ライフサイエンスコーパス: ADP

1 ADP-dependent kinases were first described in archaea, a

2 ADP-evoked fibrinogen binding was initially uniform over

3 ADP-ribosylation (ADPRylation) is a posttranslational mo

4 ADP-ribosylation factor (Arf)-like 4D (Arl4D), one of th

5 ADP-ribosylation is an intricate and versatile posttrans

6 ADP-ribosylation of Glu35 and the subsequent reduction o

7 nd expression of uncoupling protein (UCP) 3, ADP/ATP carrier protein (AAC) 1 and AAC2, and pyruvate d

8 Mutational potentiation accelerates ADP release, thereby increasing ATPase activity.

9 In the presence of actin, ADP affinity (K(AD) ) is unchanged for IFI-3a, compared

10 decreased this population in the actomyosin ADP state.

11 in the developing neuron, the protein ADAP1 (ADP-ribosylation factor GTPase-activating protein [ArfGA

12 Although ADP-ribosylation of histones by PARP-1 has been linked t

13 Furthermore, as CoA contains an ADP backbone this may extend beyond CoA-binding sites an

14 emains as the equatorial gap increases in an ADP football poised to split into half-footballs.

15 nuclear condensates or nuclear bodies in an ADP ribosylation-dependent manner.

16 PARP14 is an ADP-ribosyltransferase with multiple roles in transcript

17 These cofactors consist of an ADP core covalently bound to extra moieties.

18 HIF-1 promotes the transcription of an ADP ribosyltransferase, TiPARP, which serves to deactiva

19 enzyme, we obtain the first structure of an ADP-dependent kinase (AncMsPFK) with F6P at its active s

20 nce of additional co-factors such as AMP and ADP.

21 acetylation, ubiquitination, AMPylation, and ADP-ribosylation.

22 The apo and ADP-bound structures reveal a homo-heptamer and show a l

23 re integral to this regulation, with ATP and ADP closing the channel and MgATP and MgADP increasing c

24 differences in isomerization for the ATP and ADP growth at the barbed end exactly matches experimenta

25 nd find that the NB-ARC domain binds ATP and ADP, but does not hydrolyze these nucleotides.

26 Furthermore, excess NADPH, GTP and ADP greatly diminish N-malonylation near their nucleotid

27 resented TFs such as EZH2 affected MCF2L and ADP-ribosylhydrolase like 1 expression, among the others

28 epair, we attempted to confirm that NAD+ and ADP-ribose can be used as co-factors by human DNA ligase

29 with cysteine modifying S-nitrosylation and ADP-ribosylation reactions using a chemical nitric oxide

30 dict experimentally measured duty ratios and ADP release rates better than sequence or individual str

31 The OADP and AP methods, as well as SP and ADP, have been implemented in the open-source Python sof

32 itates the activation of members of the ARF (ADP-ribosylation factor) family of small GTPases.

33 e we report the crystal structure of an ATP (ADP:BeF(3)-bound) ground-state mimic double-ring mHsp60(

34 cate an interplay between the levels of ATP, ADP, 2-OG, PII-sensed glutamine, and NAD(+), representin

35 aptamer which binds indiscriminately to ATP, ADP, AMP, and adenosine.

36 ATP/ADP binding to Kir6.2 shuts K(ATP).

37 2+/-0.23 debanding, 1.11+/-0.24, P=0.59; ATP/ADP: sham, 6.2+/-0.9, debanding, 5.6+/-1.6, P=0.66).

38 Time-lapse imaging of autophagosomes and ATP/ADP levels in migrating cells in the rostral migratory s

39 hosphocreatine, phosphocreatine/ATP, and ATP/ADP to normalize in debanding towards sham values (phosp

40 that are regulated by the intracellular ATP/ADP ratio.

41 sions and is converted by the microglial ATP/ADP hydrolysing ectoenzyme CD39 into AMP; AMP is then co

42 ise several solute carriers, such as the ATP/ADP antiporter nucleotide transporter2 (NTT2; substantia

43 s electrophoretically transported by the ATP/ADP antiporter to the catalytic site of bound hexokinase

44 olysaccharide biosynthetic intermediate beta-ADP-heptose by the ALPK1/TIFA signaling pathway.

