戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
1                                              pS(9)-GSK3beta and CDC25A were selectively expressed in
2                                              pS-STAT3 dependency by Helicobacter coincided with trans
3 la) residues increases gamma to 36.5 +/- 1.0 pS.
4 od junctional conductance to approximately 0 pS, regardless of the time of day or the mouse strain.
5                      The 100, 700, and 1,000 pS conductances exhibited different channel characterist
6 d normalized conductance values of 0.02-0.05 pS mum(-2) and breakdown voltages of 400-600 mV.
7 wed a mean unitary conductance of 13.1+/-0.1 pS in 15 cells, which corresponded with I(K1) in sheep a
8 sponded with I(K1) in sheep atria (9.9+/-0.1 pS in 32 cells).
9 small conductance subtype, G25, was 22 +/- 1 pS; the intermediate conductance channel, G35, was 33 +/
10 diate conductance channel, G35, was 33 +/- 1 pS; and the large conductance channel, G45, was 45 +/- 1
11 ings to a single conductance level (41 +/- 1 pS, n = 12).
12 large conductance channel, G45, was 45 +/- 1 pS.
13 ance levels (28 +/- 2, 38 +/- 1 and 46 +/- 1 pS, n = 7, one level per cluster, all levels being detec
14                              Levels of IRS-1 pS(6)(1)(6) and IRS-1 pS(6)(3)(6)/(6)(3)(9) and their ac
15 in IRS-1 phosphorylated at serine 616 (IRS-1 pS(6)(1)(6)) and IRS-1 pS(6)(3)(6)/(6)(3)(9).
16        Levels of IRS-1 pS(6)(1)(6) and IRS-1 pS(6)(3)(6)/(6)(3)(9) and their activated kinases correl
17  at serine 616 (IRS-1 pS(6)(1)(6)) and IRS-1 pS(6)(3)(6)/(6)(3)(9).
18 the opening of large-conductance (237 +/- 10 pS; BK) channels.
19  oligomers producing ion conductances of <10 pS/pore.
20 nnels (i.e. single channel conductance of 10 pS and sensitivity to intracellular Ca(2+)) in PDGFRalph
21 ed the appearance of spontaneously active 10-pS channels.
22 gonucleotide experiments showed that this 10-pS channel is formed from alpha- and beta-ENaC.
23 s revealed gamma(j) of the size range 40-100 pS.
24 , a ranging conductance of approximately 100 pS that is reduced to 54% by calcium, permeating calcium
25 annel had a conductance of approximately 100 pS, consistent with the hypothesis that it underlies an
26 conductance of the channels to be 244 +/- 11 pS (n = 17; symmetrical 150 mm K(+) ) with open probabil
27 channel conductance of AMPARs in SCs is 8-11 pS, which is comparable to that in neurons.
28 e lowest conductance state (approximately 11 pS) was the most sensitive to Zn(2+) inhibition in accor
29 wer main conductance state (approximately 11 pS).
30 nrectifying single channel conductance of 11 pS, substates, and an approximately 3:1 Na(+)/K(+) perme
31 57 pS) is only 2-fold smaller than Cx43 (110 pS).
32 age gating and a unitary conductance of ~110 pS.
33 e principal unitary conductance - 22 pS, 111 pS and 178 pS.
34 ion in the prevalence of a TEA-sensitive 113 pS channel in neurones from TG2576 mice with a correspon
35 al unitary conductances of around 18 pS, 118 pS and 185 pS were also observed in cell-attached record
36 pe conductance at negative potentials was 12 pS.
37  average a single-channel conductance of 125 pS in 150 mM KCl and were found to be cation selective.
38 me of small conductance K(+) channels (13-14 pS) from 0.0007 +/- 0.0007 to 0.0053 +/- 0.0042.
39 er conductance channel of approximately 7-14 pS.
40 hannels, in addition to the approximately 14 pS (TASK-1-like) channel.
41  with conductance levels of approximately 14 pS and approximately 32 pS were recorded at a membrane p
42 operties similar to TASK-1 (approximately 14 pS), TASK-3 (approximately 32 pS) and TASK-1/3 heteromer
43 tance in symmetrical K+ was approximately 14 pS.
