ライフサイエンスコーパス: poly ADP-ribose

1 Emergent data indicate that poly(ADP-ribose) aids in the formation of nonmembranous

2 increases the binding of the macro domain to poly(ADP-ribose) and stimulates the de-PARylation activi

3 y, we demonstrate the involvement of Alc1, a poly(ADP-ribose)- and ATP-dependent remodeler, in the ch

4 f XRCC1 is required for selective binding to poly (ADP-ribose) at low levels of ADP-ribosylation, and

5 ssue, we have characterized the mechanism of poly (ADP-ribose) binding by XRCC1 and examined its impo

6 Moreover, poly(ADP-ribose) binding to the Parp9 macrodomains incre

7 nt interactions of RNA-binding proteins with poly(ADP-ribose) can affect their function.

8 he adjacent WWE domain that is known to bind poly(ADP-ribose) chains.

9 modified by poly(ADP-ribose), indicating how poly(ADP-ribose) could direct cellular organization.

10 nitiates catalytic activation and subsequent poly(ADP-ribose)-dependent DNA repair.

11 We found that BAP1 mediates rapid poly(ADP-ribose)-dependent recruitment of the polycomb d

12 Massive poly(ADP-ribose) formation by poly(ADP-ribose) polymeras

13 PARGs, which remove poly(ADP-ribose) from proteins, act in injured C. elegan

14 l intrinsic regulators of axon regeneration: poly(ADP-ribose) glycohodrolases (PARGs) and poly(ADP-ri

15 lly promoting stabilization of a new target, poly (ADP-ribose) glycohydrolase (PARG) mRNA, by binding

16 o understanding the interactions of PAR with poly(ADP-ribose) glycohydrolase (PARG) and other binding

17 ly(ADP-ribose) (PAR) polymer is catalysed by poly(ADP-ribose) glycohydrolase (PARG), whose endo-glyco

18 rase 1 (PARP1) and the deribosylating enzyme poly-(ADP-ribose) glycohydrolase (PARG), which dynamical

19 The discovery of poly(ADP-ribose) >50 years ago opened a new field, leadi

20 ease; and the incidence of nitrotyrosine and poly(ADP)ribose in the colon.

21 show that recombinant FUS binds directly to poly (ADP-ribose) in vitro, and that both GFP-tagged and

22 ates PARP1, resulting in the accumulation of poly(ADP-ribose) in the cell body and axon and limited a

23 The key acceptors of poly(ADP-ribose) include PARP-1 itself, histones, DNA re

24 Distinct properties of poly(ADP-ribose)-including its structural diversity, nuc

25 elf-assembly, are preferentially modified by poly(ADP-ribose), indicating how poly(ADP-ribose) could

26 Poly (ADP-ribose) is synthesized at DNA single-strand br

27 lgamma), which under oxidative stress become poly(ADP-ribose)lated (PARylated).

28 Our results indicate that regulation of poly(ADP-ribose) levels is a critical function of the DL

29 s work we identify a physical and functional poly(ADP-ribose)-mediated interaction of PARP1 with the

30 hesis of a negatively charged polymer called poly(ADP-ribose) or PAR on histones and other substrate

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

32 )-dependent polymerization of long chains of poly-ADP ribose (PAR) onto itself in response to DNA dam

33 NA damage, PARP1 interacts with and attaches poly-ADP-ribose (PAR) chains to EZH2.

34 nt is mediated by the zinc finger domain and poly (ADP-ribose) (PAR).

35 f human ssDNA-binding protein 1 (hSSB1) is a poly(ADP ribose) (PAR) binding domain.

36 tein hydrolase for mono-ADP-ribose (MAR) and poly(ADP-ribose) (PAR) chain removal (de-MARylation and

37 Poly(ADP-ribose) polymerases (PARP) attach poly(ADP-ribose) (PAR) chains to various proteins includ

38 ARPs that localize to DNA damage, synthesize poly(ADP-ribose) (PAR) covalently attached to target pro

39 The difficulty associated with accessing poly(ADP-ribose) (PAR) in a homogeneous form has been an

40 did not find that histone H1 accumulated on poly(ADP-ribose) (PAR) in vivo.