45 ells during S-phase as a consequence of beta-ADP-heptose/ ALPK1/TIFA/NF-kappaB signaling.

46 Channel activation requires binding of both ADP-ribose (ADPR) and Ca(2+).

47 mplex into the "old/weak" state 2 with bound ADP, which is 20 times more sensitive to force than stat

48 unchanged for IFI-3a, compared with IFI, but ADP affinity for EMB-3b is increased, compared with EMB,

49 l posttranslational modification of 53BP1 by ADP-ribosylation that is targeted by a PAR-binding E3 ub

50 als that the ATPase cycle is rate-limited by ADP release from nucleotide-binding domain 1 (NBD1).

51 site, whereas the site remained occupied by ADP in FlrC(C)-Y290A.

52 While ADP-ribosylation can be reversed by ADP-ribosylhydrolases, this protein modification can als

53 st-translational modification synthetized by ADP-ribose transferases and removed by poly(ADP-ribose)

54 k on PARPs-a family of enzymes that catalyze ADP-ribosylation, a posttranslational modification of pr

55 ha GTP-loading and pertussis toxin-catalyzed ADP-ribosylation of G(i)alpha, for which we synthesized

56 T200 levels of 0.49 ug/ml prolonged collagen-ADP closure times to > 300 s at baseline, whereas 1.35 u

57 At different concentrations, ADP triggered opposing motilities.

58 e calcium-mobilizing second messenger cyclic ADP-ribose (cADPR), CD157, a sister protein of CD38, has

59 mitochondrial matrix as well as by cytosolic ADP.

60 In response to DNA damage, ADP-ribosylated 53BP1 increased significantly, resulting

61 hydrolase activity was required for 53BP1 de-ADP-ribosylation, 53BP1 protein stability, and its funct

62 We also developed a drug-dependent ADP-ribosylation assay in primary cells that correlated

63 We found that NAD(+)-dependent ADP-ribosylation of histone H2B-Glu35 by small nucleolar

64 e of extracellular adenosine 5'-diphosphate (ADP) that activated P2Y1 purinergic receptors on neighbo

65 trong" state 1 has adenosine 5'-diphosphate (ADP)-P (i) bound to Arp2/3 complex.

66 nophosphate (AMP) and adenosine diphosphate (ADP) on flagellar beating is not fully understood.

67 resence or absence of adenosine diphosphate (ADP) suggest that motions of the catalytic core, which a

68 p47-p97 complexes in adenosine diphosphate (ADP)- and adenosine triphosphate (ATP)-bound conformatio

69 rase, DarT(Mtb) ), to mediate reversible DNA ADP-ribosylation (Jankevicius et al., 2016).

70 ons along with its cognate toxin Rv0059 (DNA ADP-ribosyl transferase, DarT(Mtb) ), to mediate reversi

71 One of these, Rv0060 (DNA ADP-ribosyl glycohydrolase, DarG(Mtb) ), functions along

72 During each ADP, participants received a priming drink of alcohol fo

73 (2+) mobilization pathway initiates an early ADP secretion, potentiating platelet activation, and a s

74 pyrene conjugated to cysteine 374 and either ADP (3.2 angstrom) or ADP-phosphate (3.0 angstrom) in th

75 physiological perturbations such as elevated ADP concentration weakens mavacamten's ability to increa

76 transient reaction intermediate, the elusive ADP.P(i) nucleotide state, which has been postulated for

77 ide donor S-nitrosoglutathione and enzymatic ADP-ribosyltransferase PtxS1-subunit of pertussis toxin,

78 ) hydrolysis assay, and 6.8 in the enzymatic ADP-ribosyltransferase inhibitor dose-response assay.

79 kinases (ADP-GKs), and bifunctional enzymes (ADP-PFK/GK).

80 In the calcium-replete ER, ADP rebinding to post-ATP hydrolysis BiP-substrate compl

81 acterized five isoforms of Manihot esculenta ADP-glucose pyrophosphorylase large subunit (MeAPL1-MeAP

82 tion defect that can be rescued by exogenous ADP.

