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1                                              NAADP binds to specific, high-affinity membrane binding
2                                              NAADP is a highly potent mobilizer of Ca(2+), which in t
3                                              NAADP is a potent second messenger that mobilizes Ca(2+)
4                                              NAADP is now established as a Ca(2+) messenger by recent
5                                              NAADP is thus a potential antidiabetic agent with therap
6                                              NAADP plays an important role in calcium signalling in t
7                                              NAADP released Ca2+ from the same thapsigargin-sensitive
8                                              NAADP triggered heterogeneous local Ca(2+) signals, incl
9                                              NAADP uptake was inhibitable by Ned-19, a NAADP mimic; d
10                                              NAADP was shown to evoke functionally relevant Ca(2+) si
11                                              NAADP-AM failed to enhance Ca(2+) responses in cardiac m
12                                              NAADP-regulated Ca(2+) release channels, likely two-pore
13 -enzyme 2'-NADP and the calcium mobilizer 2'-NAADP.
14 ation by [Ca(2+)](i), cyclic ADPR, H(2)O(2), NAADP, and negative feedback regulation by AMP and perme
15                Interestingly, 3'-NADP and 3'-NAADP have previously been used as inhibitors or signali
16 inic acid adenine dinucleotide phosphate (3'-NAADP), are substantially different from the ubiquitous
17 s (HEK293, SKBR3), and mouse pancreas, 5N(3)-NAADP selectively labeled low molecular weight sites tha
18 r concentrations of unlabeled NAADP or 5N(3)-NAADP, but not by micromolar concentrations of structura
19                                 [(32)P-5N(3)]NAADP binding was saturable and displayed high affinity
20    The proteins photolabeled by [(32)P-5N(3)]NAADP have molecular masses smaller than the sea urchin
21                                 [(32)P-5N(3)]NAADP photolabeling was irreversible in a high K(+) buff
22 g homogenates preincubated with [(32)P-5N(3)]NAADP resulted in specific labeling of 45-, 40-, and 30-
23 adenine dinucleotide phosphate ([(32)P-5N(3)]NAADP) as a photoaffinity probe.
24 toprobe based on 5-azido-NAADP ([(32)P-5N(3)]NAADP) that exhibits high affinity binding to NAADP rece
25    NAADP uptake was inhibitable by Ned-19, a NAADP mimic; dipyridamole, a nucleoside inhibitor; or Na
26 he first time provide direct evidence that a NAADP-sensitive Ca2+ release channel is present in the l
27 w that the loss of endogenous TPCs abolished NAADP-dependent Ca(2+) responses as assessed by single-c
28 ndent NAADP synthesis; second, by activating NAADP-regulated channels.
29        These data suggest that high affinity NAADP binding sites are distinct from TPCs.
30       Furthermore, labeling of high affinity NAADP binding sites was preserved in pancreatic samples
31 branes enriched with TPC2 show high affinity NAADP binding, and TPC2 underpins NAADP-induced Ca(2+) r
32 ing high potency and agonist efficacy and an NAADP derivative substituted at both the 5-position of t
33 rove that it is a pore-forming subunit of an NAADP-gated Ca(2+) channel.
34                          We conclude that an NAADP increase plays a physiologically relevant role dur
35  base-exchange reactions to produce ADPR and NAADP(+).
36 osphate (AMP), which suggests that cADPR and NAADP lead to mobilization of endogenous ADPR presumably
37 by 8-Br-cADPR, which suggests that cADPR and NAADP share a common binding site on TRPM2 that can regu
38 syl cyclase inhibitor that reduces cADPR and NAADP synthesis in mouse membrane fractions, was shown t
39                   We conclude that cADPR and NAADP, in combination with ADPR, represent physiological
40    The present study documents that TPC1 and NAADP-binding sites showed a colocalization at the acros
41 ss any AP isoenzymes and did not display any NAADP 2'-phosphatase activity.