41 Poly(ADP-ribose) (PAR) is a posttranslational modificati

42 ular DNA damage response by the synthesis of poly(ADP-ribose) (PAR) is mediated mainly by poly(ADP-ri

43 Following DNA double-strand breaks, poly(ADP-ribose) (PAR) is quickly and heavily synthesize

44 Breakdown of the poly(ADP-ribose) (PAR) polymer is catalysed by poly(ADP-

45 Poly(ADP-ribose) (PAR) polymerase 1 (PARP1) catalyzes th

46 Excessive poly(ADP-ribose) (PAR) polymerase-1 (PARP-1) activation

47 Inhibition or genetic deletion of poly(ADP-ribose) (PAR) polymerase-1 (PARP-1) is protecti

48 t MKP-1 overexpression stimulates PARP-1 and poly(ADP-ribose) (PAR) protein expression and cisplatin

49 ttranslational modification of proteins with poly(ADP-ribose) (PAR) regulates protein-protein interac

50 Over 50 years ago, the discovery of poly(ADP-ribose) (PAR) set a new field of science in mot

51 ADP-ribose (iso-ADPr), the smallest internal poly(ADP-ribose) (PAR) structural unit, binds between th

52 uction of the posttranslational modification poly(ADP-ribose) (PAR) to facilitate repair.

53 yme required for DNA repair that possesses a poly(ADP-ribose) (PAR)-binding macro domain.

54 (ADP-ribose) (MAR) or in polymeric chains as poly(ADP-ribose) (PAR).

55 the sensitivity of BRCA1-deficient cells to poly ADP ribose polymerase (PARP) inhibition is partiall

56 hway, which corresponded with an increase in poly ADP ribose polymerase cleavage.

57 Maintenance therapy with olaparib, a poly ADP ribose polymerase inhibitor given post-platinum

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

59 ADAMTS-4 directly cleaved and degraded poly ADP ribose polymerase-1 (a key molecule in DNA repa

60 1/cell-cycle, apoptotic genes, caspase-3 and poly ADP ribose polymerase-1 (PARP-1) cleavage) and was

61 logous end-joining DNA repair process and in poly ADP-ribose polymerase 1 activation.

62 2 mutant channel (C1008-->A) or silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN

63 lethality anticancer therapeutics, including poly ADP-ribose polymerase inhibitors for BRCA1- and BRC

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

65 ion, Rev1-deficiency is associated with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endo

66 is (p53, Fas, and MST1), DNA damage control (poly(ADP)-ribose polymerase and ataxia telangiectasia mu

67 e consisting of caspase-3 and -7 and cleaved poly(ADP)-ribose polymerase.

68 ch, in turn, activates the DNA repair enzyme poly(ADP)-ribose polymerase.

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

70 and RAD50 as suppressors and 53BP1, DDB1 and poly(ADP)ribose polymerase 3 (PARP3) as promoters of chr

71 hout chilling) and more than 60% cleavage of poly-ADP ribose polymerase (compared to less than 5% in

72 Assays for DNA ladder formation and poly-ADP ribose polymerase (PARP) cleavage were performe

73 aging drugs, which is further exacerbated by poly-ADP ribose polymerase (PARP) inhibitors.

74 We show that the latonduine analogs inhibit poly-ADP ribose polymerase (PARP) isozymes 1, 3, and 16.

75 eir cellular hyper-dependence on alternative poly-ADP ribose polymerase (PARP)-mediated DNA repair me

76 tion and activation of the DNA damage sensor poly-ADP ribose polymerase 1 (PARP1).

77 Poly-ADP ribose polymerase and aurora kinase inhibitors

78 cells and is catalyzed by 11 members of the poly-ADP-ribose polymerase (PARP) family of proteins (17

79 breaks (DSBs) and were modestly sensitive to poly-ADP-ribose polymerase (PARP) inhibitors olaparib an

80 otoxic alkylating agents, hyperactivation of poly-ADP-ribose polymerase (PARP) leads to cellular NAD

81 yl)ation (PARylation) is mainly catalysed by poly-ADP-ribose polymerase 1 (PARP1), whose role in gene

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

83 emicals were tested for inhibitory effect of poly (ADP-ribose) polymerase (PARP) activity in vitro an

84 activation of caspase-8 and -3, cleavage of poly (ADP-Ribose) polymerase (PARP) and apoptosis.

85 Inhibitors against poly (ADP-ribose) polymerase (PARP) are promising target

86 ion of apoptotic cell death and detection of poly (ADP-ribose) polymerase (PARP) cleavage.

87 oded by PML-RARA) are extremely sensitive to poly (ADP-ribose) polymerase (PARP) inhibition, in part

88 Poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) ol

89 recent approval of olaparib (Lynparza), the poly (ADP-ribose) polymerase (PARP) inhibitor for treati

90 izes cancer cells to DNA damaging agents, to Poly (ADP-ribose) polymerase (PARP) inhibitors and cross

91 Poly (ADP-ribose) polymerase (PARP) inhibitors have emer

92 Poly (ADP-ribose) polymerase (PARP) inhibitors have emer

93 Poly (ADP-ribose) polymerase (PARP) inhibitors have show

94 Poly (ADP-ribose) polymerase (PARP) inhibitors have show

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

96 y protein BIM, cleaved caspase 3 and cleaved poly (ADP-ribose) polymerase (PARP).

