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1                                              UTP (a P2Y(2) and P2Y(4) agonist) increased excitability
2                                              UTP activation of purinergic receptors and hydrolysis of
3                                              UTP also facilitated bladder neuron homomeric P2X(2) sus
4                                              UTP also increased expression of vitronectin, an extrace
5                                              UTP had only a slight effect, and GTP had almost none.
6                                              UTP increased calcium in pericytes leading to capillary
7                                              UTP increased hyaluronan both in the pericellular matrix
8                                              UTP increased the phosphorylation of p38, ERK, CREB, and
9                                              UTP or ADP stimulated afferents, including mouse and hum
10                                              UTP stimulation of endogenous P2Y receptors in COS 7 cel
11                                              UTP, in contrast, increases as the cells transition into
12                                              UTP-enriched TCs were found to be in two distinct fracti
13                                              UTP-gamma-aryl and cycloalkyl phosphoesters displayed on
14                                              UTP-glucose was inactive, but its (S)-methanocarba analo
15                                              UTP-induced phosphorylation of ErbB3 and EGFR was also i
16                                              UTP-induced spreading and migration of aortic SMCs did n
17 e pair (bp), fluorescein, and fluorescein-12-UTP (UTP) were separated in less than 120 s in channels
18 and dCTP bind in a very similar fashion, (2) UTP, in the presence of dCTP or CTP, binds at a site tha
19                  CTP synthetase (EC 6.3.4.2, UTP:ammonia ligase (ADP-forming)) is an essential enzyme
20 P-labeled uridine-5'-triphosphate (alpha-32P-UTP) incorporation, nuclear accumulations of 99mTc-label
21 A levels was detected by both RT-PCR and 32P-UTP in these cells.
22 the fluorinated 5'-triphosphate analogues 5F-UTP and 5F-CTP have been developed to facilitate 19F-lab
23 he availability of efficient synthesis of 5F-UTP, and for the first time, 5F-CTP, will facilitate the
24                                            A UTP cocrystal structure of one mutant shows, in contrast
25 5'-deoxyuridine phosphorylase; (iii) LipM, a UTP:5-amino-5-deoxy-alpha-D-ribose-1-phosphate uridylylt
26                            The presence of a UTP-stimulated, paxilline-sensitive large-conductance Ca
27 e family of glycosyl hydrolases, and UGP1, a UTP-glucose-1-phosphate uridylyltransferase which synthe
28  small interfering RNAs completely abolished UTP-activated sAPP alpha release.
29                                    ATP, ADP, UTP and beta-NAD elicited robust Ca(2+) transients in PD
30 purine receptor ligands (including ATP, ADP, UTP, UDP, and adenosine).
31  of 5'-nucleotidase had no effect on ATP/ADP/UTP-induced phospho- rylation of AMPK, indicating that A
32                 P2Y2 (UTP/ATP) and P2Y6 [ADP/UTP/uridine 5'-diphosphate (UDP)] have been shown to hav
33 ensitive current increased immediately after UTP stimulation and was K(+) dependent.
34 ation of FLNa induced by the P2Y(2)R agonist UTP.
35 P2Y(2) nucleotide receptor (P2Y(2)R) agonist UTP stimulates a strong and sustained release of LTA fro
36 ng the P2Y(2/4) receptor (P2Y(2/4)R) agonist UTP, electrical stimulation, or transgenic mice expressi
37 on of bradykinin or the P2Y-receptor agonist UTP augmented the nicotine-induced increase in CR to abo
38     In contrast, the P2Y(2) receptor agonist UTP caused negligible ATP release, despite promoting a r
39 cation of the selective P2Y receptor agonist UTP decreased peak amplitudes of alpha,beta-meATP-evoked
40  that the G-protein-coupled receptor agonist UTP induces the translocation of PKC delta into the nucl
41      The effects of the P2Y receptor agonist UTP on neuronal excitability and discharge properties we
42                                     Although UTP is the preferred phosphoryl donor for this reaction,
43 nd can be further inhibited by UTP, although UTP alone has little or no influence on activity; howeve
44 hat extracellular nucleotides (ATP, ADP, and UTP, but not UDP) and adenosine independently induce pho
45 re, ex vivo studies showed that both ATP and UTP (10 micromol/L) promoted migration of SMCs out of ao
46                 Enzymatic removal of ATP and UTP (by apyrase or the expression of ectopic CD39) abrog
47 ate the caspase-dependent release of ATP and UTP (in equimolar quantities) during the early stages of
48  mRNA expression were upregulated by ATP and UTP but not ADP or adenosine in vitro.
