ライフサイエンスコーパス: ADP-ribose

1 ADP-ribose can be conjugated to proteins singly as a mon

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

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

4 TRPM2's activation by Ca(2+) and ADP ribose (ADPR), an NAD(+)-metabolite produced under o

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

6 s transesterification to yield 2'-OH RNA and ADP-ribose-1",2"-cyclic phosphate products.

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

8 -ribose) polymerases (PARPs) using NAD(+) as ADP-ribose donor.

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

10 The attached ADP-ribose monomers or polymers, commonly known as poly(

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

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

13 TRPM2 is activated by ADP ribose (ADPR) binding to its C-terminal cytosolic NU

14 s-related cation channel hTRPM2, is gated by ADP-ribose (ADPR) independently of the C-terminal NUDT9H

15 This activity of TNT was not inhibited by ADP-ribose or nicotinamide, indicating low affinity of T

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

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

18 ined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the res

19 g and processing free and protein-conjugated ADP-ribose into phosphoribose forms.

20 ose) for labeling free or protein-conjugated ADP-ribose monomers and polymers at their 2'-OH termini

21 ite to better accommodate protein-conjugated ADP-ribose.

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

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

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

25 It is activated by cytosolic ADP ribose (ADPR) and contains a nudix-type motif 9 (NUD

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

27 NudT16 in complex with monomeric and dimeric ADP-ribose in identifying the active site for binding an

28 ivity of NrtR is antagonized by the effector ADP-ribose.

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

30 6A, and F61S) have reduced activity for free ADP-ribose, similar processing ability against protein-c

31 a single ADP-ribose to a target or generate ADP-ribose chains.

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

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

34 trinsic NADase activity-cleaving NAD(+) into ADP-ribose (ADPR), cyclic ADPR, and nicotinamide, with n

35 The latter involves the synthesis of long ADP-ribose chains that have specific properties due to t

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

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

38 sing ability against protein-conjugated mono(ADP-ribose), but improved catalytic efficiency for prote

39 Although stress-induced synthesis of mono(ADP-ribose) (mADPr) and poly(ADP-ribose) (pADPr) conjuga

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

41 lation refers to the addition of one or more ADP-ribose groups onto proteins.

42 lation refers to the addition of one or more ADP-ribose units onto proteins post-translationally.

43 nalysis revealed that serine serves as a new ADP-ribose acceptor site across the proteome.

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

45 s a structurally complex polymer composed of ADP-ribose units that facilitates local chromatin relaxa

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

47 novel tool to investigate different forms of ADP-ribose.

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

49 ted ARH1, the possible unbinding pathways of ADP-ribose from non-phosphorylated and phosphorylated AR

50 cofactor to transfer monomer or polymers of ADP-ribose nucleotide onto macromolecular targets such a

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

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

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

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

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

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

57 se activity and accompanied full-length poly ADP ribose polymerase (PARP) cleavage.

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

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

60 -2/Bax, TNFalpha, cleaved Caspase-3 and poly ADP-ribose polymerase (PARP).

61 Alcohol feeding induced apoptosis (poly ADP-ribose polymerase [PARP] and caspase-3 [CASP-3] clea

62 nilin-1-associated protein to attenuate poly ADP-ribose polymerase activation and mitochondrial DNA d

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

64 pathways demonstrated the activation of poly ADP-ribose polymerase-dependent cell death in bok-defici

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

66 Veliparib, a poly (ADP ribose) polymerase inhibitor, potentiated standard c

67 In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated

68 Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells

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

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

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

72 Poly (ADP-ribose) polymerase (PARP) inhibitors have shown prom

73 Poly (ADP-ribose) polymerase (PARP) is the best-known element

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

75 Poly (ADP-ribose) polymerase 1 (PARP1) has emerged as an attra

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

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

78 inhibitor, L67, in combination with a poly (ADP-ribose) polymerase inhibitor.

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

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

81 with immune checkpoint inhibitors and poly (ADP-ribose) polymerase (PARP) inhibitors in a variety of

82 being targeted with platinum drugs and poly (ADP-ribose) polymerase (PARP) inhibitors.

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

84 ells and the cleavage of caspase-3 and poly (ADP-ribose) polymerase.

85 Targeted therapies such as poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as

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

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

88 xpression of caspase-3, higher cleaved poly (ADP-ribose) polymerase levels (p < 0.007), and a higher

89 g-fold change (suppression) of cleaved poly (ADP-ribose) polymerase was greater with palbociclib plus

90 Apoptosis was characterized by cleaved poly (ADP-ribose) polymerase.

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

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

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

94 cal work, we found that combination of poly (ADP-ribose) polymerase (PARP) inhibitors with drugs that

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

96 s to involve the catalytic activity of poly (ADP-ribose) polymerase.