83 an also utilize NAD+ and, to a lesser extent ADP-ribose, as the source of the adenylate group and tha

84 CxD7L1 exhibits high affinity for ADP and ATP, a binding capacity not reported in any D7.

85 chaperone BiP, by enhancing its affinity for ADP.

86 ation downstream of P2Y(1) was essential for ADP-evoked fibrinogen binding, whereas P2Y(12) and the k

87 tidomain GTPase-activating protein (GAP) for ADP-ribosylation factor (ARF)-type GTPases.

88 ate a functional interplay between H2B-Glu35 ADP-ribosylation and H2B-Ser36 phosphorylation that cont

89 tokinases (ADP-PFKs), specific glucokinases (ADP-GKs), and bifunctional enzymes (ADP-PFK/GK).

90 Serum glucose, ADP fibrinogen, and mannose were among the strongest pre

91 ken together, these results reveal that H2AX ADP-ribosylation not only facilitates BER repair, but al

92 ion-deficient E141A mutant suggest that H2AX ADP-ribosylation plays a critical role in base excision

93 On the other hand, ADP has a high computation cost because it requires runn

94 ular mechanism of DNA damage-induced histone ADP-ribosylation remains elusive.

95 histone modifications and found that histone ADP-ribosylation was associated with histone removal at

96 at persistent antigenic stimulation impaired ADP-coupled oxidative phosphorylation.

97 n length and the relatively slow off-rate in ADP, we conclude that attachment of the tethered head is

98 examers switch from a more-solvated state in ADP to a less-solvated state in ATPgammaS, consistent wi

99 82.2 AU; P < 0.05) and an increased trend in ADP antibody (82.3 vs. 69.2 AU; P < 0.07) but not aspiri

100 e activity of other GPCR agonists, including ADP, arginine vasopressin, glucagon-like peptide 1, and

101 ion of myosin light chains, and an increased ADP:ATP ratio, destabilize the SRX population.

102 esidue 141 (E141) of variant histone H2AX is ADP-ribosylated following oxidative DNA damage.

103 lease gates access to a weak binding K.ADP-K.ADP state that can slip back along the microtubule, re-e

104 Pi release gates access to a weak binding K.ADP-K.ADP state that can slip back along the microtubule

105 Here we show during both non-ADP- and low-ADP-stimulated respiration that accelerating flux throug

106 l tension fall was caused by detachment of M.ADP.Pi myosin heads from actin and reversal of the first

107 es between conditions were found for maximal ADP-stimulated mitochondrial respiration (both for compl

108 Mechanistically, ADP-ribosylation on E141 mediates the recruitment of Nei

109 petitive CD73 inhibitor alpha,beta-methylene-ADP (AOPCP) substituted in the 2-position.

110 the transport mechanism of the mitochondrial ADP/ATP carrier to examine the structure and function of

111 They modify ADP-ribosylation factor 6 (ARF6) on lysine 3 allowing it

112 t ARH3-mutated patient cells accumulate mono(ADP-ribose) scars on core histones that are a molecular

113 DNA damage response, many noncanonical mono(ADP-ribosylating) (MARylating) PARPs are associated with

114 Moreover, we show that the mono(ADP-ribose) scars are lost from the chromatin of ARH3-de

115 irtuin family of protein deacylases and mono-ADP ribosylases, protects adult hair follicle stem cells

116 The NAD+-dependent deacetylase and mono-ADP-ribosyl transferase SIRT6 stabilizes the genome by p

117 6, including long-chain deacylation and mono-ADP-ribosylation of other proteins, have also been repor

118 ssays to identify and validate two key nodes-ADP-ribosylation factor 4 (ARF4) and valosin-containing

119 Here we show during both non-ADP- and low-ADP-stimulated respiration that acceleratin

120 Previously, we showed that ATP-DnaA, not ADP-DnaA, undergoes a conformational change at the highe

121 We also observe ADP-Mg(2+) bound in the nsp12 N-terminal nidovirus RdRp-

122 alcium-depleted ER, relative acceleration of ADP-to-ATP exchange favours substrate release.

123 ytic centre is essential for the addition of ADP-ribose moieties after DNA damage in human cells.

124 ny parameters, most notably minor amounts of ADP generated during autophosphorylation reactions or pr

125 h can greatly reduce the computation cost of ADP.