42 nels (TPCs) have been recently identified as NAADP-regulated Ca(2+) release channels, which are local
43 ls (TPCs) within the endolysosomal system as NAADP-regulated Ca(2+) channels that release organellar
44 by anti-TRP-ML1 antibody markedly attenuated NAADP-induced activation of these lysosomal Ca2+ channel
45 ng a radioactive photoprobe based on 5-azido-NAADP ([(32)P-5N(3)]NAADP) that exhibits high affinity b
46                                      5-Azido-NAADP was shown to release calcium from sea urchin egg h
47                            5-(3-Azidopropyl)-NAADP was shown to release Ca(2+) with an EC50 of 31 muM
48                            Interplay between NAADP receptors and more established intracellular Ca(2+
49 arger TPC complex is responsible for binding NAADP that is unique from the core channel itself.
50  cyclase family, catalyzes synthesis of both NAADP and cADPR in vitro However, it remains unclear whe
51 al exocytosis supports the concept that both NAADP-gated cascades match local NAADP concentrations wi
52 trolled Mg(2+), TPC2 is readily activated by NAADP with channel properties identical to those in resp
53 although both TPC1 and TPC2 are activated by NAADP, TPC1 appears to be additionally regulated by cyto
54 ated by PI(3,5)P(2) and are not activated by NAADP.
55 d recombinant TPC1 channels are activated by NAADP.
56 els (TPCs) and their potential activation by NAADP.
57 e also the acidic Ca(2+) stores mobilized by NAADP via TPC channels on the granules themselves, so th
58 ted channels regulated by mTORC1, but not by NAADP.
59 er Ca(2+) released from acidic organelles by NAADP subsequently recruits IP3 or ryanodine receptors o
60 (TPCs) have been proposed to be regulated by NAADP, recent studies have challenged this.
61 endolysosomal channels that are regulated by NAADP; however, the nature of the NAADP receptor binding
62   The molecular basis for calcium release by NAADP, however, is not clear and subject to controversy.
63    The molecular basis for Ca(2+) release by NAADP, however, is uncertain.
64 ive pore region abrogated calcium release by NAADP.
65  lysosome-related organelles are selected by NAADP.
66 ture of the intracellular stores targeted by NAADP and the molecular identity of the NAADP receptors
67 he identity of the Ca(2+) stores targeted by NAADP in conventional naive T cells is less clear.
68                       In Tpcn1/2(-/-) cells, NAADP sensitivity was restored by re-expressing wild-typ
69         In cell-free extracts of HeLa cells, NAADP was degraded to nicotinic acid adenine dinucleotid
70        Fifth, tracheal homogenates contained NAADP-binding sites of high affinity.
71              Our finding that two convergent NAADP-dependent pathways are operative in driving acroso
72 little is known about the mechanism coupling NAADP binding to calcium release.
73 ways: first, by stimulating Ca(2+)-dependent NAADP synthesis; second, by activating NAADP-regulated c
74 a rapid and transient increase in endogenous NAADP levels.
75 ly, glucose stimulation increases endogenous NAADP levels, providing strong evidence for recruitment
76 e, we demonstrate the presence of endogenous NAADP in HeLa cells.
77 ammalian cells of the presence of endogenous NAADP levels that can be regulated by a physiological st
78 PML1(D471K) was without affect on endogenous NAADP-mediated Ca(2+) signals.
79 dic-like Ca(2+) stores via the endolysosomal NAADP-sensitive two-pore channels.
80      Whereas overexpression of TPCs enhanced NAADP-mediated Ca(2+) signals, overexpression of TRPML1
81  of two-pore channel (TPC) proteins enhances NAADP-induced Ca(2+) release, whereas the NAADP response
82 ere, we show that NAADP acetoxymethyl ester (NAADP-AM), a cell-permeant NAADP analog, increases cytos
83  and nicotinic acid and metabolize exogenous NAADP to nicotinic acid adenine dinucleotide by a 2'-pho
84 us provides a potential mechanism to explain NAADP-induced Ca(2+) oscillations.
85                                     Finally, NAADP-evoked Ca(2+) oscillations in pancreatic acinar ce
86 AP isoform emerged as the best candidate for NAADP degradation in HeLa cells.
87 ely the long sought after target channel for NAADP.