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

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

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

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

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

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

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

104 y been suggested to be a target of the poly (ADP-ribose) polymerases Tankyrase 1, and we have found t

105 ) mutations that confer sensitivity to poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis), but t

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

107 ficient show a significant response to poly (ADP-ribose) polymerase (PARP) inhibitors; patients with

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

109 0 is required for HR and resistance to poly (ADP-ribose) polymerase inhibitors.

110 diotherapy, or previous treatment with poly (ADP-ribose) polymerase inhibitors.

111 to oxidative stress via regulation of poly [ADP-ribose] polymerase 1 (PARP1).

112 [also referred to as POLtheta], RAD51, poly [ADP-ribose] glycohydrolase).

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

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

115 that, besides direct cytotoxic effects, poly(ADP ribose) polymerase (PARP) inhibitors (PARPis) exhibi

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

117 Poly(ADP-ribose) (PAR) is a posttranslational modification pr

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

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

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

121 Poly(ADP-ribose) polymerase (PARP) inhibitors are increasingl

122 Poly(ADP-ribose) polymerase (PARP) inhibitors have activity i

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

124 Poly(ADP-ribose) Polymerase (PARP) is a family of enzymes, wh

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

126 Poly(ADP-ribose) polymerase 1 (PARP-1) is a multidomain multi

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

128 Poly(ADP-ribose) polymerase inhibitors (PARPi) selectively ta

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

130 Poly(ADP-ribose)ylation (PARylation) by PAR polymerase 1 (PAR

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

132 rom patient biopsies are sensitive to a poly(ADP-ribose) glycohydrolase (PARG) inhibitor.

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

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

135 their C termini: ZAPL (long) encodes a poly(ADP-ribose) polymerase (PARP)-like domain that is missin

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

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

138 n three steps to produce veliparib 1, a poly(ADP-ribose) polymerase inhibitor.

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

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

141 itive disease, bone stabilizing agents, poly(ADP-ribose) polymerase inhibitors for BRCA mutation carr

142 nthesis of mono(ADP-ribose) (mADPr) and poly(ADP-ribose) (pADPr) conjugates by pADPr polymerase (PARP

143 -1 overexpression stimulates PARP-1 and poly(ADP-ribose) (PAR) protein expression and cisplatin resis

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

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

146 s, leading to elevated DNA breakage and poly(ADP-ribose) induction that cannot be rescued by catalyti

147 damage, BRCA1 localization to DSBs, and poly(ADP-ribose) polymerase (PARP) inhibitor resistance.

148 ensitizes cells to DNA crosslinkers and poly(ADP-ribose) polymerase inhibitors.

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

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

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

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

153 monomers or polymers, commonly known as poly(ADP-ribose) (PAR), modulate the activities of the modifi

154 s, including a subset commonly known as poly(ADP-ribose) polymerases.

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

156 as a monomer or in polymeric chains as poly(ADP-ribose).

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

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

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

160 ase 1 (PARP1) and PARylation removal by poly(ADP-ribose) glycohydrolase (PARG) critically regulate DN

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

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

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

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

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

166 translational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) using NAD(+) as ADP-ribo

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

168 lytic efficiency for protein-conjugated poly(ADP-ribose).

169 omatin condensation as well as distinct poly(ADP-ribose)polymerase-1 cleavage.

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

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

172 we demonstrate that the nuclear enzyme Poly(ADP-ribose)Polymerase 1 (PARP1) is a promising target fo

173 f BRCA2, could help select patients for poly(ADP-ribose) polymerase (PARP) inhibitor or platinum chem

174 pansion of the treatment indication for poly(ADP-ribose) polymerase inhibitors to include patients wi

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

176 mers show increased resistance to human poly(ADP-ribose) glycohydrolase-mediated degradation.

177 clear LXRalpha complexes and identified poly(ADP-ribose) polymerase-1 (PARP-1) as an LXR-associated f

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

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

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

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

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

183 nases 4 and 6, angiogenesis inhibitors, poly(ADP-ribose) polymerase inhibitors, as well as chemothera

184 Bevacizumab and maintenance poly(ADP-ribose) polymerase (PARP) inhibitors both significan

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

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

187 is an important structural motif of new poly(ADP-ribose) polymerase (PARP) inhibitors, playing a usef

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

189 Through its ability to bind the ends of poly(ADP-ribose) (PAR) chains, the function of the histone va

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

191 cleolar RNAs (snoRNAs) as activators of poly(ADP-ribose) (PAR) synthesis, demonstrating that this sno

192 ational modification by the addition of poly(ADP-ribose) (PAR), which promotes protein recruitment an

193 trate that concurrent administration of poly(ADP-ribose) polymerase (PARP) and WEE1 inhibitors is eff

194 Inhibitors of poly(ADP-ribose) polymerase (PARP) have demonstrated efficacy

195 for NEDD8 in regulating the activity of poly(ADP-ribose) polymerase 1 (PARP-1) in response to oxidati

196 The success of poly(ADP-ribose) polymerase 1 (PARP-1) inhibitors in cancers

197 Furthermore, inhibition or silencing of poly(ADP-ribose) polymerase 1 (PARP1) inhibits PAR-mediated r

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

199 endonuclease trigger the recruitment of poly(ADP-ribose) polymerase 2 (PARP2) to L1 integration sites