126 a indicate that ARH3 can act as an eraser of ADP-ribose chromatin scars at sites of PARP activity dur

127 of the TrkH-TrkA complex in the presence of ADP or ATP.

128 otide and Hsp104 hexamers in the presence of ADP or ATPgammaS (adenosine 5'-O-(thiotriphosphate)).

129 length of the working stroke and the rate of ADP release in the absence of external loads by a factor

130 n 5-10 s following stimulation) secretion of ADP specifically dependent on SERCA3 stored Ca(2+) is ex

131 ely, while the projected computation time of ADP was 1628 CPU hours.

132 humans, 16 of which catalyze the transfer of ADP-ribose from NAD(+) to macromolecular targets (namely

133 roaches as well as a deeper understanding of ADP-ribosylation as a whole.

134 platelet activation, and a secondary wave of ADP secretion driven by both an IP3/SERCA2b-dependent Ca

135 de an overview of the different families of (ADP-ribosyl)hydrolases.

136 es: bias-adjusted projection (AP) and online ADP (OADP).

137 s rescued with the addition of either AMP or ADP with ATP, compared to ATP alone.

138 ysteine 374 and either ADP (3.2 angstrom) or ADP-phosphate (3.0 angstrom) in the active site.

139 erator (parOP), which requires either ATP or ADP, and which is essential for it to act as a transcrip

140 CM subunits are bound to either ATPgammaS or ADP, whereas the apo MCM2-5 interface remains open.

141 ging motor domains in the nucleotide-free or ADP states.

142 uman DNA ligase IV cannot use either NAD+ or ADP-ribose as adenylation donor for ligation.

143 ligase IV is dependent upon ATP not NAD+ or ADP-ribose.

144 onsumed during an alcohol drinking paradigm (ADP) before and after 1 week of supervised 100 mg daily

145 ay washout, and 3 alcohol drinking paradigm (ADP) sessions.

146 ticipated in two alcohol drinking paradigms (ADPs) separated by a week of open-label naltrexone (100

147 pecificities; specific phosphofructokinases (ADP-PFKs), specific glucokinases (ADP-GKs), and bifuncti

148 B in an apo state and bound to phospholipid, ADP or AMP-PNP to a resolution of 3.3-4.1 angstrom and e

149 -2/Bax, TNFalpha, cleaved Caspase-3 and poly ADP-ribose polymerase (PARP).

150 Poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib and t

151 Poly (ADP-ribose) polymerase (PARP) plays a significant role i

152 Poly (ADP-ribose) polymerase inhibitors combined with immunoth

153 Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi), is appr

154 P-3, CXCL9, CXCL10, CXCL5, ENRAGE, and poly (ADP-ribose) polymerase 1.

155 er molecular targets available such as poly (ADP-ribose) polymerase (PARP), epidermal growth factor r

156 exquisite sensitivity to inhibitors of poly (ADP-ribose) polymerase (PARP) that are being tested in c

157 cytotoxicity in a process dependent on poly (ADP-ribose) polymerase-1 (PARP-1); a NAD(+)-consuming en

158 the base excision repair (BER) protein poly (ADP-ribose) polymerase (PARP).

159 ayed synergistic cytotoxicity with the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib against

160 The poly (ADP-ribose) polymerase (PARP) inhibitor olaparib is FDA

161 R) and renders cells hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors used to treat B

162 Poly(ADP ribose) polymerase inhibitors (PARPi) have efficacy

163 Poly(ADP) ribosylation (PARylation) is important for subseque

164 Poly(ADP-ribose) (PAR) is a nucleic acid-like protein modific

165 Poly(ADP-ribose) (PAR) is rapidly synthesized from NAD(+) at

166 Poly(ADP-ribose) a dynamic and reversible posttranslational m

167 Poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glyco

168 Poly(ADP-ribose) polymerase (PARP) inhibitors have shown effi

169 Poly(ADP-ribose) polymerase (PARP) superfamily members covale

170 Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme in

171 Poly(ADP-ribose)-polymerase (PARP)-1 and PARP-2 play an essen

172 Poly(ADP-ribosyl)ation is a reversible post-translational mod

173 d compartments at DNA damage sites in a poly(ADP ribose) (PAR)-dependent manner.