88 re the long sought after target channels for NAADP.
89                   Thus, TPC1 is critical for NAADP action and is likely the long sought after target
90                   The trigger hypothesis for NAADP action proposes that calcium release from acidic s
91  Ca(2+)-permeable channels indispensable for NAADP signalling.
92                  The degradation pathway for NAADP is unknown and no enzyme that can specifically hyd
93  summary, our observations define a role for NAADP and TPC2 at lysosomal/sarcoplasmic reticulum junct
94               Here, we report a new role for NAADP in arrhythmogenic Ca(2+) release in cardiac myocyt
95 e Ca2+ stores in PC12 cells, (ii) a role for NAADP in differentiation, and (iii) that Ca2+-dependent
96   This study highlights a selective role for NAADP in stimulating exocytosis crucial for immune cell
97 uctures and dynamics, implicating a role for NAADP in the regulation of vesicular trafficking.
98 d that TPCs, not TRPMLs, are the targets for NAADP.
99       Both have been proposed as targets for NAADP.
100  increases the apparent affinity of TPC1 for NAADP by 10 nm/mV.
101 mprise a highly specialized trigger zone for NAADP-dependent Ca(2+) signaling by the vasoconstrictor
102                              Thus, TPCs form NAADP receptors that release Ca(2+) from acidic organell
103 is the first report demonstrating functional NAADP receptors in a mammalian neuron.
104                                 Furthermore, NAADP was found to be released from pancreatic islets up
105 re we show that CD38 can, in fact, hydrolyze NAADP to ADP-ribose 2'-phosphate.
106                       Our findings implicate NAADP-evoked Ca(2+) release from acidic Ca(2+) storage o
107                                 Importantly, NAADP antagonist BZ194 largely ameliorated isoproterenol
108                                 Importantly, NAADP at physiological concentrations (50-100 nM) was de
109 omiscuous enzyme described to be involved in NAADP metabolism, was not detectable in HeLa cells.
110 iculty of catching a small transient rise in NAADP levels.
111       Our data affirm a key role for TPC2 in NAADP-mediated Ca(2+) signaling and link this pathway to
112    Higher concentrations of NAADP inactivate NAADP receptors and attenuate the glucose-induced Ca(2+)
113 s with saponin and/or Triton X-100 increased NAADP synthesis, indicating that intracellular CD38 cont
114 renoreceptor signaling in the heart involves NAADP and lysosomes.
115    Here we provide details of how to isolate NAADP from cells by extraction with perchloric acid and
116 ffinity for activation of TPC1 by its ligand NAADP is not constant.
117 t that both NAADP-gated cascades match local NAADP concentrations with the efflux of acrosomal calciu
118  reconstituted and characterized a lysosomal NAADP-sensitive Ca2+ release channel using purified lyso
119       Furthermore, the identity of lysosomal NAADP-sensitive Ca2+ release channels was also investiga
120 nterestingly, the activity of this lysosomal NAADP-sensitive Ca2+ release channel increased when the
121  refined and improved a method for measuring NAADP levels and presented it in a manner accessible to
122             Thus, TPC1 and TPC2 both mediate NAADP-induced Ca(2+) release, but the subsequent amplifi
123 rms localize to acidic organelles to mediate NAADP-dependent calcium release.
124 iated mechanism, but the mechanism mediating NAADP-induced intracellular Ca2+ release remains unclear
125                         The second messenger NAADP triggers Ca(2+) release from endo-lysosomes.
126                  Hence, the second messenger NAADP, promoting efflux of calcium from lysosome-like co
127            Moreover, the NADP(+) metabolite, NAADP(+), regulates intracellular calcium homeostasis vi
128 ma in either the nanomolar or low micromolar NAADP concentration range, where TPC1 was found to be re
129                                    Moreover, NAADP activates TPCs to drive exocytosis in a way that i
130      However, whether TPCs constitute native NAADP receptors is unclear.
131                                Nevertheless, NAADP is not presently classified as a second messenger
132                                     Notably, NAADP-mediated Ca(2+) release in intact cells is regulat
133 for the first time (i) the presence of novel NAADP-sensitive Ca2+ stores in PC12 cells, (ii) a role f
134 t of charged groups to the nicotinic acid of NAADP is associated with loss of activity, suggesting th
135 n kinase II inhibitors suppressed actions of NAADP in myocytes.