44 tween dark-adapted rods is approximately 140 pS, regardless of the time in the circadian cycle.
45 sed SR Ca(2+) indicator), IP(3) activated 15 pS sarcolemmal cation channels, generated a whole-cell c
46 , which increased from ~12 (proximal) to 150 pS mum(-2) (distal).
47 er limit for the membrane conductance of 158 pS.
48 uctance 13 picosiemens (pS) at +60 mV and 16 pS at -60 mV.
49 subunits and has a unitary conductance of 16 pS.
50 nitary junctional conductance (gamma(j); 160 pS) was only slightly altered, and the relative cation/a
51  NMCC exhibits a unitary conductance of ?160 pS and high, voltage-independent open probability.
52 e a single-channel conductance (gamma) of 17 pS and that an average of just seven receptors mediates
53  unitary conductance - 22 pS, 111 pS and 178 pS.
54  principal unitary conductances of around 18 pS, 118 pS and 185 pS were also observed in cell-attache
55 ad a single-channel conductance of around 18 pS, and inactivated with a time constant of 98 +/- 4 ms
56                                   Between 18 pS and 41 pS conductance levels, direct transitions were
57 annel in Task-1(-/-) cells and a smaller (18 pS) K(+)-channel in Task-3(-/-) cells.
58 conductances of around 18 pS, 118 pS and 185 pS were also observed in cell-attached recordings from t
59 lta1-54 produced approximately 90 pS and 188 pS channels, respectively.
60 exhibited a limiting slope conductance of 19 pS and were not observed in dendritic membrane patches.
61 tance reached a maximum of approximately 190 pS at saturating [K(+)], a value 4- to 5-fold larger tha
62 onductance (gamma) from gamma = 6.9, to 11.2 pS, when glutamate was increased from 10 mum to 10 mm.
63 r that those of KCNQ4 and KCNQ5 (2.1 and 2.2 pS, respectively).
64 channel conductance was determined to be 3.2 pS, but unlike any other known wild-type human potassium
65 urrents had a unitary conductance of about 2 pS.
66  had unitary conductances of approximately 2 pS.
67 Icat2) with a conductance of approximately 2 pS.
68 PTA), 1 nm and 10 nm Ang II activated both 2 pS TRPC1/C5 channels and 15-45 pS TRPC6 channels in the
69 and with excellent detection sensitivity (~2 pS).
70 YM 2081 exhibited conductance levels of 2-20 pS.
71  estimated to be 115 +/- 34 pS and 74 +/- 20 pS, at 150 mV and 75 mV, respectively, in satisfactory a
72 K), indirectly activates an approximately 20 pS channel in isolated glomus cells.
73 of mCx30.2 hemichannels was approximately 20 pS, about twice the cell-cell channel conductance.
74 ation with single-channel conductances of 20 pS for inward currents and 80 pS for outward currents.
75 threshold [Ca(2+)]i for activation of the 20 pS channel in cell-attached patches was approximately 20
76             The reversal potential of the 20 pS channel was estimated to be -28 mV.
77                                       The 20 pS channel was not sensitive to voltage.
78                                       The 20 pS channel was permeable to K(+), Na(+) and Cs(+) but no
79 a(2+) channel with FPL64176 activated the 20 pS channel when 1 mm Ca(2+) was present in the external
80  side of inside-out patches activated the 20 pS channel.
81                   We detected a 40-pS and 20-pS potassium channel in the basolateral membrane of the
82 ons between the closed and approximately 200-pS conductance state.
83 ons between the closed and approximately 200-pS open state while simultaneously reducing transitions
84 EK-2L phenotype shows a full open state (202 pS) with several short-lived sub-conductance levels.
85  However, membrane stretch can activate a 21-pS nonselective cation channel.
86 m) reduced the frequency of observance of 21-pS alpha-ENaC channels and simultaneously induced the ap
87 educed the frequency of observance of the 21-pS alpha-ENaC channel but induced the appearance of a 5-
88 el currents had a unitary conductance of 210 pS, typical of Cx50.
89 ere three principal unitary conductance - 22 pS, 111 pS and 178 pS.
90 imately 52 pS) and large ( approximately 220 pS) unitary conductance levels.
