ライフサイエンスコーパス: ADP

1 ADP acts as a strong ATPase inhibitor of cytosol-specifi

2 ADP inhibition of bacterial Hsp90 can be relieved by bac

3 ADP inhibition of human and yeast cytosolic Hsp90 can be

4 ADP-glucose pyrophosphorylase (AGPase) controls bacteria

5 ADP-ribosylation (ADPr) regulates important patho-physio

6 ADP-ribosylation is a posttranslational modification tha

7 ADP-ribosylation is a PTM, in which ADP-ribosyltransfera

8 ADP-Ribosylation is reversed by hydrolases that cleave t

9 ADP-ribosylation of proteins is emerging as an important

10 ADP-ribosylhydrolases (ARH1, ARH2 and ARH3) are a family

11 ADP-ribosyltransferases (ARTs) modify proteins with sing

12 ADP-ribosyltransferases promote repair of DNA single str

13 Sir2, Sir3, Sir4, nucleosomes, and O-acetyl-ADP-ribose.

14 third C. difficile toxin, is a binary actin-ADP-ribosylating toxin that causes depolymerization of a

15 ic signature by reducing the actin-activated ADP release rate to become rate-limiting.

16 ults in a slow transition between actomyosin.ADP states and increases the time myosin is strongly bou

17 cted that MYO1C(35) populated the actomyosin.ADP closed state (AMD(C)) 5-fold more than the actomyosi

18 ate (AMD(C)) 5-fold more than the actomyosin.ADP open state (AMD(O)) and to a greater degree than MYO

19 2R) activation elicits afterdepolarizations (ADPs) in subcortically projecting (SC) pyramidal neurons

20 the rate of ATP synthesis, plotted against [ADP], remains low until [ADP] reaches about 30 mum and t

21 and excitability were related to the altered ADPs and AHPs.

22 These results suggest that altering ADP inhibition may be a mechanism of Hsp90 regulation.

23 Here, we describe an AMP/ADP-independent mechanism that triggers AMPK activation

24 se structures support the role of SUR1 as an ADP sensor and highlight the lasso extension as a key re

25 ification motif where lysine can serve as an ADP-ribose acceptor site.

26 Cat-1) is a signaling scaffold as well as an ADP-ribosylation factor-GTPase-activating protein.

27 UNC50 acted by recruiting GBF1, an ADP ribosylation factor-guanine nucleotide exchange fact

28 activities from a single Sde polypeptide: an ADP-ribosyltransferase and a nucleotidase/phosphohydrola

29 SAN4825, an ADP-ribosyl cyclase inhibitor that reduces cADPR and NAA

30 Our experiments suggest that an ADP-driven downward movement of the p97 N-terminal domai

31 by targeting the NADPH binding site using an ADP-TAMRA probe in a high-throughput screening assay.

32 itylate serine residues in substrates via an ADP-ribosylated ubiquitin intermediate.

33 presence of the non-hydrolyzable ATP analog, ADP-beryllium fluoride, we observe additional interactio

34 nucleotide conditions in which both ATP and ADP are present.

35 Elevated extracellular ATP and ADP levels are associated with cellular injury, inflamma

36 se 1 (NTPDase1) degrades the purines ATP and ADP that are key regulators of inflammation and clotting

37 Importantly, in some cell types AMP/ATP and ADP/ATP ratios remain unchanged during acute glucose sta

38 conformational changes between the ATP- and ADP-bound states explain the coupling of ATP hydrolysis

39 calize to the plasma membrane, caveolae, and ADP-ribosylation factor-6+ (Arf6+) endocytic compartment

40 h effects were independent of DNA damage and ADP-ribosylation.

41 h the enzymatic activity of deacetylases and ADP ribosyltransferases.

42 yl transfers (UDP-glucose), and electron and ADP-ribosyl transfers (NAD(P)H/NAD(P)(+)) to drive metab

43 was dependent on both its RING E3 ligase and ADP-ribosylation factor (ARF) GTPase activity.

