated the magnitude of rotation angle
76 -site, rearrangement of peptidyl-tRNA in the P-site, and availability of cognate aa-tRNA correspondin
77 amycin M occupies portions of both the A and P-site, and induces a conformational change in the ribos
78 ee main pockets in the binding site (D-site, P-site, and the rim of the S1-site) leads to higher affi
79 d to an E site, rotate into a pre-insertion (PS) site, and ultimately align in the catalytic (A) site
80 hannel blocker, or 2',5'-dideoxyadenosine, a P-site antagonist of transmembrane adenylate cyclases.
81                             In addition, the P sites are not simple spectators and directly participa
82 st that movements of tRNA into the P/E and A/P sites are separable events.
83 onstants for the binding of carbachol to the P-site are about an order of magnitude larger (i.e., ind
84 RNA and binding of the tRNA to the ribosomal P-site - are as important for re-initiation as for de no
85  the translocation of tRNA from the A to the P site as the small ribosome subunit spontaneously rotat
86 sed affinities for tRNA binding to the A and P sites as well as the cricket paralysis virus internal
87  places the initiation codon directly in the P site, as on HCV-like IRESs and, as we show here, SV 26
88 rombin can make stronger interactions in the P-site, as a result of its exclusive 60-loop, makes of t
89 yl-tRNAs and tRNA(fMet) dissociated from the P site at a similar low rate, even in the presence of va
90 tronic heterogeneity and the distribution of Pd sites at the NP surface, with these two factors playi
91 oacyl tRNA substrate analog at the ribosomal P site, at 3.1 A resolution.
92                             In the ribosomal P site, bases C74 and C75 of tRNA, form Watson-Crick bas
93 RNA or damage to the DNA, and is termed the "P" site because it supports proofreading.
94             Point mutation of the seven (S/T)P sites between amino acids 567 and 760 reduces mitotic
95 we solved the crystal structures of proposed P site binding domains from two intergenic region IRES R
96  was weaker in five of the six positions but P site binding was unaffected.
97 ll subunit around C967 and C1400 during tRNA P-site binding sensitive to the type of mRNA that is use
98 py a different site in the ribosome than the P-site-binding TCV TSS, suggesting that these two TSS em
99 cating that approximately half of the center P sites bound stigmatellin more slowly and in a differen
100 e P-loop and thereby mimics C74 and C75 of a P-site bound tRNA.
101 ioned next to the anticodon stem-loop of the P site-bound initiator tRNA.
102 and molecular dynamics simulations show that P site-bound peptidyl-D-aa-tRNA can trap the ribosomal p
103  of the large ribosomal subunit and with the P site-bound tRNA through its extended C terminus.
104  binding of the tRNAs to the ribosomal A and P sites, but prevents correct positioning of their CCA-e
105 gger the removal of deacylated tRNA from the P site by moving RRF toward the ribosomal E site, and su
106  coarse-grained molecular simulations of the P-site/catalytic site binding reactions that precede EGF
107                        The f(5)C(34) enabled P-site codon binding to these normally isoleucine codons
108 es corresponding to direct contacts with the P-site codon or tRNA in bacterial 70S complexes confer G
109 ity of A-site tRNAs, in combination with the P-site codon third nucleotide.
110 e combination of the third nucleotide of the P-site codon, and all 3 nt of the A-site codon.
111 second intron and polyadenylation at the (pA)p site compete during processing of the B19V pre-mRNA.
112 proteins by using ribosomes that contain 30S P sites composed only of RNA.