91 arge-conductance channel ( approximately 220 pS).
92 y coupled with an average conductance of 220 pS, whereas coupling is undetectable in blue-green cone
93 etrical junctional conductances G(j) (40-223 pS) and a rank order: Rod(C)-large single cone, rod-larg
94  conductance channel ( approximately 185-224 pS).
95 ether, these findings identified a novel 225 pS channel as the native mitochondrial ryanodine recepto
96                                      The 225 pS cation-selective channel exhibited multiple subconduc
97 nnels have a conductance of approximately 23 pS.
98 23C single-channel conductance from 40 to 23 pS but did not produce complete block.
99 e sum of these two conductances averaged 235 pS.
100 ction and caused a reduction in NPo of a 238 pS arterial KCa channel current and an increase in [Ca(2
101 +) current with a unitary conductance of 246-pS in freshly isolated coronary SMCs.
102 as a low conductance (7 pS) channel and a 25-pS channel, the most striking finding was the presence o
103 nels x open probability (NP(o)) of a 230-250 pS K(+) channel was significantly increased after FN app
104 ichannels with a unitary conductance of ~250 pS, and was not due to elevated mutant protein expressio
105 conductance states in the range of 15 to 250 pS, with a larger open probability at 0 mV as compared w
106 ngle channels had a conductance close to 250 pS, within the range of all known BKCa channels.
107 M) K(+) the channel mean conductance was 265 pS, the current reversing at approximately 0 mV.
108 vealed that the channel conductance of 25-27 pS was unaffected by the agonists.
109  high main conductances (approximately 25-28 pS) for gamma2 or delta subunit-containing receptors whe
110  two main conductance levels of 45 pS and 28 pS when the extracellular Ca(2+) concentration was 0.5 m
111 >288 pS for most flickers, but within 15-288 pS for the remaining flickers.
112 ef capacitance flicker (<2 s) with G(p) >288 pS for most flickers, but within 15-288 pS for the remai
113                             Large G(p) (>288 pS) might discharge transmitter rapidly and thereby caus
114 y >375 pS and increased rapidly at > or =299 pS ms(-1).
115  increased with depolarization from 15 +/- 3 pS/pF at -80 mV to 29 +/- 5 pS/pF at -40 mV.
116 n of openings to conductance levels above 30 pS, resulting in larger peak ensemble currents that deca
117 n of openings to conductance levels above 30 pS, resulting in larger peak ensemble currents that deca
118 TP and glibenclamide sensitivities of the 30 pS K channel in TAL cells were absent in mice lacking CF
119 R has been proposed as a regulator of the 30 pS, ATP-sensitive renal K channel (Kir1.1, also known as
120 f 500 picosiemens (pS) in mammals and of 300 pS in yeast.
121 ine with a large conductance for K(+) of 300 pS.
122  of approximately 14 pS and approximately 32 pS were recorded at a membrane potential of -60 mV.
123 proximately 14 pS), TASK-3 (approximately 32 pS) and TASK-1/3 heteromer (approximately 32 pS).
124 pS) and TASK-1/3 heteromer (approximately 32 pS).
125 nductance Ca(2+)-activated K(+) channels (32 pS at -100 mV) which were sensitive to charybdotoxin and
126 nels with a single-channel conductance of 33 pS.
127 -1 cells with a main conductance state of 33 pS.
128 f the hexamer was estimated to be 115 +/- 34 pS and 74 +/- 20 pS, at 150 mV and 75 mV, respectively,
129 have unitary conductance of approximately 35 pS with symmetrical 150 mM KCl solutions.
130 nal conductances averaging approximately 350 pS.
131 The coupling was characterized by small (350 pS or less) junctional conductance (G(j)), which showed
132 nalysis of cultured astrocytes revealed a 37 pS lactate-permeable ion channel activated by cell depol
133 ion pore conductance (G(p)) was usually >375 pS and increased rapidly at > or =299 pS ms(-1).
134        In its place we observed a larger (38 pS) K(+)-channel in Task-1(-/-) cells and a smaller (18
135 herms with gamma(max)(Ca(2+)) of 9.5 +/- 0.4 pS and gamma(max)(Ba(2+)) of 10.3 +/- 0.5 pS.