44 -oxadiazole analog in complex with Sirt2 and ADP-ribose reveals its orientation in a still unexplored

45 mediators such as thromboxane A2 (TxA2) and ADP, which are agonists for G-protein-coupled receptors

46 ion structures of MsbA with ADP-vanadate and ADP reveal an unprecedented closed and an inward-facing

47 hen the delay between the synaptic input and ADPs is relatively long (e.g., several hundred milliseco

48 increases in matrix [Mg(2+)], [NAD(+)], and [ADP].

49 The dependencies on energy state and [ADP] near the threshold can be fitted by the Hill equati

50 xins introduce protein modifications such as ADP-ribosylation to manipulate host cell signaling and p

51 ssibly, other mitochondrial proteins such as ADP/ATP carrier proteins.

52 tone genes that can be manipulated to assess ADP-ribosylation events in vivo.

53 lHR and pHRed, to quantitatively assess ATP, ADP, and pH levels in MDA-MB-231 metastatic cancer cells

54 Renal cortical concentrations of ATP, ADP, AMP, cAMP, creatinine phosphate and ATP:AMP ratio w

55 These results imply that an ATP/ADP heterodimer of cytosolic Hsp90 is the predominant ac

56 one function are regulated by binding of ATP/ADP to mtHsp70's nucleotide-binding domain.

57 cellular levels of citrate, the ratio of ATP/ADP, phospholipid content, and ATP citrate lyase express

58 rapidly after reperfusion and ratios of ATP/ADP/AMP after reperfusion are significantly correlated t

59 ocyte infiltration by phosphohydrolyzing ATP/ADP.

60 All ACKs utilize ATP/ADP as the phosphoryl donor/acceptor in the respective d

61 rface of the cell, correlating with high ATP:ADP ratios close to the ventral membrane, which rapidly

62 a 2.45-, 3.17- and 2.12-fold increase in ATP:ADP, ATP:AMP and energy charge after portal venous reper

63 llular energetics and that intracellular ATP:ADP ratio is related to the ability of cancer cells to e

64 tion is pharmacologically inhibited, the ATP:ADP ratio decreases.

65 Specifically, we find that the ATP:ADP ratio increases in cells in denser matrices, where m

66 P, with feedback by the energy state ([ATP]/[ADP][Pi ]) regulating the pathway.

67 sulting in the rate being coupled to ([ATP]/[ADP][Pi ])(3) .

68 tor 1 (HPF1) is required for PARP1 to attach ADP-ribose groups onto the hydroxyl oxygen of the Ser re

69 Moreover, RECQ1 regulates PARP1 auto-(ADP-ribosyl)ation and the choice between long-patch and

70 the full-length constructs isomerized before ADP release, which has not been observed previously in t

71 t cleave the glycosidic bonds either between ADP-ribose units or between the protein proximal ADP-rib

72 -ribosylation acceptor sites but also boosts ADP-ribosylated peptide identifications.

73 r than the IC50 were required to ablate both ADP-ribosylation and XRCC1 chromatin binding following H

74 in ADP is consistent with SNF1 activation by ADP in vivo Downstream of SNF1, the Cat8 and Adr1 transc

75 This protein modification is often added by ADP-ribosyltransferases, commonly known as PARPs, but it

76 9)), we demonstrate an inverse regulation by ADP and Iloprost, suggesting that these are central modu

77 chlorophyll a/b-binding protein gene (CAB1), ADP-glucose pyrophosphorylase gene (APL3), and chalcone

78 bonded heterohexamers in which the catalytic ADP-ribosyltransferase subunit is activated when exposed

79 nd ARH3) are a family of enzymes to catalyze ADP-ribosylation, a reversible and covalent post-transla

80 deletion of Parp1 rescued normal cerebellar ADP-ribose levels and reduced the loss of cerebellar neu

81 ne dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR) are Ca(2+)-mobilizing messengers impo

82 athway involving the second messenger cyclic ADP-ribose (cADPR).

83 7) are NAD(+)-dependent protein deacetylases/ADP ribosyltransferases, which play decisive roles in ch

84 pression and function inhibits ANT-dependent ADP/ATP exchange.