174 Here, we show that tankyrase, a poly(ADP-ribosyl) polymerase that regulates beta-catenin leve

175 matic tissues, much less is known about poly(ADP-ribosyl)ation in the germline, where DNA double-stra

176 t forms DNA adducts, thereby activating poly(ADP-ribose) polymerases (PARPs) to initiate DNA repair.

177 rates through the addition of mono- and poly(ADP-ribose) (PAR)(1-5).

178 Poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glycohydrolase (PARG) are key enzymes in BER

179 t enzymes, including sirtuins, CD38 and poly(ADP-ribose) polymerases.

180 modify numerous proteins with mono- and poly(ADP-ribose) signals that are important for the subsequen

181 damage-repair-targeting agents such as poly(ADP-ribose)-polymerase inhibitors.

182 finger in ZBTB24 binds PARP1-associated poly(ADP-ribose) chains and mediates the PARP1-dependent recr

183 ects replication forks from stalling at poly(ADP-ribose) polymerase 1 (PARP1)-DNA complexes trapped b

184 erase 1 (PARP1) and stimulates its auto-poly(ADP-ribosyl)ation.

185 Synthetic lethality between poly(ADP-ribose) polymerase (PARP) inhibition and BRCA defici

186 PAR degradation by poly(ADP-ribose) glycohydrolase (PARG) is essential for progr

187 ADP-ribose transferases and removed by poly(ADP-ribose) glycohydrolase (PARG), which plays important

188 BTB24 protects them from degradation by poly(ADP-ribose) glycohydrolase (PARG).

189 nd break repair; a process regulated by poly(ADP-ribose) metabolism.

190 cule inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP1) for the detection of ca

191 oteomic analyses uncover a new role for poly(ADP-ribosyl)ation (PARylation) in regulating the chromat

192 for several NAD-consuming enzymes (e.g. poly(ADP-ribose) polymerases, sirtuins, and others).

193 iosis, beyond its enzymatic activity in poly(ADP-ribose) catabolism.

194 SCA7 patients displayed increased poly(ADP-ribose) in cerebellar neurons, supporting poly(ADP-r

195 NA damage, neuroinflammation, increased poly(ADP-ribose) polymerase-1 (PARP1) activity, single-cell s

196 These interventions also increased poly(ADP-ribosyl) polymerase and sirtuin activity, suggesting

197 n of downstream effector TCDD-inducible poly(ADP-ribose) polymerase (TiPARP) during infection.

198 Although the well-known poly(ADP-ribosylating) (PARylating) PARPs primarily function

199 nation of LuTate and the small molecule Poly(ADP-ribose) polymerase-1 (PARP) inhibitor, talazoparib l

200 The synthesis of poly(ADP-ribose) (PAR) reconfigures the local chromatin envir

201 d irreversibly inhibits the activity of poly(ADP-ribose) polymerase 1, an important anticancer target

202 The success of poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors (PARPi) to

203 The process of poly(ADP-ribosyl)ation and the major enzyme that catalyses th

204 utes) through mechanisms that depend on poly(ADP-ribose) polymerases (PARP) and the catalytic subunit

205 forks is a prominent mechanism of PARP (Poly(ADP-ribose) Polymerase) inhibitor (PARPi) resistance in

206 ge by inhibiting the DNA repair protein poly(ADP-ribose) polymerase (PARP).

207 s the central DNA damage sensor protein poly(ADP-ribose) polymerase 1 (PARP1) and activates caspase-3

208 ere, we have found that a host protein, poly(ADP-ribose) polymerase 1 (PARP1), facilitates IFNAR degr

209 ere, we report that a cellular protein, poly(ADP-ribose) polymerase 1 (PARP1), plays a critical role

210 or enzyme that catalyses this reaction, poly(ADP-ribose) polymerase 1 (PARP1), were discovered more t

211 cludes elevated CD38 NADase and reduced poly(ADP-ribose) polymerase and SIRT1 activities, respectivel

212 ion, induction of autophagy, and robust poly(ADP-ribose) polymerase (PARP) cleavage indicative of DNA

213 onse to a variety of cellular stresses, poly(ADP-ribose) polymerase 1 (PARP1) has vital roles in orch

214 bose) in cerebellar neurons, supporting poly(ADP-ribose) polymerase-1 upregulation.