136 reduced gamma to 8.7 +/- 0.5 and 6.7 +/- 0.4 pS, respectively, both significantly below that of chann
137 (QCA) construct with a gamma of 17.7 +/- 0.4 pS.
138 cetylcholine receptor channels (42.7 +/- 1.4 pS, n = 8, compared with 70.9 +/- 1.6 pS for wild-type,
139 ger when activated by 4BP-TQS (100.3 +/- 2.4 pS) than when activated by ACh (90.0 +/- 2.7 pS), provid
140 uced the channel conductance to 8 pS and 8.4 pS, respectively.
141  (10 microM) did not affect conductance (9.4 pS), but did increase P(o) and short and long open times
142 ingly in heterologous cells (approximately 4 pS).
143  GABA(C) receptor gamma is estimated to be 4 pS.
144  activities with a unitary conductance of 40 pS.
145                             We detected a 40-pS and 20-pS potassium channel in the basolateral membra
146                         Between 18 pS and 41 pS conductance levels, direct transitions were asymmetri
147 so caused the appearance of approximately 42 pS (TASK-1/3-like) and approximately 74 pS (TASK-3-like)
148 tates with a conductance of approximately 42 pS; transitions between fully open and closed states wit
149                                       The 42 pS channel was the most abundant, contributing approxima
150 increased those of TASK-1/3 and TASK-3 to 42 pS and 74 pS, respectively.
151 ivated both 2 pS TRPC1/C5 channels and 15-45 pS TRPC6 channels in the same outside-out patches.
152 h conductances states of about 15, 30 and 45 pS.
153 lycine had two main conductance levels of 45 pS and 28 pS when the extracellular Ca(2+) concentration
154 ying, high conductance channels (gamma = 470 pS).
155 the single channel conductance from 96 to 49 pS.
156 f 98 pS during the subjective day and of 493 pS during the subjective night.
157 e average chord conductance was 24.4 +/- 0.5 pS (n = 11), between 0 and -200 mV, and was 9.6 +/- 0.7
158 th substantially reduced gamma (11.4 +/- 0.5 pS).
159 d a single-channel conductance of 19 +/- 0.5 pS, and made up the majority of the sustained K(+) curre
160 .4 pS and gamma(max)(Ba(2+)) of 10.3 +/- 0.5 pS.
161 ective and had a conductance of 224 +/- 11.5 pS in symmetrical 150 mM K(+) solutions were identified.
162 ddition, a subconductance state at 124 +/- 5 pS was identified.
163 onductance decreased thus: Ba2+ > Ca2+ (14.5 pS) > Mg2+ > Zn2+ (20 mM external cation, 1 mM H2O2).
164 on from 15 +/- 3 pS/pF at -80 mV to 29 +/- 5 pS/pF at -40 mV.
165 ave a single channel conductance of 42 +/- 5 pS for T(4)Vpu and 76 +/- 5 pS for T(5)Vpu in 0.5m KCl.
166 orming subunits is larger (approximately 7.5 pS) than that of Kv4 channels expressed singly in hetero
167 ance of 42 +/- 5 pS for T(4)Vpu and 76 +/- 5 pS for T(5)Vpu in 0.5m KCl.
168 conductances of KCNQ2 and KCNQ3 (6.2 and 8.5 pS, respectively) were much higher that those of KCNQ4 a
169 aC channel but induced the appearance of a 5-pS channel, presumably a alphabetagamma-ENaC channel.
170  HTC hepatoma cells evoked the opening of 50 pS K+-permeable channels, consistent with intermediate c
171 onal conductance between paired rods was 500 pS and the coupling coefficient (the ratio of voltage re
172  states with conductance of approximately 52 pS in magnitude occur at substantially lower ( approxima
173 lian cells exhibits small ( approximately 52 pS) and large ( approximately 220 pS) unitary conductanc
174 small-conductance channel ( approximately 52 pS).
175 ad 3 subconductance states of 14, 32, and 53 pS.
176 f 7 kcal/mol and a maximum conductance of 53 pS compared to the experimental value of 6 pS.
177 se reconstituted into lipid bilayers form 53-pS channels activated by Ca(2+) and thiol oxidants and i
178 four chord conductances of 18, 30, 41 and 54 pS.