200 exquisitely sensitive to inhibition of poly(ADP-ribose) polymerase has ushered in a new era of resea

201 mages DNA and causes hyperactivation of poly(ADP-ribose) polymerase, resulting in extensive NAD(+)/AT

202 amage was associated with activation of poly(ADP-ribose) polymerase, which led to consumption of NAD(

203 This work focuses on the regulation of poly(ADP-ribose) polymerase-1 (PARP-1) expression by MKP-1.

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

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

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

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

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

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

210 cleaved CASP8/3 [caspase-8/3] and PARP [poly(ADP-ribose) polymerase] formation).

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

212 o contain other factors, including PML, poly(ADP-ribose) polymerase 1 (PARP1), ligase IIIalpha, and o

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

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

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

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

217 Methods: Using a radiolabeled poly(ADP-ribose) polymerase (PARP) inhibitor, (125)I-KX1, we

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

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

220 ese, an important DNA damage regulator, poly(ADP-ribose) polymerase 1 (PARP1), was discovered.

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

222 4 associates with the DNA damage sensor poly(ADP-ribose) polymerase 1 (PARP-1) and that the associati

223 on of E4orf4 with the DNA damage sensor poly(ADP-ribose) polymerase 1 (PARP-1).

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

225 of enzymes consume NAD(+) as substrate: poly(ADP-ribose) polymerases, ADP-ribosyl cyclases (CD38 and

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

227 This was linked to suppressed poly(ADP-ribose) polymerase-1 activity and was reversible on

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

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

230 tive lesions and a conserved N-terminal poly(ADP-ribose)-dependent recruitment motif, with later rete

231 llenges including the complexity of the poly(ADP-ribose) (PAR) chains, low abundance of the modificat

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

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

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

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

236 n tankyrase-1 (TNKS) is a member of the poly(ADP-ribose) polymerase (PARP) superfamily of proteins th

237 nd promote the rapid proteolysis of the poly(ADP-ribose) polymerase 1 (PARP-1), but the mechanism of

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

239 targets in anticancer therapy, are the poly(ADP-ribose) polymerases (PARPs).

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

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

242 ntly mutated in human cancers, binds to poly(ADP-ribose) (PAR) immediately following DNA damage and m

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

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

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

246 LL) cells exhibit a high sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors.

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

248 ancer but also creates vulnerability to poly(ADP-ribose) polymerase (PARP) inhibitors.

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

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

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

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

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

254 is expressed alone, it associates with poly(ADP-ribose) (PAR) chains and is recruited to DNA damage

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

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

257 r DNA repair targeted therapies such as poly-ADP ribose polymerase (PARP) inhibitors.

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

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

260 d the ZnF domain of SIRT1 interact with poly-ADP ribose (PAR) in response to DNA damage, and are resp

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

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

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

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

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

266 AD(+)-converting enzymes, such as CD38, poly-ADP-ribose polymerases, and sirtuins (SIRTs).

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

268 And its derived poly-ADP-ribose polymers show increased resistance to human p

269 r protein PARylation catalyzed by human poly-ADP-ribose polymerase 1 (PARP1) and PARP2.

270 effectuated by associated reduction in poly-ADP-ribose chain formation.

271 Mechanistically, poly-ADP-ribose polymerase 1 (PARP1) represses expression of

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

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

274 homologs) and SIRT1 is an inhibitor of poly-ADP-ribose polymerase-1 (PARP1).

275 he accumulation of three test proteins, poly-ADP-ribose polymerases 1 and 2 (PARP1/2) and histone PAR

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

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

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

279 Poly-(ADP-ribose) polymerase inhibitors (PARPi) selectively ki

280 m-containing therapy and inhibitors of poly-(ADP-ribose)-polymerase (PARP)(14,15).

281 f ATM-mutant cells to topotecan or the poly-(ADP-ribose) polymerase (PARP) inhibitor olaparib reflect

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

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

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

285 structure of adenosine-5-diphosphate-ribose (ADP-ribose) in complex with non-phosphorylated and phosp

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

287 ibosyltransferases either conjugate a single ADP-ribose to a target or generate ADP-ribose chains.

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

289 d named ELTA (enzymatic labeling of terminal ADP-ribose) for labeling free or protein-conjugated ADP-

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

291 Nevertheless, accurate assignment of the ADP-ribose acceptor site(s) within the modified proteins

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

293 Inhibitors of the ADP-ribose polymerase Tankyrase (Tnks) have become lead

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

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

296 hydrolyze the nicotinamide and transfer (tz)ADP-ribose to an arginine analogue, respectively.

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

298 re of Tpt1 in a product-mimetic complex with ADP-ribose-1"-phosphate in the NAD(+) site and pAp in th

299 y modify themselves and target proteins with ADP-ribose (termed PARylation).

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