136               Our data extend the actions of NAADP to the endothelium both in vitro and in vivo, poin
137              Consistently, administration of NAADP to type 2 diabetic mice improved glucose tolerance
138 , we show that intravenous administration of NAADP-AM into anesthetized rats decreases mean arterial
139                 Extracellular application of NAADP has been shown to elicit intracellular Ca(2+) sign
140 hannels (TPC), a recently described class of NAADP- and PI(3,5)P2-sensitive Ca(2+)-permeable cation c
141                     Higher concentrations of NAADP inactivate NAADP receptors and attenuate the gluco
142    We demonstrate that liposomal delivery of NAADP mediated release of Ca2+ from acidic Ca2+ stores a
143 onsible for controlling the pH dependence of NAADP synthesis by the cyclase.
144 say is highly selective for the detection of NAADP under cell extract conditions.
145 M to 1 microM, but this activating effect of NAADP was significantly reduced when the concentrations
146 ryanodine receptors abolished the effects of NAADP on neurite length and reduced the magnitude of NAA
147 nodine blocked the Ca2+-releasing effects of NAADP, cADPR, and caffeine, but not IP3.
148 vidence for AP as the metabolizing enzyme of NAADP in cells that do not express CD38.
149 wo-pore channels (TPCs) comprise a family of NAADP receptors, with human TPC1 (also known as TPCN1) a
150 in a high K(+) buffer, a hallmark feature of NAADP binding in the egg system.
151 key to the investigation of the functions of NAADP as a Ca2+ -releasing second messenger.
152     These observations support generation of NAADP and cADPR by intracellular CD38, which contributes
153  base-exchange reaction in the generation of NAADP.
154 rent study, we demonstrate the importance of NAADP in the generation of Ca(2+) signals in murine naiv
155                                  Infusion of NAADP into intact cardiac myocytes induced global Ca(2+)
156      Selective pharmacological inhibition of NAADP-evoked Ca(2+) release or genetic ablation of endol
157 ores, supporting emerging interpretations of NAADP physiology and pharmacology in heart.
158 nist Ned-19, we addressed the involvement of NAADP in the generation of Ca(2+) signals evoked by TCR
159  neurite length and reduced the magnitude of NAADP-mediated Ca(2+) signals.
160 thod to prevent the endogenous metabolism of NAADP by chelating Ca2+ with bis-(o-aminophenoxy)ethane-
161                            Microinjection of NAADP mimicked the fertilization cortical response, sugg
162 tes critical evaluation of current models of NAADP-triggered activation of the TPC family.
163 hat exhibited the diagnostic pharmacology of NAADP-sensitive Ca(2+) release.
164  be introduced at the 8-adenosyl position of NAADP while preserving high potency and agonist efficacy
165 urthermore, the single channel properties of NAADP-activated TPC2delN were not affected by TRPML1.
166 HEK293 cells, resulting in reconstitution of NAADP 2'-phosphatase activity in cell-free extracts.
167 anelles, using organelle pH as a reporter of NAADP action.
168                     In contrast, the role of NAADP in Ca(2+) signaling or the identity of the Ca(2+)
169  a basis for the recently-discovered role of NAADP in reperfusion-induced cell death.
170 r understanding of the physiological role of NAADP.
171                                 Synthesis of NAADP catalyzed by CD38 is known to have strong preferen
172 r Ca(2+) channels are the primary targets of NAADP.
173 omes and sarcoplasmic reticulum dependent on NAADP and TPC2 comprise an important element in beta-adr
174  the second messengers IP3 and cADPR (ER) or NAADP (acidic organelles).