49 , release of TSP-1 was stimulated by ATP and UTP but not by 2-methylthio-ADP or adenosine.
50                    Apical release of ATP and UTP can activate P2Y(2) receptors in the aldosterone-sen
51   In the present study, we show that ATP and UTP have strikingly opposite effects on human acute myel
52                        Extracellular ATP and UTP induce chemotaxis, or directed cell migration, by st
53 r (P2Y2R) activated by extracellular ATP and UTP molecules released following injury/stress.
54                        Extracellular ATP and UTP nucleotides increase the proliferation and engraftme
55 is model, an initial stimulus evokes ATP and UTP release from a single cell.
56                      The nucleotides ATP and UTP represent one class of find-me signals, but their me
57 ive EcCTPS crystals soaked in either ATP and UTP substrates or ADP and CTP products.
58 ne and pyrimidine nucleotides (e.g., ATP and UTP) are strongly implicated in this process following t
59 , extracellular nucleotides (such as ATP and UTP) have emerged as key immunomodulators.
60 lular purines and pyrimidines (e.g., ATP and UTP), released during bladder distension or from damaged
61 ltiple factors, such as nucleotides, ATP and UTP.
62 ed protein kinases or Akt inhibited ATP- and UTP-induced TSP-1 expression.
63  C5a-mediated actin polymerization, C5a- and UTP-stimulated intracellular calcium mobilization, and t
64 er, they all possess conserved catalytic and UTP recognition domains, often accompanied by various au
65 ditionally, the enzyme utilizes both CTP and UTP equally well as substrates.
66 arbamoylase is feedback inhibited by CTP and UTP in the presence of CTP.
67 ffects of allosteric effectors, ATP, CTP and UTP on the kinetics of the quaternary structure change o
68 rted by Tlc4, it was an inhibitor of CTP and UTP uptake and demonstrated a K(i) similar to that of GD
69 xpression stimulated by prostaglandin E2 and UTP was not observed in cells lacking Gbeta-subunits.
70 oncentration ratios of ATP/ADP, GTP/GDP, and UTP/UDP were 1.9 +/- 1.39, 1.12 +/- 0.50, and 0.79 +/- 0
71                                CTP, GTP, and UTP, as well as ATP, supported transfer but with lesser
72   Many of the pools, including ATP, GTP, and UTP, begin to decrease while the cells are still in mid-
73  for ATP and undetectable with GTP, ITP, and UTP.
74      The crystal structures of apo MEAT1 and UTP-bound MEAT1 refined to 1.56 A and 1.95 A, respective
75 . aureus alpha-phosphoglucomutase (PgcA) and UTP:alpha-glucose 1-phosphate uridyltransferase (GtaB) h
76 an be limiting in phosphatide synthesis, and UTP, which activates P2Y receptors coupled to neurite ou
77 espite the fact that its precursors, UDP and UTP, are not.
78 show here that adenosine, ADP, ATP, UDP, and UTP all stimulate calcium mobilization in bone marrow-de
79  ADP, ATP, CDP, CTP, FAD, GDP, GTP, UDP, and UTP.
80                                       Apical UTP or ATP-gamma-S stimulation of monolayers mounted in
81 m serum starvation-induced apoptosis by ATP, UTP, and ATPgammaS, an effect mediated via P2Y2 receptor
82 rved in the presence of CTP followed by ATP, UTP, and GTP.