85 ing; (ii) enhanced the after-depolarization (ADP); (iii) reduced fast and medium after-hyperpolarizat

86 ently reported that an M. pneumoniae-derived ADP-ribosylating and vacuolating toxin called community-

87 & Microbe, Vareechon et al. (2017) describe ADP-ribosylation of Ras as a strategy to inhibit assembl

88 ThcD) fragmentation methods when determining ADP-ribose acceptor sites within complex cellular sample

89 Adenosine diphosphate (ADP) enhances platelet activation by virtually any other

90 ne triphosphate (ATP)/adenosine diphosphate (ADP) metabolite ratio which strongly correlated with for

91 rst five catabolites: adenosine diphosphate (ADP), adenosine monophosphate (AMP), inosine monophospha

92 e triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP); and antioxidant

93 Protein adenosine diphosphate (ADP)-ribosylation is a physiologically and pathologicall

94 rack changes in substrate specificity during ADP-dependent kinase evolution along with the structural

95 st publicly available database encapsulating ADP-ribosylated proteins identified from the past 40 yea

96 enine nucleotide translocase (ANT) exchanges ADP/ATP through the mitochondrial inner membrane, and An

97 All these changes facilitate ADP-RA to bind ARH1.

98 ion of VAC-INVcis-QTL were also detected for ADP-glucose pyrophosphorylase, fumarase, and phosphogluc

99 improves the overall localization scores for ADP-ribosylation acceptor sites but also boosts ADP-ribo

100 Using the glycolytic ADP-dependent kinases of archaea, including the orders T

101 pecifically associated with the small GTPase ADP-ribosylation factor 1 (Arf1) to mediate uniform dist

102 lthough redundancy between H2BE18 and H2BE19 ADP-ribosylation is also apparent following DSBs in vivo

103 ETA has ADP-ribosylation activity and decisively affects the pro

104 CHIKV nsP3 macrodomain is able to hydrolyze ADP-ribose groups from mono(ADP-ribosyl)ated proteins.

105 as utilized a variety of methods to identify ADP-ribosylated proteins, recent proteomics studies brin

106 lic signaling and suggest that a decrease in ADP levels is important in GSIS.

107 sso extension as a key regulatory element in ADP's ability to override ATP inhibition.

108 A concomitant increase in ADP is consistent with SNF1 activation by ADP in vivo Do

109 ional landscape of the interdomain linker in ADP-bound DnaK and supported our simulations by strategi

110 ] are much higher than [ADP] and change in [ADP] is primarily responsible for the change in energy s

111 increases rapidly with further increase in [ADP].

112 Exchange of activating ATP to inactivating ADP triggers short helical segments in the K(+)-transloc

113 Here, we present an inactive ADP-bound structure of KtrAB from Vibrio alginolyticus,

114 tissue from Mc4r-/- mice exhibited increased ADP stimulated respiratory capacity.

115 Finally, the D2R-induced ADP is blocked by inhibitors of cAMP/PKA signaling, inse

116 nt regulator of the basal and stress-induced ADP-ribosylome.

117 These D2R-induced ADPs only occur following synaptic input, which activate

118 ic stimulation from facilitating D2R-induced ADPs, suggesting that this phenomenon depends on the rec

119 (Orbitrap, FT) scans, which produced intense ADP-ribose fragmentation ions.

120 the active site nucleotide species in Dop is ADP and inorganic phosphate rather than ATP, and that no

121 en complemented by recent advances that link ADP-ribosylation to stress responses, metabolism, viral

122 nd implications of this unexpected, O-linked ADP-ribosylation are speculated on.

123 ance of KATP/Ca(2+) signaling control by low ADP.Mg(2+) rather than by high ATP levels; and a role fo

124 cycle intermediates, malonyl-CoA, and lower ADP levels.

125 itochondrial content in the KO rats, maximal ADP-stimulated respiration was higher in permeabilized m

126 nnate immune response requires ExoS-mediated ADP-ribosylation of Ras in neutrophils.