113 conserved 18S rRNA residues corresponding to P-site contacts in bacterial ribosomes, are critical for
114                                          The P-site contributes to catalytic efficiency by transientl
115  Cy3-labeled ribosomal protein L11 and A- or P-site Cy5-labeled tRNA or Cy3- and Cy5-labeled tRNAs.
116    After translational termination, mRNA and P site deacylated tRNA remain associated with ribosomes
117 c 80S ribosomes remain associated with mRNA, P-site deacylated tRNA, and release factor eRF1 and must
118 l eight aa-tRNAs in both the ribosomal A and P sites despite substantial differences in tRNA sequence
119                          Mutation of the 30S P site destabilized tRNAs to various degrees, depending
120                         rRNA residues in the P site display reduced cleavage in AUG versus AUC PICs;
121 ial in their direct binding to the ribosomal P-site due to the hallmark occurrence of the three conse
122 nition of peptidyl-tRNA in the small subunit P site during EF-G-catalyzed translocation.
123 ecoding of mRNA and for translocation to the P site during protein synthesis.
124 mplex from the A site of the ribosome to the P site during protein synthesis.
125  pe/E-tRNA maintains tight interactions with P-site elements of the swiveled 30S head.
126 P-tRNA is contacted by domain IV of EF-G and P-site elements within the 30S subunit body, whereas the
127 sed Hoxb7creEGFP mice with mice carrying lox-p sites flanking critical regions of fgfr1 and/or fgfr2.
128 ull accommodation of Met-tRNA(i)(Met) in the P site for AUG selection.
129 mylmethionyl-tRNA (fMet-tRNA(fMet)) into the P site for start codon recognition.
130 that favors its extension into the ribosomal P-site had the opposite effect.
131  to the A-site whenever it is vacant and the P-site has peptidyl-tRNA; and association of the EF-Tu t
132 eciprocal crosstalk does not occur at PX(S/T)P sites, i.e., at sites phosphorylated by proline-direct
133 ositioning of mRNA upstream of the ribosomal P site in 48S complexes formed on AUG codons following i
134 sion beyond the first shell of As(5+) at the P site in struvite.
135 tional change is transmitted from one center P site in the dimer to the other upon stigmatellin bindi
136 oduced kinase-activating mutations after Lox-P sites in the mouse Stk39 gene, which encodes the termi
137                            Eleven AML1c (S/T)P sites in the transcriptional activating domain are pho
138 porter gene constructs in vivo, we show that P sites in these modules mediate activation by proneural
139 nase and has lower activity toward other Tyr(P) sites in these proteins.
140 obtained for carbachol binding to the A- and P-sites in E and of 2 and 32 mM for carbachol binding to
141 nd 32 mM for carbachol binding to the A- and P-sites in EC.
142 ny of eight candidate phosphorylation sites (P-sites) in either of the two C-terminal (CT) domains.
143 CTD phosphorylation, specifically at the S/T-P sites, in a mammalian cell lysate.
144  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
145 e-quarters of the frameshift sequence in the P site, indicating that the 5' bases of the expanded ant
146 nly the adduct in the minor groove at the 3'-P site inhibited 3'-P, suggesting the importance of the
147                            Stigmatellin, a Q(P) site inhibitor, inhibits electron transfer from iron-
148 1)), stabilized with the quinol oxidation (Q(P)) site inhibitor stigmatellin alone or in combination
149 ction of a series of forskolin analogs and a P-site inhibitor, 2'-d3'-AMP.
150 s the same position in the catalytic site as P-site inhibitors and substrate analogs.
151                       These were examined as P-site inhibitors of adenylyl cyclase.
152 phosphorylation at the phosphorylation site (P-site) inhibits holoenzyme reassociation with the catal
153 ycin cassette inserted into intron 1 and lox P sites inserted into intron 1 and intron 4.
154 voking a closed conformation and more stable P site interaction of Met-tRNAi; however, physical evide
155 e RNA initiation site and the intron and (pA)p site is increased.
156 ction between the initiator tRNA and the 30S P site is tuned to balance efficiency and accuracy durin
157 ranslocation of peptidyl-tRNA from the A- to P-site is insensitive to perturbation of either.
158 a Efl1, suggesting that the integrity of the P-site is interrogated during maturation.
159  terminal loop of 25S rRNA Helix 84 when the P-site is occupied.