215 The anti-cancer drug target poly(ADP-ribose) polymerase 1 (PARP1) and its close homologue

216 to the automated radiosynthesis of the poly(ADP-ribose) polymerase (PARP) inhibitor [(18)F]olaparib.

217 dered GLS(high) cells vulnerable to the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib, and p

218 This facilitates the poly(ADP-ribose)-dependent assembly of the LIG4/XRCC4 complex

219 t ATAD5-depleted cells are sensitive to poly(ADP)ribose polymerase (PARP) inhibitors and that the pro

220 rstanding acquired tumour resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and other thera

221 mutated breast cancers are sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors and platinum ag

222 on levels show increased sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors, especially whe

223 perform HDR, conferring sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi).

224 ples, RITA, AF, and Onc-1 sensitized to poly(ADP-ribose) polymerase inhibitors both in vitro and ex v

225 r (mCRPC) and may confer sensitivity to poly(ADP-ribose) polymerase inhibitors.

226 Moreover, through its association with poly(ADP-ribose) chains, ZBTB24 protects them from degradatio

227 y, we found that ZBTB24 associates with poly(ADP-ribose) polymerase 1 (PARP1) and stimulates its auto

228 NAD(+) consumers in mammalian cells are poly-ADP-ribose-polymerases (PARPs).

229 Blocking poly-ADP-ribose gylcohydrolase also enhanced this association

230 Here we report that both BRCA1 poly-ADP ribosylation (PARsylation) and the presence of BRCA1

231 uit and activate PARP1/2, which deposit poly-ADP-ribose (PAR) to recruit XRCC1-Ligase3 and other repa

232 ) is a substrate for PARP-enzymes (mono/poly-ADP-ribosylation) and sirtuins (deacetylation).

233 The success of poly-ADP ribose polymerase inhibitors in the treatment of bre

234 PSKalpha exhibited lower expression of poly-ADP-ribose polymerase 1 (PARP1) gene, leading to a highe

235 Inhibitors of poly-ADP-ribose polymerase 1 (PARPi) are highly effective in

236 inding domain and, at least in part, on poly-ADP ribose polymerase (PARP) activity.

237 of target proteins, leading to mono- or poly-ADP-ribosylation (MARylation or PARylation).

238 In this study, we present ADP-dependent glucokinase (ADPGK) as a novel glucose sen

239 ion from SERCA3-dependent stores and primary ADP secretion are blocked by the NAADP receptor antagoni

240 ion from SERCA3-dependent stores and primary ADP secretion were unaffected by inhibition of the produ

241 augmentation, decomposition and Procrustes (ADP) transformation, such as LASER and TRACE, are popula

242 One of the kinase reaction products, ADP, is transported back to the mitochondrial matrix via

243 subsidized by the Assistive Devices Program (ADP).

244 phosphate-ribose polymerases (PARPs) promote ADP-ribosylation, a highly conserved, fundamental posttr

245 vides insights into the functions of protein ADP-ribosylation, and suggests activating TiPARP as an a

246 l structures of a complex consisting of Prp2-ADP and the G-patch domain of Spp2 demonstrate that the

247 s and found that the FACT complex recognized ADP-ribosylated histones and mediated the removal of his

248 ck along the microtubule, re-engage, release ADP, and try again to take an ATP-driven forward step.

249 NUDT16 has hydrolase activities that remove ADP-ribosylation of 53BP1 to regulate 53BP1 stability an

250 in the ARH3 (ADPRHL2) hydrolase that removes ADP-ribose from proteins have been associated with neuro

251 g GTPase-independent mechanism that requires ADP-ribosylation factor 1 (Arf1).

252 mily members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins u

253 erves to regulate Hsp104 activity by slowing ADP release.

254 converts the AncMsPFK enzyme into a specific ADP-GK.

255 ion differs from that described for specific ADP-GK enzymes, where each substrate independently cause

256 he catalytic cycle, as reported for specific ADP-PFK.