175                                     Overall, NAADP exhibited a similar profile in mediating Ca(2+) re
176                         High-affinity [(32)P]NAADP binding still occurs in Tpcn1/2(-/-) tissue, sugge
177 low concentration and to compete with [(32)P]NAADP in a competition ligand binding assay with an IC(5
178 mpetition ligand binding assays using [(32)P]NAADP.
179 toxymethyl ester (NAADP-AM), a cell-permeant NAADP analog, increases cytosolic Ca(2+) concentration i
180             Application of membrane-permeant NAADP acetoxymethyl ester to PASMCs elicited a biphasic
181 cotinic acid adenine dinucleotide phosphate (NAADP(+)), both of which have been shown to modulate cal
182 nicotinamide adenine dinucleotide phosphate (NAADP) and Ca(2+).
183 cotinic acid adenine dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR) are Ca(2+)-mobilizi
184 cotinic acid adenine dinucleotide phosphate (NAADP) and its recently identified molecular target, two
185 cotinic acid adenine dinucleotide phosphate (NAADP) antagonist BZ194 (200 mum) had no effect on eithe
186 cotinic acid adenine dinucleotide phosphate (NAADP) as well as by inositol 1,4,5-trisphosphate (IP3)
187 cotinic acid adenine dinucleotide phosphate (NAADP) evokes highly localized intracellular Ca(2+) sign
188 cotinic acid adenine dinucleotide phosphate (NAADP) from NAD phosphate (NADP).
189 cotinic acid adenine dinucleotide phosphate (NAADP) in cell extracts using surface-enhanced Raman spe
190 cotinic acid adenine dinucleotide phosphate (NAADP) in the control of Ca(2+)-dependent functions.
191 cotinic acid adenine dinucleotide phosphate (NAADP) in the insulin-secreting beta-cell line MIN6.
192 cotinic acid adenine dinucleotide phosphate (NAADP) is a Ca(2+) releasing intracellular second messen
193 cotinic acid adenine dinucleotide phosphate (NAADP) is a messenger that regulates calcium release fro
194 cotinic acid adenine dinucleotide phosphate (NAADP) is a novel metabolite of NADP that has now been e
195 cotinic acid adenine dinucleotide phosphate (NAADP) is a potent and widespread calcium-mobilizing mes
196 cotinic acid adenine dinucleotide phosphate (NAADP) is a potent second messenger that mobilizes Ca(2+
197 cotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger for mobilizing Ca(2+) from
198 cotinic acid adenine dinucleotide phosphate (NAADP) is a ubiquitous messenger proposed to stimulate C
199 cotinic acid adenine dinucleotide phosphate (NAADP) is a ubiquitous second messenger providing a Ca(2
200 cotinic acid adenine dinucleotide phosphate (NAADP) is a widespread and potent calcium-mobilizing mes
201 cotinic acid adenine dinucleotide phosphate (NAADP) is an agonist-generated second messenger that rel
202 cotinic acid adenine dinucleotide phosphate (NAADP) is capable of inducing global Ca2+ increases via
203 cotinic acid adenine dinucleotide phosphate (NAADP) is increasingly being demonstrated to be involved
204 cotinic acid adenine dinucleotide phosphate (NAADP) is the least well understood in terms of its mole
205 cotinic acid adenine dinucleotide phosphate (NAADP) is the most potent Ca(2+)-mobilizing messenger th
206 cotinic acid adenine dinucleotide phosphate (NAADP) is the most potent Ca(2+)-releasing second messen
207 cotinic acid adenine dinucleotide phosphate (NAADP) levels in cells has been, and remains, key to the
208 cotinic acid adenine dinucleotide phosphate (NAADP) on neurite length and cytosolic Ca(2+) levels.
