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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
14 ation by [Ca(2+)](i), cyclic ADPR, H(2)O(2), NAADP, and negative feedback regulation by AMP and perme
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
20 The proteins photolabeled by [(32)P-5N(3)]NAADP have molecular masses smaller than the sea urchin
22 g homogenates preincubated with [(32)P-5N(3)]NAADP resulted in specific labeling of 45-, 40-, and 30-
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
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
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
40 The present study documents that TPC1 and NAADP-binding sites showed a colocalization at the acros
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
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
57 e also the acidic Ca(2+) stores mobilized by NAADP via TPC channels on the granules themselves, so th
59 er Ca(2+) released from acidic organelles by NAADP subsequently recruits IP3 or ryanodine receptors o
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.
66 ture of the intracellular stores targeted by NAADP and the molecular identity of the NAADP receptors
73 ways: first, by stimulating Ca(2+)-dependent NAADP synthesis; second, by activating NAADP-regulated c
75 ly, glucose stimulation increases endogenous NAADP levels, providing strong evidence for recruitment
77 ammalian cells of the presence of endogenous NAADP levels that can be regulated by a physiological st
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
93 summary, our observations define a role for NAADP and TPC2 at lysosomal/sarcoplasmic reticulum junct
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
101 mprise a highly specialized trigger zone for NAADP-dependent Ca(2+) signaling by the vasoconstrictor
109 omiscuous enzyme described to be involved in NAADP metabolism, was not detectable in HeLa cells.
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
115 Here we provide details of how to isolate NAADP from cells by extraction with perchloric acid and
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
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
124 iated mechanism, but the mechanism mediating NAADP-induced intracellular Ca2+ release remains unclear
128 ma in either the nanomolar or low micromolar NAADP concentration range, where TPC1 was found to be re
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
138 , we show that intravenous administration of NAADP-AM into anesthetized rats decreases mean arterial
140 hannels (TPC), a recently described class of NAADP- and PI(3,5)P2-sensitive Ca(2+)-permeable cation c
142 We demonstrate that liposomal delivery of NAADP mediated release of Ca2+ from acidic Ca2+ stores a
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
149 wo-pore channels (TPCs) comprise a family of NAADP receptors, with human TPC1 (also known as TPCN1) a
152 These observations support generation of NAADP and cADPR by intracellular CD38, which contributes
154 rent study, we demonstrate the importance of NAADP in the generation of Ca(2+) signals in murine naiv
156 Selective pharmacological inhibition of NAADP-evoked Ca(2+) release or genetic ablation of endol
158 nist Ned-19, we addressed the involvement of NAADP in the generation of Ca(2+) signals evoked by TCR
160 thod to prevent the endogenous metabolism of NAADP by chelating Ca2+ with bis-(o-aminophenoxy)ethane-
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.
173 omes and sarcoplasmic reticulum dependent on NAADP and TPC2 comprise an important element in beta-adr
177 low concentration and to compete with [(32)P]NAADP in a competition ligand binding assay with an IC(5
179 toxymethyl ester (NAADP-AM), a cell-permeant NAADP analog, increases cytosolic Ca(2+) concentration i
181 cotinic acid adenine dinucleotide phosphate (NAADP(+)), both of which have been shown to modulate cal
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
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
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
229 al systems that are widely used for studying NAADP-evoked Ca(2+) signaling, including sea urchin eggs
234 Third, tracheal homogenates could synthesize NAADP by base exchange from exogenous NADP and nicotinic
236 Taken together, these data demonstrate that NAADP functions as a second messenger in tracheal smooth
239 evolution and provide further evidence that NAADP mediates calcium release from acidic stores throug
243 troversial, although evidence indicates that NAADP mobilizes Ca(2+) from lysosome-related acidic comp
246 1 and TPC2) are endolysosomal proteins, that NAADP-mediated calcium signals are enhanced by overexpre
250 sosomes to the plasma membrane and show that NAADP evokes Ca(2+) influx independent of ryanodine rece
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
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
265 t of extracellular Ca(2+) and blocked by the NAADP antagonist Ned-19 or the vacuolar H(+)-ATPase inhi
268 ermed TPC1 and TPC2, are responsible for the NAADP-mediated Ca(2+) release but the underlying mechani
271 l smooth muscle, and therefore, steps in the NAADP signaling pathway might provide possible new drug
275 d by NAADP and the molecular identity of the NAADP receptors remain controversial, although evidence
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
285 possess the hallmark properties ascribed to NAADP receptors, including nanomolar ligand affinity [3-
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
297 lusion, our results support a model in which NAADP mediates glucose-induced Ca(2+) signaling in pancr
299 egion and that treatment of spermatozoa with NAADP resulted in a loss of the acrosomal vesicle that s
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