83  possesses one major binding region for ATP, UTP, and GTP that partially overlaps with a previously d
84 ted with several nucleotides, including ATP, UTP, and ADP, in the presence or absence of selective in
85 nzoyl ATP (BzATP), alpha,beta methylene ATP, UTP, 2-methylthioATP (MeSATP), and ATPgammaS increased [
86                              Mismatched ATP, UTP, or CTP could mediate excision of 3'-terminal CMP to
87 fied that is activated via nucleotides (ATP, UTP) binding apical P2 receptors and increasing [Ca(2+)]
88                     Purinergic agonists (ATP/UTP) stimulated release of accumulated mucins in the Mun
89 tudies indicate a key role of the apical ATP/UTP-P2Y(2)-receptor system in the inhibition of ENaC P(o
90 nergic receptor subtypes, the Gq-coupled ATP/UTP-sensing P2Y2 receptor and the Gs-coupled A2b adenosi
91 ivation of P2Y (most likely, endothelial ATP/UTP-selective P2Y(2)) receptors, rather than via its dep
92 do not express CD39, that do not express ATP/UTP receptor P2Y2, and in controls.
93                   We then identified the ATP/UTP receptor P2Y(2) as a critical sensor of nucleotides
94 ucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) reactivity and activation
95 ucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL)-positive cells were detect
96 ucleotidyl transferase-mediated biotinylated UTP nick end labeling assay revealed substantial deterio
97 ucleotidyl transferase-mediated biotinylated UTP nick end labeling positive, and they can be mitotica
98 ucleotidyl transferase-mediated biotinylated UTP nick end labeling) positive or apoptotic nuclei.
99 ucleotidyl transferase-mediated biotinylated UTP nick end labeling) staining in the cortex.
100 ucleotidyl transferase-mediated biotinylated UTP nick end labeling, cleaved caspase-3, and p53.
101 ucleotidyl transferase-mediated biotinylated UTP nick end labeling, hallmarks of apoptosis, were seen
102 ucleotidyl transferase-mediated biotinylated UTP nick end labeling-positive matrices and p53 at the o
103 ucleotidyl transferase-mediated biotinylated UTP nick end labeling-positive nuclei increased dramatic
104 ucleotidyl transferase-mediated biotinylated UTP nick end labeling.
105 ted from P2Y(2)R knockout mice restored both UTP-induced spreading and migration.
106                                   Thus, both UTP- and iNOS-generated reactive species contribute to E
107  stacks against the uracil base of the bound UTP, which on its other face also stacks with an essenti
108              The structure of p48 with bound UTP and Mn(2+) provides insights into the mechanism of n
109                                        Brain UTP, CTP, and CDP-choline were all elevated 15 min after
110 human (h) P2Y receptors (P2YRs) activated by UTP (P2Y2/4R) or UDP (P2Y6R).
111  to the nucleus continues to be activated by UTP by a mechanism dependent on Src kinase activity.
112 F109203x and Go6983 blocked BK activation by UTP in control epithelia, suggesting that PKC-mediated p
113 lcholine and phosphatidylethanolamine and by UTP-mediated activation of P2Y receptors.
114 coronary artery endothelial cells (HCAEC) by UTP/ATP increased the mRNA level of TF but not of its co
115  reversed P2X3 current inhibition induced by UTP-sensitive P2Y receptor activation.
116 bited by CTP and can be further inhibited by UTP, although UTP alone has little or no influence on ac
117 The feedback inhibition of uridine kinase by UTP and CTP in cell-free extracts was alleviated by incr
118    One of the operons regulated (in part) by UTP-sensitive reiterative transcription in E. coli is th
119 Activation of epithelial P2Y(2) receptors by UTP generated two patterns of [Ca(2+)](i) change: 2-10 m
120 2+ uptake and reduced stored Ca2+ release by UTP (400 microM) that activates a different family of in
121 ay, partially inhibited sAPPalpha release by UTP, whereas inhibitors of Src-dependent epidermal growt
122 -fluoromethylenetriphosphate (beta,gamma-CHF-UTP, 1) by (19)F NMR under conditions we previously pres
123                         Under current clamp, UTP increased action potential (AP) firing in response t
124 ma-methylene substitution on the non-cognate UTP/dT scaffold ( approximately 3-fold decrease in kpol)
125 eractions alone are not sufficient to confer UTP selectivity.