209 cotinic acid adenine dinucleotide phosphate (NAADP) potently releases Ca(2+) from acidic intracellula
210 cotinic acid adenine dinucleotide phosphate (NAADP) releases Ca(2+) from the acidic Ca(2+) stores of
211 cotinic Acid Adenine Dinucleotide Phosphate (NAADP) stimulates calcium release from acidic stores suc
212 cotinic acid adenine dinucleotide phosphate (NAADP) strongly activate natively expressed TRPM2 channe
213 cotinic acid adenine dinucleotide phosphate (NAADP) with substitution at either the 4- or the 5-posit
214 cotinic acid adenine dinucleotide phosphate (NAADP), a novel Ca2+-mobilizing messenger, with that of
215 cotinic acid adenine dinucleotide phosphate (NAADP), and the mammalian target of rapamycin (mTOR).
216 cotinic acid adenine-dinucleotide phosphate (NAADP), and the specific engagement of the two-pore chan
217 cotinic acid adenine dinucleotide phosphate (NAADP), the most potent Ca(2+) mobilizing second messeng
218 cotinic acid adenine dinucleotide phosphate (NAADP)-evoked Ca(2+) release in many diverse cell types.
219 cotinic acid adenine dinucleotide phosphate (NAADP)-evoked Ca(2+) release was also impaired using eit
220 cotinic acid adenine dinucleotide phosphate (NAADP)-mediated Ca(2+) release from intracellular stores
221 cotinic acid adenine dinucleotide phosphate (NAADP).
222 cotinic acid adenine dinucleotide phosphate (NAADP).
223 cotinic acid adenine dinucleotide phosphate (NAADP).
224 cotinic acid adenine dinucleotide-phosphate (NAADP), a potent calcium messenger, is able to trigger c
225 detect no requirement for cyclic ADP ribose, NAADP-dependent lysosomal Ca2+ release, activation of th
226                                      Second, NAADP increased cytosolic calcium in isolated cells when
227                          With a SERS sensor, NAADP can be detected in less than 1 min without any spe
228                             To further study NAADP binding sites, we have synthesized and characteriz
229 al systems that are widely used for studying NAADP-evoked Ca(2+) signaling, including sea urchin eggs
230           In contrast, several 5-substituted NAADP derivatives showed high potency for binding and fu
231  that these truncated proteins still support NAADP-induced Ca(2+) release.
232  WT but not CD38(-/-) mouse hearts supported NAADP and cADPR synthesis.
233      In contrast, TPC3 expression suppressed NAADP-induced Ca(2+) release.
234 Third, tracheal homogenates could synthesize NAADP by base exchange from exogenous NADP and nicotinic
235            Additionally, we demonstrate that NAADP dilates aortic rings in an endothelium- and NO-dep
236  Taken together, these data demonstrate that NAADP functions as a second messenger in tracheal smooth
237                          We demonstrate that NAADP is neither generated nor broken down during sample
238 ides the first conclusive demonstration that NAADP is a genuine second messenger.
239  evolution and provide further evidence that NAADP mediates calcium release from acidic stores throug
240              We provide strong evidence that NAADP-mediated modulation of couplon activity plays a ro
241                            It was found that NAADP activates lysosomal Ca2+ release channels at conce
242                            We show here that NAADP-mediated Ca(2+) release from endolysosomal Ca(2+)
243 troversial, although evidence indicates that NAADP mobilizes Ca(2+) from lysosome-related acidic comp
244                              We propose that NAADP is functioning as an autocrine/paracrine hormone i
245                              We propose that NAADP regulates endolysosomal Ca(2+) storage and release
246 1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpre
247                               We report that NAADP satisfies all five criteria as follows.
248                           Here, we show that NAADP acetoxymethyl ester (NAADP-AM), a cell-permeant NA
249                           Our data show that NAADP and physiological stimuli alter the pH within intr
250 sosomes to the plasma membrane and show that NAADP evokes Ca(2+) influx independent of ryanodine rece
251                            Here we show that NAADP evokes localized Ca(2+) signals by mobilizing a ba
252                           Here, we show that NAADP is effectively transported into selected cell type
253                        Our results show that NAADP mediates complex global and local Ca(2+) signals.
254                                 We show that NAADP potentiates neurite extension in response to serum
255                         We further show that NAADP-evoked Ca(2+) signals hyperpolarize endothelial ce
256                   Recent studies showed that NAADP-induced Ca(2+) release is mediated by the two-pore
257              It has recently been shown that NAADP mediates Ca2+ mobilization by insulin in human pan
258 in intracellular organelles and suggest that NAADP signals through pH as well as Ca(2+).