127 CD73 mRNA, and alphabeta-methylene-ADP-inhibitable ecto-AMPase activity were elevated in th

128 osin VI motor domain in rigor (4.6 A) and Mg-ADP (5.5 A) states bound to F-actin.

129 the conversion of phosphoenolpyruvate and Mg-ADP to pyruvate and Mg-ATP.

130 RNA viruses that binds to the small molecule ADP-ribose.

131 ly defined its substrate specificity as mono(ADP-ribosyl)ated aspartate and glutamate but not lysine

132 ble to hydrolyze ADP-ribose groups from mono(ADP-ribosyl)ated proteins.

133 Therefore, nsP3 mono(ADP-ribosyl)hydrolase activity is critical for CHIKV rep

134 well described, the enzymes involved in mono-ADP-ribosylation (MARylation) have been less well invest

135 our results establish ARH3 as a serine mono-ADP-ribosylhydrolase and as an important regulator of th

136 RECQL5 both with and without the nucleotide ADP in two distinctly different ('Open' and 'Closed') co

137 An accounting of ADP is critically important for designing and interpreti

138 e, we have created ADPriboDB - a database of ADP-ribosylated proteins.

139 ed a statistically significant enrichment of ADP-ribosylated proteins in non-membranous RNA granules.

140 older to be without significant evidence of ADP.

141 and have led to the discovery of hundreds of ADP-ribosylated proteins in both cultured cells and mous

142 le carriers displayed enhanced inhibition of ADP-induced platelet aggregation by the nitric oxide don

143 results demonstrate that very low levels of ADP-ribosylation, synthesized by either PARP1 or PARP2,

144 The modification of serines by molecules of ADP-ribose plays an important role in signaling that the

145 To determine the molecular origin of ADP inhibition, we identify residues that preferentially

146 fy proteins with single units or polymers of ADP-ribose to regulate DNA repair.

147 he domain-docked conformation in presence of ADP and ATP.

148 In the presence of ADP or maltose, MalE.MalFGK2 remains essentially in a se

149 ce of nucleotide, but not in the presence of ADP.

150 re relatively insensitive to the presence of ADP.

151 stain electron microscopy in the presence of ADP/MgCl2 Single-particle analysis yielded a low-resolut

152 anslocase, which results in a slower rate of ADP or ATP translocation across the mitochondrial membra

153 various roles of PARPs and the regulation of ADP-ribosylation of protein substrates.

154 nstead suggest that the selective release of ADP from a postrigor myosin motor head promotes highly s

155 evel in the CII domain rises, the release of ADP from CI slows down, making the inactive conformation

156 The release of ADP has the opposite effect.

157 and cell biological evidence for the role of ADP-ribosylation factor 1 (ARF1)-GTPase and its effector

158 To appreciate the diverse roles of ADP-ribosylation across the proteome, we have created AD

159 adg1 mutation disables the small subunit of ADP-glucose pyrophosphorylase, the first step in starch

160 r a more detailed molecular understanding of ADP-induced protein phosphorylation could identify (1) c

161 Here we focused on ADP ribosylation factor (Arf) GTPases, which orchestrate

162 tivation occurs solely via changes in AMP or ADP, the classical activators of AMPK.

163 that preferentially stabilize either ATP or ADP.

164 .Pi.2K(+) and Na(+)-bound E1 approximately P.ADP suggest that the dimensions of the respective bindin

165 anges in the atomic displacement parameters (ADPs) on crossing T*.

166 Parp9 ADP-ribosylation activity therefore restrains the E3 fun

167 Dtx3L/Parp9 ADP-ribosylates the carboxyl group of Ub Gly76.

168 + ATP [Formula: see text] acetyl phosphate + ADP), with the exception of the Entamoeba histolytica AC

169 Poly ADP-ribose polymerases (PARPs) catalyze massive protein

170 l-cycle, apoptotic genes, caspase-3 and poly ADP ribose polymerase-1 (PARP-1) cleavage) and was rever

171 ncrease in Bcl2-like protein 4, cleaved Poly ADP-Ribosyl Polymerase 1 and cleaved Caspase 3 levels wi

172 ADAMTS-4 directly cleaved and degraded poly ADP ribose polymerase-1 (a key molecule in DNA repair an

173 ant channel (C1008-->A) or silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN trans

174 erived DNA were resistant to platin- or poly ADP ribose polymerase inhibitor-based chemotherapy.