126                                 In contrast, UTP-induced spreading and migration did not occur in SMC
127 karyotic UDP-GlcNAc biosynthesis, converting UTP and N-acetylglucosamine-1-phosphate (GlcNAc-1P) to U
128                            In addition, CTP, UTP and nearly all UDP-activated sugars that serve as do
129 el the interactions of myosin with ATP, CTP, UTP, aza-ATP, ITP, and GTP (in decreasing order of effec
130 lates GpppA, GDP, and dGTP but not ATP, CTP, UTP, ITP, or m(7)GTP.
131 r activity than ATP, PSTK utilizes GTP, CTP, UTP and dATP as phosphate-donors.
132 leotide substrates, including ATP, GTP, CTP, UTP, and NAD.
133 as well as other nucleotides, including CTP, UTP, and GTP, had no effect on topoisomerase I cleavage
134 des has determined that Tlc4 transports CTP, UTP, and GDP.
135 estabilization of the R state by CTP and CTP/UTP, consistent with the T and R state crystallographic
136    Addition of CTP or the combination of CTP/UTP to the substrates significantly decreased the rate o
137 l-Lys-Arg-chloromethylketone also diminished UTP-induced sAPP alpha release.
138                                     Enolase, UTP-glucose-1-phosphate uridylyltransferase and polygala
139 djacent, does not coincide with the expected UTP binding site in apo Escherichia coli CTPS, suggestin
140 gulation of HAS2 expression by extracellular UTP, which is likely to contribute to the previously rep
141  explored the possibility that extracellular UTP or its breakdown products UDP and UMP act as mediato
142         Enzyme activity requires NTP, favors UTP, is stimulated by calcium, and initially produces 4
143 e relative fraction and sizes of fluorescent UTP-labeled transcripts in the nucleoplasm.
144 tance attributable to a reduced affinity for UTP.
145 on state for bond formation and cleavage for UTP/dT incorporation compared with ATP/dT incorporation.
146 compounds: choline, uridine (a precursor for UTP, CTP, and CDP-choline), and a PUFA (e.g., docosahexa
147 establish multicolor labeling strategies for UTP-enriched transcription compartments (TCs) and probe
148                                 Furthermore, UTP did not induce PLCgamma1 phosphorylation, and the ph
149                                 Furthermore, UTP particularly blocked the G1/S transition of GC cells
150                                 Furthermore, UTP selectively induces ICAM-1 expression in WT but not
151             Levels of ATP, ADP, ADP-glucose, UTP, UDP, and UDP-glucose were altered in a light-depend
152 secretion response was BzATP >> ATP > ADP >> UTP, and removal of external Ca(2+) dramatically suppres
153 t with lesser efficiency (ATP >> CTP > GTP > UTP).
154                   It can hydrolyze ATP, GTP, UTP, and CTP.
155  binds 40S subunits and hydrolyzes ATP, GTP, UTP, and CTP.
156 rthermore, analog nucleotides including GTP, UTP and CTP, do not show serious interferences and this
157 icked by other Mg-nucleotides including GTP, UTP, AMP-PCP and ATP-gamma-S, but not by PP(i) or AMP, s
158 de uniporter Npt2(Ct), which transports GTP, UTP, CTP, and ATP.
159 ed with no observed [(3)H]adenosine or [(3)H]UTP transport.
160                                   The higher UTP values might be related to elevated UDP-glucose/gala
161                             To determine how UTP is able to synergistically inhibit ATCase in the pre
162 flumic acid) and agonists (Forskolin + IBMX, UTP).
163 sociated temporally with a 20-nM increase in UTP and ATP content of bronchoalveolar lavage fluid, hyp
164         ATP and other nucleotides, including UTP, decrease ENaC activity via apical P2Y2 receptors.
165 into a (U,G)-adding enzyme that incorporates UTP and GTP instead of CTP and ATP; we transformed the r
166 to known ligands of the EGFR did not inhibit UTP-induced EGFR phosphorylation.
167  and silencing of ErbB3 expression inhibited UTP-induced phosphorylation of both ErbB3 and EGFR.
168 gene expression can be regulated by internal UTP levels, which reflect the availability of external p
169 n concomitant depletion of the intracellular UTP and CTP pools.
