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1 pS(9)-GSK3beta and CDC25A were selectively expressed in
2 pS-STAT3 dependency by Helicobacter coincided with trans
4 od junctional conductance to approximately 0 pS, regardless of the time of day or the mouse strain.
7 wed a mean unitary conductance of 13.1+/-0.1 pS in 15 cells, which corresponded with I(K1) in sheep a
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
13 ance levels (28 +/- 2, 38 +/- 1 and 46 +/- 1 pS, n = 7, one level per cluster, all levels being detec
20 nnels (i.e. single channel conductance of 10 pS and sensitivity to intracellular Ca(2+)) in PDGFRalph
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
28 e lowest conductance state (approximately 11 pS) was the most sensitive to Zn(2+) inhibition in accor
30 nrectifying single channel conductance of 11 pS, substates, and an approximately 3:1 Na(+)/K(+) perme
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
37 average a single-channel conductance of 125 pS in 150 mM KCl and were found to be cation selective.
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
45 sed SR Ca(2+) indicator), IP(3) activated 15 pS sarcolemmal cation channels, generated a whole-cell c
50 nitary junctional conductance (gamma(j); 160 pS) was only slightly altered, and the relative cation/a
52 e a single-channel conductance (gamma) of 17 pS and that an average of just seven receptors mediates
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
58 conductances of around 18 pS, 118 pS and 185 pS were also observed in cell-attached recordings from t
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.
64 channel conductance was determined to be 3.2 pS, but unlike any other known wild-type human potassium
68 PTA), 1 nm and 10 nm Ang II activated both 2 pS TRPC1/C5 channels and 15-45 pS TRPC6 channels in the
71 estimated to be 115 +/- 34 pS and 74 +/- 20 pS, at 150 mV and 75 mV, respectively, in satisfactory a
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
79 a(2+) channel with FPL64176 activated the 20 pS channel when 1 mm Ca(2+) was present in the external
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.
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-
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
95 ether, these findings identified a novel 225 pS channel as the native mitochondrial ryanodine recepto
100 ction and caused a reduction in NPo of a 238 pS arterial KCa channel current and an increase in [Ca(2
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
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
112 ef capacitance flicker (<2 s) with G(p) >288 pS for most flickers, but within 15-288 pS for the remai
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
125 nductance Ca(2+)-activated K(+) channels (32 pS at -100 mV) which were sensitive to charybdotoxin and
128 f the hexamer was estimated to be 115 +/- 34 pS and 74 +/- 20 pS, at 150 mV and 75 mV, respectively,
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
136 reduced gamma to 8.7 +/- 0.5 and 6.7 +/- 0.4 pS, respectively, both significantly below that of chann
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
141 (10 microM) did not affect conductance (9.4 pS), but did increase P(o) and short and long open times
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
153 lycine had two main conductance levels of 45 pS and 28 pS when the extracellular Ca(2+) concentration
157 e average chord conductance was 24.4 +/- 0.5 pS (n = 11), between 0 and -200 mV, and was 9.6 +/- 0.7
159 d a single-channel conductance of 19 +/- 0.5 pS, and made up the majority of the sustained K(+) curre
161 ective and had a conductance of 224 +/- 11.5 pS in symmetrical 150 mM K(+) solutions were identified.
163 onductance decreased thus: Ba2+ > Ca2+ (14.5 pS) > Mg2+ > Zn2+ (20 mM external cation, 1 mM H2O2).
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
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
177 se reconstituted into lipid bilayers form 53-pS channels activated by Ca(2+) and thiol oxidants and i
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 +
187 l currents with a unitary conductance of 2.6 pS which were not inhibited by either ET(A) or ET(B) rec
189 rees C, LDS-P5 formed narrow pores (58 +/- 6 pS) with low open probability, whereas OG-P5 formed larg
191 ously observed single-channel conductance (6 pS at pH 3) implies an open channel probability of 10(-6
196 single-channel conductance is as low as 1.67 pS and that channel activation is a one-step process.
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
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
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
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
214 nt has a unitary conductance of 61.7 +/- 5.8 pS, similar to that reported for wild-type alpha7, but a
219 9 pA and single-channel conductance is 74-80 pS; 2), in optimal recording conditions the maximal sing
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
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
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
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
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
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
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
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
278 isomerization of phosphorylated-Ser/Thr-Pro (pS/T-P) motifs found in numerous signaling proteins regu
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
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
295 intrinsically low catalytic activity toward pS and pT substrates, suggesting that its primary physio
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,