97 005) concomitant with an increase in cleaved poly (ADP-ribose) polymerase 1 (P < 0.05), indicative of

98 Poly (ADP-ribose) polymerase 1 (PARP-1) is a constitutiv

99 Inhibition of beta-catenin, poly (ADP-ribose) polymerase 1 (PARP1), or enhancer of z

100 langiectasia mutated (ATM), but dependent on poly (ADP-ribose) polymerase 1 (PARP1), which ADP ribosy

101 lementing protein 1, DNA polymerase beta, or poly (ADP-ribose) polymerase 1 activity, all of which fa

102 reatly reduced or ablated by an inhibitor of poly (ADP-ribose) polymerase activity.

103 termined by Western blot analysis of cleaved poly (ADP-ribose) polymerase and caspase 3.

104 caspase-8, and caspase-9 activation and less poly (ADP-ribose) polymerase cleavage compared with WT l

105 downregulation of glucose transporter-1 and poly (ADP-ribose) polymerase cleavage while preserving t

106 pectively, and high selectivity toward other poly (ADP-ribose) polymerase enzymes.

107 a potential marker of long-term response to poly (ADP-ribose) polymerase inhibition and that restora

108 Purpose Data suggest that DNA damage by poly (ADP-ribose) polymerase inhibition and/or reduced v

109 reased sensitivity to ionizing radiation and poly (ADP-ribose) polymerase inhibition.

110 rpose Durable and long-term responses to the poly (ADP-ribose) polymerase inhibitor olaparib are obse

111 Olaparib is an oral poly (ADP-ribose) polymerase inhibitor with activity in

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

113 Poly (ADP-ribose) polymerase inhibitors (PARPis) are cli

114 d treatments such as antiangiogenic drugs or poly (ADP-ribose) polymerase inhibitors offer potential

115 vic radiotherapy, or previous treatment with poly (ADP-ribose) polymerase inhibitors.

116 overexpression of caspase-3, higher cleaved poly (ADP-ribose) polymerase levels (p < 0.007), and a h

117 is, and activation of caspase-3, -7, -8, -9, poly (ADP-ribose) polymerase, and lamin A/C.

118 thodologies for studying robust responses of poly (ADP-ribose) polymerase-1 (PARP-1) to DNA damage wi

119 Poly (ADP-ribose) polymerase-1 (PARP1) is a highly conse

120 ent of targeted agents such as inhibitors of poly (ADP-ribose) polymerase-1 and mTOR and immunomodula

121 Purpose To determine whether cotargeting poly (ADP-ribose) polymerase-1 plus androgen receptor is

122 of UVA laser induced damage in cells lacking poly (ADP-ribose) polymerase-1.

123 of their breakage, and to be antagonized by poly (ADP-ribose) polymerase/RECQ1-regulated restart.

124 caspase-9 and caspase-3 and the cleavage of poly (ADP-ribose) polymerase; (5) upregulating pancreati

125 nents of the topoisomerase IIbeta (TOP2beta)/poly(ADP ribose) polymerase 1 (PARP1) complex are necess

126 ingly, mtp53 depletion profoundly influenced poly(ADP ribose) polymerase 1 (PARP1) localization, with

127 e-9 and -3 that, in turn, led to cleavage of poly(ADP ribose) polymerase and Mcl-1.

128 rate alpha-ketoglutarate or treatment with a poly(ADP ribose) polymerase inhibitor protects reductive

129 ase and cleavage of caspases 3, 8, and 9 and poly(ADP ribose) polymerase, and suppressed survivin, my

130 large Ca(2+) and Na(+) influx, activation of poly(ADP ribose) polymerase-1 (PARP-1), and delayed Ca(2

131 l series of tetrahydropyridophthlazinones as poly(ADP-ribose) polymerase (PARP) 1 and 2 inhibitors.

132 t its chromatin accumulation was enhanced in poly(ADP-ribose) polymerase (PARP) 1(-/-) compared with

133 nM), we observed loss of CIPs and increased poly(ADP-ribose) polymerase (PARP) activation [also obse

134 We found that poly(ADP-ribose) polymerase (PARP) activation distinguis

135 (COX-2 and IL-1beta) and apoptotic markers (poly(ADP-ribose) polymerase (PARP) and caspase 3).

136 n BC3 and BCBL1 PEL cells but did not induce poly(ADP-ribose) polymerase (PARP) cleavage in virus-neg

137 hrome c release, activation of caspases, and poly(ADP-ribose) polymerase (PARP) cleavage.