170                             Intraventricular UTP injection transiently decreased blood flow monitored
171         In addition to established invariant UTP-binding determinants, we have identified and verifie
172    This is consistent with a binding step (K(UTP)=17+/-6 muM) followed by a conformational change (k=
173 e demonstrate functional conservation of key UTP-binding and metal-ion-coordinating residues and iden
174  (CaCC) is activated by Ca(2+) agonists like UTP.
175 We found that uridine triphosphate-mediated (UTP-mediated) Cl(-) secretion was reduced during the per
176 We found that uridine triphosphate-mediated (UTP-mediated) Cl- secretion was reduced during the perio
177  patterns of [Ca(2+)](i) change: 2-10 microm UTP induced [Ca(2+)](i) oscillations, whereas 100 microm
178 [Ca(2+)](i) oscillations, whereas 100 microm UTP induced a sustained [Ca(2+)](i) increase, both in th
179 wth factor 1 (IGF-1)-inducible mitochondrial UTP carrier (PNC1/SLC25A33) promotes cell growth.
180                                   10-100 mum UTP strongly up-regulated HAS2 expression, although the
181 ty and can cut DNA with GTP and CTP (but not UTP).
182 1 cells with A77-1726 (20 microM), a de novo UTP synthesis inhibitor, and 1400W completely reversed t
183 sP4 is unable to transfer other nucleotides (UTP, CTP, GTP, and dATP) to the acceptor RNA in the abse
184 ngement allows for independent adaptation of UTP and CTP binding affinities while efficiently utilizi
185      Efflux was induced with the addition of UTP (100 microM, 10.2 +/- 1.5 nmol min(-1)), which was b
186 scratch wounds or stimulation by addition of UTP caused a brief internalization of EGFR, which parall
187                           The application of UTP (P2Y2 and P2Y4 agonist) sensitized colonic sensory n
188 er, these results explain how the binding of UTP can enhance the binding of CTP and why UTP binds mor
189 uggest the transient compartmentalization of UTP-enriched aggregates and their dynamic reorganization
190 of a prereaction ternary complex composed of UTP, TbTUT4, and UMP, which mimics an RNA substrate, and
191             By lowering the concentration of UTP needed for the initiation of RNA replication, CRE-de
192 ing that the intracellular concentrations of UTP and CTP may precisely regulate hCTPS activity.
193 ted with increased urinary concentrations of UTP and the ATP hydrolytic product, ADP.
194    As reported herein, low concentrations of UTP did not support negative-strand RNA synthesis when C
195 lls, are sensitive to high concentrations of UTP or CTP.
196 is of SG RNA at the lowest concentrations of UTP/CTP and that the single SVcpc mutation enhances the
197                   The facilitatory effect of UTP on P2X(2) sustained currents was mediated by a G-pro
198  receptor/PKC pathway, whereas the effect of UTP on P2X(3) fast currents was G-protein independent.
199                             These effects of UTP on bladder neuron excitability were blocked by the P
200 m BAPTA-AM completely blocked the effects of UTP on K(+) channel activation, indicating that the apam
201 erminal phosphate group into gamma-esters of UTP analogues.
202 th the templating base with the exception of UTP opposite purine deoxyribonucleoside.
203 ried in a hyperbolic manner as a function of UTP concentration.
204 rescence-based assay measuring inhibition of UTP-induced intracellular calcium release in 1321N1 astr
205 anisms in which high intracellular levels of UTP promote reiterative transcription that adds extra U
206 pendent VPg uridylylation lowers the K(m) of UTP required for viral RNA replication and that CRE-depe
207 respectively, reveal an unusual mechanism of UTP selection and domain organization previously unseen
208  1/59,000, 1/135,000 for misincorporation of UTP, ATP, and CTP opposite CMP in the template, respecti
209 te toward T while the additional presence of UTP makes the steady state vanishingly short.
210  ATCase is proposed in which the presence of UTP stabilizes the T state even more than CTP alone.
211  tetraphosphate and to a reduced response of UTP.
212            The EGFR-dependent stimulation of UTP-induced ERK1/2 phosphorylation in HSG cells is inhib
213 strong response to methylene substitution of UTP.