175 erases (PARPs) catalyze massive protein poly ADP-ribosylation (PARylation) within seconds after the i

176 uitment of DNA repair factors via their poly ADP-ribose (PAR) binding domains.

177 Poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as

178 Inhibitors against poly (ADP-ribose) polymerase (PARP) are promising targeted age

179 mediated by the zinc finger domain and poly (ADP-ribose) (PAR).

180 urpose Data suggest that DNA damage by poly (ADP-ribose) polymerase inhibition and/or reduced vascula

181 rpose To determine whether cotargeting poly (ADP-ribose) polymerase-1 plus androgen receptor is super

182 Rucaparib is an inhibitor of nuclear poly (ADP-ribose) polymerases (inhibition of PARP-1 > PARP-2 >

183 s were tested for inhibitory effect of poly (ADP-ribose) polymerase (PARP) activity in vitro and in v

184 ely, and high selectivity toward other poly (ADP-ribose) polymerase enzymes.

185 omoting stabilization of a new target, poly (ADP-ribose) glycohydrolase (PARG) mRNA, by binding a uni

186 Durable and long-term responses to the poly (ADP-ribose) polymerase inhibitor olaparib are observed i

187 eficient cancers are hypersensitive to Poly (ADP ribose)-polymerase (PARP) inhibitors, but can acquir

188 ential marker of long-term response to poly (ADP-ribose) polymerase inhibition and that restoration o

189 Poly(ADP-ribosyl)ation (PARylation) is a post-translational m

190 Poly(ADP-ribosyl)ation (PARylation) is mainly catalysed by po

191 equired for DNA repair that possesses a poly(ADP-ribose) (PAR)-binding macro domain.

192 Olaparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, has previously

193 colorectal cancer by interacting with a poly(ADP-ribose) polymerase (PARP) tankyrase.

194 provides further evidence that use of a poly(ADP-ribose) polymerase inhibitor in the maintenance trea

195 Rucaparib, a poly(ADP-ribose) polymerase inhibitor, has anticancer activit

196 had received previous treatment with a poly(ADP-ribose) polymerase inhibitor.

197 AD50 as suppressors and 53BP1, DDB1 and poly(ADP)ribose polymerase 3 (PARP3) as promoters of chromoso

198 -1 overexpression stimulates PARP-1 and poly(ADP-ribose) (PAR) protein expression and cisplatin resis

199 erization with Parp9 enables NAD(+) and poly(ADP-ribose) regulation of E3 activity.

200 Tankyrase 1 and 2 are poly(ADP-ribose) polymerases that function in pathways critic

201 whereas DNA repair pathways mediated by poly(ADP)ribose polymerase 1 (PARP1) serve as backups.

202 reaks and disruption of this pathway by Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) is toxi

203 spase-3, cleaved caspase-7, and cleaved poly(ADP-ribose) polymerase (PARP).

204 The nuclear enzyme poly(ADP-ribose) polymerase 1 (PARP1) has been shown to facil

205 epressor (Ahrr/AhRR) and TCDD-inducible poly(ADP-ribose)polymerase (Tiparp/TiPARP) by AhR ligands wer

206 ns of PARP-1 occur independently of its poly(ADP-ribosyl) transferase activity.

207 rapidly modified by tankyrase-mediated poly(ADP-ribosyl)ation, which promotes the proteolysis of Axi

208 Moreover, poly(ADP-ribose) binding to the Parp9 macrodomains increases

209 The discovery of poly(ADP-ribose) >50 years ago opened a new field, leading th

210 PNKP and implicates hyperactivation of poly(ADP-ribose) polymerase/s as a cause of cerebellar ataxia

211 l the mechanisms by which inhibition of poly(ADP-ribose) polymerases (PARPs) elicits clinical benefit

212 te aspartate residues in the process of poly(ADP-ribosyl)ation.