160        Receptor phosphorylation on CT domain P-sites is critical in signaling because of the binding
161                                  Whereas the Pd site is tetrahedral in 2, the Pt site is square-plana
162   Selective adsorption of CO at these atomic Pd sites is shown to either prevent the uptake of hydrog
163                First, the ability of a bound P-site ligand to increase the substrate acetylation rate
164 eal the ribosome aminoacyl (A) and peptidyl (P) site locations.
165                            Mutations in this P-site loop blocked 60S maturation but were suppressed b
166 on of wild-type ribosome shows that that the P-site loop is inherently flexible, i.e. it is extended
167          These analyses suggest that the L11 P-site loop normally helps to optimize ribosome function
168 is structure, a series of mutants within the P-site loop were created and analyzed.
169      A mutant that favors interaction of the P-site loop with the terminal loop of Helix 84 promoted
170                        We call this the L11 'P-site loop'.
171 s that decrease fidelity, we found that many P-site mutations increase the stringency of start codon
172 ar low rate, even in the presence of various P-site mutations.
173  base of the gorge and a peripheral site (or P-site) near the gorge entrance.
174 w mechanism when tRNA(Pro) is stalled in the P-site next to an empty A-site and a fast mechanism duri
175 uired to stabilize the initiator tRNA in the P site of 40S subunit.
176 affinity of tRNA to either the A site or the P site of Escherichia coli 70S ribosomes.
177            The model overlaps with the Glc-1-P site of other PPases such as Pseudomonas aeruginosa dT
178 eraction, which induces +1 frameshift in the P site of ribosome.
179 of initiator tRNA and the start codon in the P site of the 30S ribosomal subunit.
180  most likely accommodation of tRNA(i) in the P site of the 40 S subunit driven by base pairing betwee
181  find that BlaS enhances tRNA binding to the P site of the large ribosomal subunit and slows down spo
182 y, suggesting that deacylated tRNA binds the P site of the ribosome via the E site.
183 rom isotopic substitution in either the A or P site of the ribosome.
184  of the peptidyl-tRNA from the A site to the P site of the ribosome.
185 veal the dynamics of the interactions in the P site of the ribosome.
186 termediates wherein peptidyl-tRNA enters the P site of the small ribosomal subunit via reversible, sw
187         Purified CDK2 phosphorylated the S/T-P sites of the HBV and DHBV CTD in vitro.
188 phosphorylates the functionally critical S/T-P sites of the hepadnavirus core CTD and is incorporated
189 the anticodon stem loops reside in the A and P sites of the small subunit, while the acceptor ends in
190 ments within the aminoacyl (A) and peptidyl (P) sites of the ribosome.
191  T is strongly enhanced when it binds to the P-site of AChE, and this fluorescence is partially quenc
192 ed and aminoacylated tRNAs to the A-site and P-site of E. coli ribosomes afforded an accurate estimat
193 referred translocation of triazoles into the P-site of HIV reverse transcriptase (RT).
194 selective inhibitor of the substrate binding P-site of SYK.
195 sferase that methylates G1575 of rRNA in the P-site of the small (40S) ribosomal subunit.
196 r with a similar efficiency in cis, with the P-sites of both receptor monomers being phosphorylated t
197  tRNA decodes AUA and AUG in both the A- and P-sites of the metazoan mitochondrial ribosome.
198 Adjacent transfer RNAs (tRNAs) in the A- and P-sites of the ribosome are in dynamic equilibrium betwe
199 l algorithm, and deduce events at the A- and P-sites of the ribosome.
200 rent triplet in the "takeoff site", i.e. the P-site on the 5' side of the hungry codon, and an identi
201     Due to the geometrical separation of the Pd sites on the surfaces, the steric approach of the rea
202 (a) complex or its activity, but (4) another PS site on FV(a) does have a regulatory role.
203 bound in various combinations to the A-site, P-site, or E-site of ribosomes, and their effect on conf
204  the same tRNA exhibit significantly similar P-site pairing preferences.