214 ns of pyrazofurin (inhibits the synthesis of UTP and CTP) were added to SVpzf-infected cells, the yie
215 phorbol ester pre-treatment had no effect on UTP-stimulated sAPP alpha release, indicating a PKC-inde
216              Stopped-flow kinetic studies on UTP binding followed by UMP incorporation into an EC as
217 results also indicate that release of ATP or UTP across the apical or basolateral membrane elicits qu
218 ryl acceptors, dCK can utilize either ATP or UTP as phosphoryl donors.
219 focal abluminal application of either ATP or UTP at the downstream end of cannulated arteries evoked
220  (HCAEC) and that P2Y2R activation by ATP or UTP induces dramatic up-regulation of tissue factor (TF)
221                           Exposure to ATP or UTP inhibited AML-cell migration in vitro.
222 mpaired by apyrase and facilitated by ATP or UTP.
223 s of initiating nucleotides GTP, ATP, CTP or UTP to bind.
224 eferred substrate compared with GTP, CTP, or UTP.
225 nreactive with GDP, GTP, GpppA, ATP, CTP, or UTP.
226                     Addition of ADP, GTP, or UTP to culture medium elevated the ATP concentration.
227  dATP, and ATP-agarose, but not CTP, GTP, or UTP, and exhibits ATPase activity.
228 and reduced AA release after thapsigargin or UTP treatment with decreased ERK1/2 and cPLA(2) phosphor
229  label from [alpha-(32)P]CTP or [alpha-(32)P]UTP into a RNase-sensitive and DNase-resistant product w
230 -(32)P]ATP and the formation of [gamma-(32)P]UTP is monitored by high-performance liquid chromatograp
231 verall conversion of UDP-Gal to [gamma-(32)P]UTP was linear between 0.5 and 30 nM UDP-Gal.
232                                        P2Y2 (UTP/ATP) and P2Y6 [ADP/UTP/uridine 5'-diphosphate (UDP)]
233 ow that UL84 has NTPase activity, preferring UTP.
234 , chelation of intracellular Ca(2+) prevents UTP-stimulated increases in diacylglycerol at the Golgi.
235 ding, subunit oligomerization and processive UTP incorporation, and predict druggable pockets.
236 d in the presence of the substrates/products UTP and UDP-glucose to nominal resolutions of 1.64 Angst
237  exhibited a >60% reduction in purinoceptor (UTP)-regulated CaCC activity.
238 he triphosphate moiety overlaps the putative UTP triphosphate binding site, explaining how CTP compet
239 idyltransferases that specifically recognize UTP and belong to a large enzyme superfamily typified by
240    RNAi knockdown of AC1 selectively reduced UTP-induced cAMP elevation and chloride secretion.
241 ntroduction of FLNa in FLNa RNAi SMC rescued UTP-induced LTA expression.
242 idered as contributing to the small residual UTP response.
243 tol-4,5-bisphosphate (PIP(2)) fully reverses UTP-mediated regulation of P2X3 channel activity.
244                       The effects of several UTP analogs on the RdRp activity of the norovirus and fe
245 ng the arrangement of U3 RNA and the several UTP complexes that form a chaperone-like structure aroun
246 13-dibutyrate (PDBu) or a natural stimulant, UTP, time lapse live cell imaging movies indicated phosp
247 the K(m) and IC(50) values for the substrate UTP and the product CTP, respectively, were close to the
248 g that, although they are poorer substrates, UTP and GTP can also be utilized by Ssl2.
249 tocellular apoptosis as assessed by terminal UTP nick-end labeling when compared to ConA-treated Wt m
250  Here, we show by X-ray crystallography that UTP binds to a unique site on each regulatory chain of t
251                                We found that UTP depleted PIP(2) abundance in the apical membrane whi
252                   In addition, we found that UTP-stimulated LTA secretion is not sensitive to brefeld
253 munoprecipitation experiments indicated that UTP causes association of the EGFR with another member o
254                Agonist studies revealed that UTP, but not 2',3'-O-(4-benzoyl)benzoyl-ATP, 2-methylthi
255 answell cell migration assay, we showed that UTP significantly increased SMC spreading on collagen I
256                                          The UTP-stimulated iodide efflux was shown to be Ca(2+) depe
257                  Specific siRNAs against the UTP receptor P2Y2, and inhibitors of UDP receptors P2Y6
258                                       As the UTP/CTP concentrations were increased, the SVpzf system,
259 ed knock-in phenotypes, we have assessed the UTP and RNA binding sites in RET2.