179 isy open state with a mean conductance of 54 pS (+40 mV).
180 ed three conductance levels of 15, 35 and 55 pS.
181 with unitary conductance of approximately 56 pS.
182 43, while its single channel conductance (57 pS) is only 2-fold smaller than Cx43 (110 pS).
183 d bilayers, with a unitary conductance of 57 pS in 1 M KCl and numerous larger conductance levels.
184 ad a single-channel conductance of 6 +/- 0.6 pS, inactivated with a time constant of 23 +/- 2 ms at +
185 /- 1.4 pS, n = 8, compared with 70.9 +/- 1.6 pS for wild-type, n = 6).
186 2+) chelator BAPTA-AM activated the same 2.6 pS SOC in coronary artery.
187 l currents with a unitary conductance of 2.6 pS which were not inhibited by either ET(A) or ET(B) rec
188 l with a single channel conductance of ~28.6 pS.
189 rees C, LDS-P5 formed narrow pores (58 +/- 6 pS) with low open probability, whereas OG-P5 formed larg
190 single-channel conductance was measured as 6 pS with open probability of < or =0.03.
191 ously observed single-channel conductance (6 pS at pH 3) implies an open channel probability of 10(-6
192  increases gamma to the resolvable range (>6 pS).
193 3 pS compared to the experimental value of 6 pS.
194 tween this open state and a approximately 65-pS subconductance state.
195  average junctional conductance is about 650 pS.
196 single-channel conductance is as low as 1.67 pS and that channel activation is a one-step process.
197 uctance states of about 18, 34 and 51 and 68 pS, and a reversal potential of 0 mV.
198 d), with conductances ranging from 28 to 689 pS, except for their ionic selectivity, which was slight
199 , between 0 and -200 mV, and was 9.6 +/- 0.7 pS (n = 8), between 0 and 50 mV; these magnitudes and th
200  increasedgamma to 23 +/- 1.0 and 26 +/- 0.7 pS, respectively.
201 pS) than when activated by ACh (90.0 +/- 2.7 pS), providing evidence that activation by allosteric an
202  single MCU conductance is approximately 6-7 pS (105 mM [Ca(2+)]), and MCU flux appears to be modulat
203 openings with an apparent conductance of 9.7 pS, consistent with recent reports of native and recombi
204              As well as a low conductance (7 pS) channel and a 25-pS channel, the most striking findi
205 ocked by Gd(3+), have a conductance of 50-70 pS and, like many other TRP channels, open at very posit
206 S and the embryonic DmInsP(3)R isoform is 70 pS; 3), ug3 mutation affects sensitivity of the DmInsP(3
207  at S368, reduced the incidence of 55- to 70-pS channels, and reduced by 10-fold the selective permea
208 those of TASK-1/3 and TASK-3 to 42 pS and 74 pS, respectively.
209 y 42 pS (TASK-1/3-like) and approximately 74 pS (TASK-3-like) channels, in addition to the approximat
210 ol (OAG) induced single channel activity (75 pS) that was not observed in TRPC7-/- cells but was resc
211 ith alpha4beta2 nAChRs (gamma = 31.3 +/- 0.8 pS), replacement of MA 0' residues by arginine in alpha4
212 d a single-channel conductance of 11 +/- 0.8 pS, did not inactivate with prolonged membrane depolariz
213 y rectified, K+-specific current with a 10.8 pS unitary conductance at -100 mV.
214 nt has a unitary conductance of 61.7 +/- 5.8 pS, similar to that reported for wild-type alpha7, but a
215 ) channels with a unitary conductance of 7.8 pS were resolved in excised patches of ICC.
216 e similar in conductance to ANO1 channels (8 pS) expressed in HEK293 cells.
217 (1 mM), reduced the channel conductance to 8 pS and 8.4 pS, respectively.
218  transition conductances (gamma(j)) of 30-80 pS.
219 9 pA and single-channel conductance is 74-80 pS; 2), in optimal recording conditions the maximal sing
220 uctances of 20 pS for inward currents and 80 pS for outward currents.