213 Veliparib, an oral poly(ADP-ribose) polymerase inhibitor, has been shown to enha

214 endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap formation s

215 ors (PARPi), a cancer therapy targeting poly(ADP-ribose) polymerase, are the first clinically approve

216 eading the way for the discovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and the

217 Further, we observed that the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib synergi

218 Resolution at telomeres requires the poly(ADP-ribose) polymerase tankyrase 1, but the mechanism th

219 gets are the tankyrase proteins (TNKS), poly(ADP-ribose) polymerases (PARP) that regulate Wnt signali

220 BRCA2 and are selectively sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors.

221 responsible for cellular sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi) in BRCA1-defic

222 The vault-interacting domain of vault poly(ADP-ribose)-polymerase (INT) has been used as a shuttle

223 participate in DNA damage response via poly(ADP-ribosylation).

224 ), matrix metalloproteinases (MMPs) and poly-ADP-ribose-polymerase-1 (PARP-1) in diabetic kidney remo

225 down-regulated iNOS, nitrotyrosine, and poly-ADP-ribosyl polymerase expression and inhibited CAR-indu

226 mage, PARP1 interacts with and attaches poly-ADP-ribose (PAR) chains to EZH2.

227 ion (PARylation) is mainly catalysed by poly-ADP-ribose polymerase 1 (PARP1), whose role in gene tran

228 PARP1-dependent poly-ADP-ribosylation (PARylation) participates in the repair

229 Here, we found unlike PARP1-mediated Poly-ADP-Ribosylation (PARylation) at genomic damage sites, P

230 We also found that tankyrase1-mediated poly-ADP-ribosylation of TRF1 is important for both the inter

231 PARP1) and erasers (e.g. PARG, ARH3) of poly-ADP-ribosylation (PARylation) are relatively well descri

232 domains that interpret either mono- or poly-ADP-ribosylation and the implications for cellular proce

233 This modification can occur as mono- or poly-ADP-ribosylation.

234 are critical for both the mono- and the poly-ADP-ribosylhydrolase activity of ARH3.

235 s (DSBs) and were modestly sensitive to poly-ADP-ribose polymerase (PARP) inhibitors olaparib and BMN

236 sensitizing BRCA1-deficient tumours to poly-ADP-ribose polymerase-1 (PARP) inhibitors.

237 Poly-(ADP-ribose) polymerase (PARP) inhibitors (PARPis) select

238 imaging strategy for DLBCL that targets poly[ADP ribose] polymerase 1 (PARP1), the expression of whic

239 k repair but also elevated levels of protein ADP-ribosylation.

240 Herein, we investigated the protein ADP-ribosylation factor-like GTPase 13b (ARL13b) as a mo

241 odified by ARTs, the sites on these proteins ADP-ribosylated following DNA damage and the ARTs that c

242 ribose units or between the protein proximal ADP-ribose and a given amino acid side chain.

243 acyclin, we determined how Iloprost reverses ADP-mediated signaling events.

244 The Rho ADP-ribosylating C3 exoenzyme (C3bot) is a bacterial pro

245 the adenosine-5-diphosphate-ribosylarginine (ADP-RA) complex (51.56%) than that of the non-phosphoryl

246 Defected SCS ADP-forming beta subunit (SCS A-beta) is linked to letha

247 aracterized by a specific increase in serine-ADP-ribosylation in vivo under untreated conditions as w

248 " with advanced ages do not have significant ADP because they have protective factors for amyloid and

249 y be important for aging without significant ADP.

250 the functional consequences of site-specific ADP-ribosylation on those substrates.

251 nverted membrane vesicles under steady-state ADP-phosphorylating conditions.

252 titative temporal phosphoproteomics to study ADP-mediated signaling at unprecedented molecular resolu

253 mally used for Ub conjugation to substrates, ADP-ribosylation of the Ub carboxyl terminus precludes u

254 tivated following DNA damage and synthesizes ADP-ribose polymers that XRCC1 binds directly.