205 , however, we find that ribosomes carrying a P-site peptidyl-D-aa-tRNA partition into subpopulations
206 sphorylation reaction lead to selectivity in P-site phosphorylation, we performed coarse-grained mole
207 reduced by accommodation of Met-tRNAi in the P site (PIN state) and by their interactions with the an
208  bound in a state not fully engaged with the P site ("POUT") to a closed, arrested conformation with
209                                       At the P-site, proline is slow in forming peptide bonds.
210           We conclude that (1) the C2 domain PS site provides all but approximately 1 kT of the free
211 ike structure in the A site, whereas the 40S P site remains unoccupied during this initial step.
212            Initiation from the A but not the P site requires PKI.
213 A within the second intron (in which the (pA)p site resides) interfered with the polyadenylation, lea
214 u sites with increased reactivity, while the Pd sites responsible for unselective decarbonylation pat
215 responding codon move spontaneously into the P site, resulting in a complex with a 3 nt longer spacer
216 anslocation of the expanded anticodon to the P site results in movement of mRNA by four nucleotides,
217 rearrange to hand off the A-site tRNA to the P site, revealing an active role for ribosomal RNA in th
218 within the first intron (upstream of the (pA)p site) stimulated the polyadenylation; in contrast, spl
219                   Mutation G2252U of the 50S P site stimulates mRNA slippage, suggesting that decreas
220                 Isotopomers of the ribosomal P-site substrate, the trinucleotide peptide conjugate CC
221 talyze the covalent linkage of an A-site and P-site substrate; however, the product did not contain a
222             There are also overlaps with the P-site, suggesting that RRF flexibility plays a role in
223 e of insertion of a NeoR gene flanked by lox P sites targeted to the first intron of the Th gene.
224          The role of Au is to isolate single Pd sites that facilitate the coupling of critical surfac
225 king a peptidyl group is translocated to the P site, the mRNA slips to allow re-pairing of the tRNA w
226                              Upstream of the P-site, the proximity of positions (-)3/(-)4 to rpS5(S7p
227 ricts the mRNA entry channel and narrows the P site to enclose tRNAi, thus elucidating key events in
228 odon-anticodon" helix is translocated to the P site to restore the correct reading frame.
229  from the A site to the P site, and from the P site to the E site.
230  direct movement of the tRNAs from the E and P sites to the P and A sites, respectively).
231 esults identify molecular signaling from the P-site to Tif6 via Efl1, suggesting that the integrity o
232 ranslocating tRNAs from the ribosomal A- and P-sites to the P- and E-sites.
233  show that a loop of Rpl10 that embraces the P-site transfer ribonucleic acid was required for releas
234 ain near the exit channel and Rqc2p over the P-site transfer RNA (tRNA).
235 olysis of the nascent protein chain from the P-site transfer RNA.
236  leading to a spring-like deformation of the P-site transfer RNA.
237 al A site and releasing the peptide from the P-site transfer RNA.
238 ns formed between EF4, the ribosome, and the P site tRNA and illuminate the GTPase activation mechani
239          Furthermore, the acylation state of P site tRNA has a dramatic effect on the frequency of in
240 base-pair formation between G2252 and C74 of P site tRNA was disrupted, indicating that this conserve
241                eIF1 also mediates release of P site tRNA, whereas eIF3j ensures subsequent dissociati
242 , as observed in the presence of EF4-GDP and P site tRNA.
243 residue adjacent to the acceptor stem of the P site tRNA.
244 ted bidirectionally to codons cognate to the P site tRNA.
245       At TS formation the 2' OH group of the P-site tRNA A76 forms a hydrogen bond with the oxygen at
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
249  to the Thermus thermophilus ribosome with a P-site tRNA at 2.9 angstroms resolution.
250 acing between the SD sequence and P codon on P-site tRNA binding and RF2-dependent termination.