257 amino-terminal RhoGAP and a carboxy-terminal ADP-ribosyltransferase domain.

258 ion speed can be 16-16 000 times faster than ADP.

259 We show that ADP-ribosylation factor 1 (ARF1), bridging integrator 1

260 pport the increasingly compelling view that (ADP-ribosyl)hydrolases are a vital element within ADP-ri

261 The ADP component of these metabolites base-pairs with the D

262 The ADP release rate (k(-D) ) in the absence of actin is com

263 The ADP.BeF(3) (-)-stabilized complex did not require the Ch

264 tudies performed with wild-type H2AX and the ADP-ribosylation-deficient E141A mutant suggest that H2A

265 abundant Rossmann-fold motifs that bind the ADP moiety of NADH, NADPH, FADH and ATP.

266 Blocking the ADP signal reduced rotavirus replication, inhibited rota

267 Both the ADP off-rate and the ATP on-rate at physiological ATP co

268 iated with higher alcohol craving during the ADP (F(1,81) = 4.88, p = 0.030).

269 The RhoGAP-, but not the ADP-ribosyltransferase domain of the related effector pr

270 l complex, and the cryo-EM structures of the ADP-bound successor mHsp60(14)-(mHsp10(7))(2) complex, a

271 ogical roles, as well as the activity of the ADP-ribose (ADPR) transferase enzymes (PARP family membe

272 rane vesicles requires the activation of the ADP-ribosylation factor ARF GTPase by the SEC7 domain of

273 ne nucleotide exchange factors (GEFs) on the ADP-ribosylation factor (ARF) family of small GTPases in

274 s-containing R403Q myosin, recapitulated the ADP-induced destabilization of the SRX state.

275 5 architecture with two active subunits, the ADP ribosyl transferase PltA and the DNase CdtB, linked

276 and that the ATP monomer is flatter than the ADP form.

277 Our results suggest that the ADP-binding function acquired by CxD7L1 evolved to enhan

278 We demonstrate that the ADP-ribose chromatin scars result in reduced endogenous

279 PARP catalytic domains transfer the ADP-ribose moiety from NAD(+) to amino acid residues of

280 vealed that ALA3 functions together with the ADP ribosylation factor GTPase exchange factors GNOM and

281 Moreover, loss of this ADP-ribosylation enhances serine-139 phosphorylation of

282 The ATPase-catalysed conversion of ATP to ADP is a fundamental process in biology.

283 TrkA forms a tetrameric ring when bound to ADP and constrains TrkH to a closed conformation.

284 TrkA, which closes the channel when bound to ADP and opens it when bound to ATP.

285 he crystal structure of mouse DHX36 bound to ADP.

286 1987 and 2016 were identified and linked to ADP claims.

287 ons, underscored by a decrease in the ATP-to-ADP ratio in Cox6a2(-/-) PV(+) interneurons.

288 ides increased the EC(50) for trinitrophenyl-ADP binding to NBS2, but only in the presence of Mg(2+),

289 e loss of the small guanosine triphosphatase ADP-ribosylation factor 1 (Arf1) or its effector, phosph

290 By using ADP-ribosylation factor 6 (ARF6) small interfering RNA,

291 d to enhance blood-feeding in mammals, where ADP plays a key role in platelet aggregation.

292 Whereas ADP-DnaA was predominantly monomeric, AMP-PNP-DnaA (a no

293 While ADP-ribosylation can be reversed by ADP-ribosylhydrolase

294 timal DNA damage response is associated with ADP-ribosylation of histones.

295 Branches with ADP-Arp2/3 complex are more sensitive to debranching by

296 (glia maturation factor) than branches with ADP-P (i) -Arp2/3 complex.

297 tin's ability to polymerize as compared with ADP G-actin.

298 crystal structure of CxD7L1 in complex with ADP to 1.97 angstrom resolution.

299 tation impeded the interaction of PROM1 with ADP-ribosylation factor-like protein 13B, a key regulato

300 continuously supports H(+)-ATP synthase with ADP until glucose or creatine is available.

301 ibosyl)hydrolases are a vital element within ADP-ribosyl signaling pathways and they hold the potenti