255 cells, [ATP] and [Pi ] are much higher than [ADP] and change in [ADP] is primarily responsible for th

256 Our data demonstrate that ADP-triggered phosphorylation occurs predominantly withi

257 Our observations suggest that ADP at physiological levels is important to Hsp90 struct

258 The ADP ribosylation factor (Arf) and the coat protein compl

259 The ADP-ribosylated moiety of ubiquitin is a substrate for t

260 ding to actin in the ADP-bound state and the ADP-release rate from myosin-S1 alone.

261 polymerase (PARP) family of enzymes and the ADP-ribosylation reactions that they catalyze.

262 t the activation of other GPCRs, such as the ADP receptors and protease-activated receptors, can also

263 ng of myosin Ic to actin is dominated by the ADP state for small external forces and by the ATP state

264 , suggesting that D2R activation elicits the ADP by stimulating cAMP/PKA signaling.

265 e find that knocking out D2Rs eliminates the ADP in a cell-autonomous fashion, confirming that this A

266 d the rate of myosin binding to actin in the ADP-bound state and the ADP-release rate from myosin-S1

267 By contrast, in the ADP-bound state, exemplified by the Escherichia coli Hsp

268 ARL13B is a member of the ADP ribosylation factor family of regulatory GTPases, bu

269 d the unique fragmentation properties of the ADP-ribose moiety were used to trigger targeted fragment

270 Members of the ADP-ribosylation factor (ARF) small GTPase family regula

271 We show that the ADPs for I ions yield extended flat regions in the poten

272 Protection from these ADP factors may be important for aging without significa

273 ell-autonomous fashion, confirming that this ADP depends on D2Rs.

274 ed on the ability of NKA to transform ATP to ADP and free phosphate, the latter reacting with ammoniu

275 Specifically, the ratio of ATP to ADP was highest at perinuclear areas of dense mitochondr

276 telet protein phosphorylation in response to ADP and Iloprost, which inversely overlap and represent

277 ting a failure by these mutants to translate ADP binding into a movement of the N-terminal domain.

278 d ATP or (tz) ATP to the corresponding N(tz) ADP(+) .

279 The N(tz) ADP(+) /N(tz) ADPH cycle can be monitored in real time b

280 phate dehydrogenase and reoxidation to N(tz) ADP(+) by glutathione reductase.

281 nicotinamide's glycosidic bond yielding (tz)ADP-ribose.

282 ientists and clinicians to better understand ADP-ribosylation at the molecular level.

283 s, plotted against [ADP], remains low until [ADP] reaches about 30 mum and then increases rapidly wit

284 a preference for GDP-glucose and can utilize ADP-glucose to some extent too.

285 oiety into hydrophobic subpockets in various ADP-ribosyltransferases.

286 bit protein synthesis of mammalian cells via ADP-ribosylation of the eukaryotic elongation factor-2.

287 active Vps4 hexamer with its cofactor Vta1, ADP.BeFx, and an ESCRT-III substrate peptide.

288 ADP-ribosylation is a PTM, in which ADP-ribosyltransferases use nicotinamide adenine dinucle

289 ar adenosine nucleotides: ATP inhibits while ADP activates.

290 ies of the different enzymes associated with ADP-ribosylation and the consequences of this PTM on sub

291 helps two residues form hydrogen bonds with ADP-RA; and (3) Tyr-211 is also less flexible in the pho

292 These values aligned closely with ADP centile values published for term infants from 36 to

293 nanometre-resolution structures of MsbA with ADP-vanadate and ADP reveal an unprecedented closed and

294 tide (NAD(+)) to modify target proteins with ADP-ribose.

295 ss flexible in the phosphorylated state with ADP-RA complex, which helps stabilize the cation-pi inte

296 ss flexible in the phosphorylated state with ADP-RA complex, which helps two residues form hydrogen b

297 sion in predicting exceptional aging without ADP.

298 contribution with exceptional aging without ADP.

299 operationalized "exceptional aging" without ADP by considering individuals 85 years or older to be w

300 "Exceptional aging" without ADP may be possible with a greater number of protective