260 shift of conserved cationic Arg3.29 from the UTP gamma position to the delta position of Up4U and Up4
261 ing the involvement of these pathways in the UTP-induced HAS2 response.
262 44 and 435 positioned in the vicinity of the UTP binding site are critical for RET2 activity on singl
263 f the triphosphate moieties with that of the UTP substrate.
264 viously determined crystal structures of the UTP-bound and apo forms of the minimal trypanosomal TUTa
265 red viral RNA synthesis as a function of the UTP/CTP concentrations.
266 ncing of hBest1 in CFPAC-1 cells reduced the UTP-stimulated iodide efflux by around 40%.
267 n, thereby creating a cavity adjacent to the UTP-binding site.
268  and highly ordered water molecules with the UTP's base, ribose and phosphate moieties.
269 ological effects and metabolic conversion to UTP analog are L-ala,SP prodrug-dependent in cardiomyocy
270 Y6 and P2Y14, indicated that the response to UTP was mediated mainly through P2Y2 and to a lesser ext
271                               In response to UTP, phosphorylation of GolgiCKAR was sustained the long
272 ent with reduced afferent fiber responses to UTP and ADP in Na(v)1.9(-/-) mice.
273 y, and terminal deoxynucleotidyl transferase UTP nick-end labeling (TUNEL) staining of histologic sec
274 s) selectively bind uridine 5'-triphosphate (UTP) and catalyze the addition of uridine 5'-monophospha
275 cells stimulated by uridine-5'-triphosphate (UTP) and PMA, agonists inducing LB fusion with the PM, b
276              Docked uridine 5'-triphosphate (UTP) formed a nucleobase pi-pi complex with conserved Ph
277 dy we revealed that Uridine-5'-triphosphate (UTP) uptake in living cells labeled transcription-relate
278 ch as ATP, ADP, and uridine 5'-triphosphate (UTP), among others, may serve as extracellular signaling
279 ceptor activated by uridine-5'-triphosphate (UTP), which is widely expressed in the body, e.g., in in
280 rocortisone (HC) on uridine-5'-triphosphate (UTP)-stimulated ion transport in differentiated, pseudos
281 tions in intracellular uridine triphosphate (UTP) and cytidine triphosphate (CTP).
282                 Apical uridine triphosphate (UTP) stimulation was shown to increase short circuit cur
283 eas the other displays a more compact TUTase-UTP complex.
284 ws no appreciable conformational change upon UTP binding and apparently does not require RNA substrat
285 r (bp), fluorescein, and fluorescein-12-UTP (UTP) were separated in less than 120 s in channels of de
286 ; a pyrimidine (e.g., uridine, converted via UTP to brain CTP); and a PUFA (e.g., docosahexaenoic aci
287 gative-strand RNA synthesis, especially when UTP concentrations were limiting.
288 C0 conditions, activation only occurred when UTP was added after NS11021.
289                                      Whereas UTP is discriminated by 77,000-fold compared with dTTP,
290 f UTP can enhance the binding of CTP and why UTP binds more tightly in the presence of CTP.
291   Furthermore, stimulation of HSG cells with UTP induced phosphorylation of ErbB3, and silencing of E
292 nding site, explaining how CTP competes with UTP while CTP resistance mutations are acquired without
293 dition site) and mechanism (competition with UTP for occupancy of the NTP addition site) that differ
294 ET1 catalytic core alone and in complex with UTP analogs.
295  by EGF was attenuated by costimulation with UTP.
296 hosphorylated at the highest efficiency with UTP as donor.
297 f Grb2 when stimulated with EGF but not with UTP or injury.
298 e different kinetic properties observed with UTP to those with ATP.
299 te and the uridylyltransferase reaction with UTP to produce UDP-GlcNAc.
300 ed; and 3) secreted liquid when treated with UTP or forskolin or subjected to cyclic compressive stre

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