251 lization of the deformed conformation of the P-site tRNA by BlaS strongly inhibits peptidyl-tRNA hydr
252 inetic mechanisms, where the identity of the P-site tRNA dictates the kinetic route that is taken.
253 lity plays a role in removing the deacylated P-site tRNA during termination of translation.
254                               The deacylated P-site tRNA has moved into a partly translocated pe/E ch
255 de (nt), the dissociation rate (k(off) ) for P-site tRNA increases by > 100-fold.
256           Here, we sought evidence of A- and P-site tRNA interaction by examining bias in codon pair
257 IRES) utilizes a unique mechanism, involving P-site tRNA mimicry, to directly assemble 80S ribosomes
258 irical testing allowed the rate constant for P-site tRNA slippage (k(s)) to be estimated as k(s) appr
259                  These analyses suggest that P-site tRNA slippage is the driving force for +1 ribosom
260 g broken, in such a manner as to release the P-site tRNA so that it may exit as a free molecule and b
261 rlapping binding sites of RRF, EF-G, and the P-site tRNA suggest that the binding of EF-G would trigg
262        Binding of the anticodon stem-loop of P-site tRNA to the ribosome is sufficient to lock the he
263  mechanism by bending the 3' terminus of the P-site tRNA toward the A site of the large ribosomal sub
264 93U, changing the h31 loop located below the P-site tRNA(i)(Met), show phenotypes indicating defectiv
265 ose proximity of the SD clearly destabilizes P-site tRNA, RF2-dependent termination and EF-Tu-depende
266 ast, eIF1A-CTT appears to interfere with the P-site tRNA-head interaction in the 'closed' complex and
267 s mediated by a UG base pair adjacent to the P-site tRNA-mimicking domain.
268 rface between the PTC and the CCA end of the P-site tRNA.
269 ine near the critical A76 2'-OH group on the P-site tRNA.
270 raction between the translocase eEF2 and the P-site tRNA.
271 lex with mRNA and the anticodon stem-loop of P-site tRNA.
272  added to the E site of ribosomes containing P-site tRNA.
273 ter bond that links the polypeptide with the P-site tRNA.
274 16S rRNA, contact the anticodon stem-loop of P-site tRNA.
275 enosine at A76, which mimics the 3' end of a P-site tRNA.
276                             Furthermore, the P-site tRNA/L1 stalk of FSmRNA-programmed pretranslocati
277           Helix 69 interacts with both A and P site tRNAs and contains five modifications.
278 n overlapping the binding sites of the A and P site tRNAs, and RbfA's functionally important C termin
279 iring to the -1 frame of the A site or A and P sites tRNAs.
280 overlapping the positions of mRNA and A- and P-site tRNAs.
281 ridge B2a and contacts the D stems of A- and P-site tRNAs.
282 osed' complex and is likely ejected from the P-site upon start codon recognition.
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
285 tion rate (k(off)) of various tRNAs from the P site were measured.
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  tethers of intermediate length bound to the P-site, whereas those with long tethers reached the A-si
292 A that demarcates the boundary between A and P sites, which is potentially important to prevent slipp
293 number of mRNA nucleotides downstream of the P-site, which suggests that ABCE1/Pelota/Hbs1 would disa
294 producing energetic electrons at the surface Pd sites, which enhances the sites' intrinsic catalytic
295 RNA is captured in transition toward the 30S P site, while its 3' acceptor end contacts both the A an
296 ter carbon of the peptidyl-tRNA bound to the P site, while preventing the nucleophilic attack of wate
297 eral conserved serine/threonine-proline (S/T-P) sites whose phosphorylation state is known to regulat
298  MRK preferentially phosphorylates R-P-X-S/T-P sites, with the preference for arginine at position -3
299 s activated by PEs to phosphorylate the (S/T)P sites within the AML1c molecule and markedly enhance t
300  that Pin1 binds c-Fos through specific pS/T-P sites within the c-Fos TAD, and that this interaction

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