221 f the fully open channel is approximately 85 pS, and it is permeable to Lucifer yellow, Alexa Fluor(3
222 e of the adult head DmInsP(3)R isoform is 89 pS and the embryonic DmInsP(3)R isoform is 70 pS; 3), ug
223 l currents with a unitary conductance of 1.9 pS.
224 1-44 and Delta1-54 produced approximately 90 pS and 188 pS channels, respectively.
225  satisfactory agreement with the value of 90 pS measured at 75 mV.
226 audin-2 channels display conductances of ~90 pS.
227 reatment or during perinatal development, 90-pS stretch-activated cation channels that could be block
228 ctional conductance has a median value of 98 pS during the subjective day and of 493 pS during the su
229 n1 with three related ligands that include a pS-P substrate peptide, and two pS-P substrate analogue
230 by applying the chirality descriptors pR and pS.
231 vealed that VH1 is highly active toward both pS/pT and pY peptides.
232 irement for IL-11 signaling via constitutive pS-STAT3 in Helicobacter-induced gastric carcinogenesis.
233 es that are phosphorylated (i.e., containing pS, pT, or pY) from those that are nonphosphorylated (i.
234 phase, phosphorylation of Emi1 generates a D-pS-G-X-X-pS degron to recruit the SCF(betaTrCP) ubiquiti
235 imeras consisting of alternating TMO and DNA-pS subunits exhibit higher binding affinity toward compl
236 p-ACC1 peptide, with the sequence 1258-DSPPQ-pS-PTFPEAGH-1271), which provides molecular evidence for
237 Fam20C is a kinase that phosphorylates S-x-E/pS motifs on proteins in milk and in the extracellular m
238 idification postdraw by complexing H-fibroin pSs, creating Ca(2+)-stabilized crystalline beta-nanodom
239 gnostic phosphate OH stretch (indicative for pS, pT, or pY) can be distinguished from the alcohol OH
240 criptional role and obligate requirement for pS-STAT3 in gastric cancer that could be extrapolated to
241  infection in mice, we reveal a key role for pS-STAT3 in promoting Helicobacter-induced gastric patho
242 nalysis of the monophosphorylated peptide FQ[pS]EEQQQTEDELQDK shows that in the resulting c- and z-ty
243 w a high variety of conductance states (from pS to nS) that are dependent both on the lipid compositi
244  mucosa of mice and patients with gastritis, pS-STAT3 was constitutively expressed irrespective of He
245 that the suppressed gastric tumorigenesis in pS-STAT3-deficient gp130 (F/F) mice associated with redu
246 s (pS) and morpholinos, to create morpholino-pS hybrid oligonucleotides.
247 enables the easy incorporation of morpholino-pS moieties and therapeutically relevant sugar modificat
248 basis of a recurrent GSK-3 consensus motif ((pS/pT)XXX(S/T)), but this prediction has not been tested
249 previously unrecognized 14-3-3-binding motif-pS/pT (X1-2)-COOH, referred to here as mode III.
250  of these moieties (i.e., containing neither pS, pT, pY nor S, T, Y).
251     Here, we reveal that genetic ablation of pS-STAT3 in the gp130 (F/F) spontaneous gastric cancer m
252 gh increased IFN-gamma induced activation of pS(727)-Stat1 and inhibition of pY(705)-Stat3 phosphoryl
253      Notably, the protumorigenic activity of pS-STAT3 aligned with its capacity to primarily augment
254 sies did not show significant correlation of pS(9)-GSK3beta and CDC25A expression (P<0.2).
255  NPM-ALK in 293T cells led to an increase of pS(9)-GSK3beta (glycogen synthase kinase 3 beta) compare
256 ary homolog (ERH) as interacting partners of pS-STAT3 that are pivotal for its transcriptional activi
257                           Phosphorylation of pS(9)-GSK3beta by NPM-ALK was mediated by the PI3K/AKT s
258 ial mitochondrial functions, yet the role of pS-STAT3 among epithelial cancers is ill-defined.