259 curs in Tpcn1/2(-/-) tissue, suggesting that NAADP regulation is conferred by an accessory protein.
260 yanodine, or xestospongin C, suggesting that NAADP-mediated Ca(2+) signals interact with both ryanodi
261                                          The NAADP bolus plays a physiological role upon delivery to
262 Ca(2+) released from the ER can activate the NAADP pathway in two ways: first, by stimulating Ca(2+)-
263      However, the expression of TPCs and the NAADP-induced local Ca(2+) signals have not been examine
264               Ruthenium red also blocked the NAADP-elicited Ca2+ release.
265 t of extracellular Ca(2+) and blocked by the NAADP antagonist Ned-19 or the vacuolar H(+)-ATPase inhi
266 emical analogue NADP and were blocked by the NAADP antagonist trans-Ned-19.
267                                   First, the NAADP antagonist Ned-19 inhibited contractions in trache
268 ermed TPC1 and TPC2, are responsible for the NAADP-mediated Ca(2+) release but the underlying mechani
269                              To identify the NAADP binding site, we employed a photoaffinity labeling
270 ected that this will enhance research in the NAADP field.
271 l smooth muscle, and therefore, steps in the NAADP signaling pathway might provide possible new drug
272 on with perchloric acid and then measure the NAADP using a radioreceptor assay.
273 gulated by NAADP; however, the nature of the NAADP receptor binding site is unknown.
274  specific labeling and identification of the NAADP receptor.
275 d by NAADP and the molecular identity of the NAADP receptors remain controversial, although evidence
276                      Hence, by virtue of the NAADP/TPC pathway, cytolytic granules generate Ca(2+) si
277 cellular pathway pharmacologically using the NAADP antagonist Ned-19 or genetically using Tpcn2(-/-)
278 ods and a pharmacological approach using the NAADP antagonist Ned-19, we addressed the involvement of
279 es NAADP-induced Ca(2+) release, whereas the NAADP response was abolished in pancreatic beta cells fr
280 osis and cytosolic pH but coincides with the NAADP-dependent fertilization Ca(2+) wave.
281  (SR) had no effect on the activity of these NAADP-activated Ca2+ release channels.
282 e is known about the functional role of this NAADP uptake system.
283                                        Thus, NAADP signaling appears an attractive novel target for a
284 Ca(2+) stores and ryanodine receptors and to NAADP antagonist BZ194.
285  possess the hallmark properties ascribed to NAADP receptors, including nanomolar ligand affinity [3-
286 AADP) that exhibits high affinity binding to NAADP receptors.
287 ating that intracellular CD38 contributes to NAADP production.
288 flash was eliminated in eggs desensitized to NAADP.
289 hat release organellar Ca(2+) in response to NAADP.
290                                 Responses to NAADP were abolished by disrupting the lysosomal proton
291 ere the Ca(2+) stores that were sensitive to NAADP in naive T cells.
292 h affinity NAADP binding, and TPC2 underpins NAADP-induced Ca(2+) release from lysosome-related store
293 ion of nanomolar concentrations of unlabeled NAADP or 5N(3)-NAADP, but not by micromolar concentratio
294 tes the egg by Ca(2+) release dependent upon NAADP, and accordingly, we report that fertilization als
295      These results demonstrate that a VEGFR2/NAADP/TPC2/Ca(2+) signaling pathway is critical for VEGF
296                         To determine whether NAADP functions as a second messenger in tracheal smooth
297 lusion, our results support a model in which NAADP mediates glucose-induced Ca(2+) signaling in pancr
298 ) with an EC50 of 31 muM and to compete with NAADP for receptor binding with an IC50 of 56 nM.
299 egion and that treatment of spermatozoa with NAADP resulted in a loss of the acrosomal vesicle that s
300 response, suggesting that it occurred within NAADP-sensitive acidic Ca(2+) stores.

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