259 (ESCs), we found that approximately 2.4% of (pS/pT)XXX(S/T) sites are phosphorylated in a GSK-3-depen
260 acy, comparable to that of a chimeric 2'-OMe-pS/pO control, during in vitro bioassay screens designed
261 relative to the lines producing pS1, pS2, or pS(T) However, the betaA-betaB loop Asn-55-His and Lys-5
262 d pharmacophores, namely, phosphorothioates (pS) and morpholinos, to create morpholino-pS hybrid olig
263     Here, by coupling serine-phosphorylated (pS)-STAT3-deficient Stat3(SA/SA) mice with chronic H. fe
264 receptor substrate-1 (IRS1) phosphorylation (pS(307) IRS1/total IRS1) and serine/threonine-protein ki
265  Akt while enhancing serine phosphorylation (pS(307)) of IRS1.
266         By contrast, serine phosphorylation (pS) of STAT3 can augment its nuclear transcriptional act
267 t exhibits no activity toward phosphoserine (pS) or phosphothreonine (pT) peptides.
268 tified in each sample in vivo phosphoserine (pS) phosphorylation sites at pS434, pS440, and pS441, as
269 +) complexation by H-fibroin phosphoserines (pSs) and a shift in secondary structure from random coil
270 of protein phosphatases toward phosphoseryl (pS) and phosphothreonyl (pT) peptides.
271 ly 700, and approximately 1,000 picosiemens (pS) in symmetrical 150 mm CsCl were observed.
272 e single channel conductance 13 picosiemens (pS) at +60 mV and 16 pS at -60 mV.
273  mean conductance of 224 +/- 26 picosiemens (pS).
274 from 7.8 +/- 0.5 to 5.0 +/- 0.5 picosiemens (pS).
275 possessing a conductance of 500 picosiemens (pS) in mammals and of 300 pS in yeast.
276 of adaptive evolution of these two genes, pN/pS > 1, was demonstrated.
277 how that KSHV Rta protein contains potential pS/T-P motifs and binds directly to Pin1.
278 isomerization of phosphorylated-Ser/Thr-Pro (pS/T-P) motifs found in numerous signaling proteins regu
279  phosphoserine- or phosphothreonine-proline (pS/T-P) motifs in target proteins.
280 or threonine residues that precede prolines (pS/T-P), such as the transcription factors p53 and c-Jun
281 e only phosphorylated residue in the protein pS(16); therefore, changes in the LRAP-HAP interaction a
282 hosphosite-specific antibody that recognizes pS(355,356).
283                                          RSX(pS/pT)XP and RXPhiX(pS/pT)XP are two canonical consensus
284                      RSX(pS/pT)XP and RXPhiX(pS/pT)XP are two canonical consensus binding motifs for
285  kinase B substrate consensus sequence RXRXX(pS/pT) and a phosphospecific antibody that recognizes se
286  which lacks a PBD consensus binding site (S(pS/pT)(P/X)), and that Dbf4 inhibits Cdc5 function durin
287 s mapped to residues 146 to 148 within the S(pS/T)P motif, and the phosphorylation site was identifie
288 cal; it does not require either a complete S-pS/pT-P motif in Mtrm or key residues in the Polo-box do
289 els, enhanced its phosphorylation at serine (pS) 279/282, and increased VSMC proliferation both in vi
290 found that Pin1 binds c-Fos through specific pS/T-P sites within the c-Fos TAD, and that this interac
291 on in the phosphorylation of Ser(727)-Stat1 (pS(727)-Stat1), and IFN-gamma induced dephosphorylation
292 s producing potato Rubisco incorporating the pS(T)-subunit, which reduced CE and CO(2)/O(2) specifici
293 by the amino acid residues C-terminal to the pS, pT, or pY residue.
294 omoting the cis-trans isomerization of these pS/T-P bonds.
295  intrinsically low catalytic activity toward pS and pT substrates, suggesting that its primary physio
296 d more stringent sequence specificity toward pS/pT than pY substrates.
297 s (pS1, pS2, and pS3) or the potato trichome pS(T)-subunit.
298 at include a pS-P substrate peptide, and two pS-P substrate analogue inhibitors locked in the cis and
299 anonical 14-3-3 binding site (RSXpSXP, where pS denotes phosphoserine) located in the amino-terminal
300 osphorylation of Emi1 generates a D-pS-G-X-X-pS degron to recruit the SCF(betaTrCP) ubiquitin ligase,

 
Page Top