138 vidence is provided that the activity of the poly(ADP-ribose) polymerase (Parp) enzyme is required fo

139 Prior work has established that the poly(ADP-ribose) polymerase (PARP) enzyme Tankyrase (TNK

140 The poly(ADP-ribose) polymerase (PARP) enzymes were initiall

141 e a critical function of some members of the poly(ADP-ribose) polymerase (PARP) family in clearance o

142 The mammalian poly(ADP-ribose) polymerase (PARP) family includes ADP-r

143 ld, leading the way for the discovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and

144 highly toxic DNA strand breaks that trigger poly(ADP-ribose) polymerase (Parp) hyperactivation, cell

145 nfer cellular sensitization to radiation and poly(ADP-ribose) polymerase (PARP) inhibition.

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

147 ng agents melphalan and cisplatin and to the poly(ADP-ribose) polymerase (PARP) inhibitor veliparib (

148 We report results for veliparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, combined w

149 Olaparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, has previo

150 nction and was recently reported as a potent poly(ADP-ribose) polymerase (PARP) inhibitor.

151 and breaks and disruption of this pathway by Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) is

152 Poly(ADP-ribose) polymerase (PARP) inhibitors have activ

153 eterogeneous responses to platinum drugs and poly(ADP-ribose) polymerase (PARP) inhibitors in clinica

154 ical trials exploiting this concept by using poly(ADP-ribose) polymerase (PARP) inhibitors in patient

155 In the present study we observed that the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib a

156 eutic drugs that block DNA repair, including poly(ADP-ribose) polymerase (PARP) inhibitors, fail due

157 tizes tumors to DNA cross-linking agents and poly(ADP-ribose) polymerase (PARP) inhibitors, we sought

158 provide insight into why clinical trials of poly(ADP-ribose) polymerase (PARP) inhibitors, which req

159 DNA-damaging agents, including cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors.

160 compromised DNA repair and are sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors.

161 A1 or BRCA2 and are selectively sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors.

162 This study explores the role of poly(ADP-ribose) polymerase (PARP) on global gene expres

163 The poly(ADP-ribose) polymerase (PARP) Tankyrase (TNKS and T

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

165 ed caspase 3, cleaved caspase 9, and cleaved poly(ADP-ribose) polymerase (PARP), suggesting that impa

166 ed by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation

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

168 of Ewing sarcoma cells to the inhibition of poly(ADP-ribose) polymerase (PARP).

169 ivo, we show that the anti-apoptotic protein poly(ADP-ribose) polymerase (PARP)14 promotes aerobic gl

170 ere, we show that the loss of TCDD-inducible poly(ADP-ribose) polymerase (Tiparp), an ADP-ribosyltran

171 B and SP1 bind to a composite element in the poly(ADP-ribose) polymerase 1 (PARP-1) promoter in a mut

172 Here, we identify poly(ADP-ribose) polymerase 1 (PARP1) as a previously un

173 investigated the regulation of mitochondrial poly(ADP-ribose) polymerase 1 (PARP1) by the cyclic aden

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

175 Poly(ADP-ribose) polymerase 1 (PARP1) inhibitors were re

176 Poly(ADP-ribose) polymerase 1 (PARP1) interacts genetica

177 n Xenopus egg extract assays, we showed that poly(ADP-ribose) polymerase 1 (PARP1) is modified by SUM

178 poly(ADP-ribosyl)ation mediated primarily by poly(ADP-ribose) polymerase 1 (PARP1) is responsible for

179 ity in identifying ADP-ribosylation sites on Poly(ADP-ribose) Polymerase 1 (PARP1) with mass spectrom

180 h increased expression of DNA ligase 3alpha, poly(ADP-ribose) polymerase 1 (PARP1), and X-ray repair

181 -ribose (PAR) chains, primarily catalyzed by poly(ADP-ribose) polymerase 1 (PARP1), is crucial for ce

182 apurinic/apyrimidinic endonuclease 1 (APE1), poly(ADP-ribose) polymerase 1 (PARP1), X-ray repair cros

183 D(+)-dependent auto-poly-ADP-ribosylation of poly(ADP-ribose) polymerase 1 (PARP1).

184 poly(ADP-ribose) (PAR) is mediated mainly by poly(ADP-ribose) polymerase 1 (PARP1).

185 Poly(ADP-ribose) polymerase 1 (PARP1, also known as ARTD

186 oskeleton while promoting the degradation of poly(ADP-ribose) polymerase 1, an inhibitor of osteoclas

187 hat the SNAT2 ER-alpha-ERE complex contained poly(ADP-ribose) polymerase 1, Lupus Ku autoantigen prot

188 t assay, quantification of 8-oxoguanine, and poly(ADP-ribose) polymerase 1.

189 Increasing evidence define Poly(ADP-ribose) polymerase 3 (PARP3, also known as ARTD

190 increase in caspase-3, cytochrome c release, poly(ADP-ribose) polymerase activation, down-regulation

191 including HMGN1 and RFC1; and regulation of poly(ADP-ribose) polymerase activity.

192 ROS and poly(ADP-ribose) polymerase also reduce sirtuin, PGC-1al

193 1-XPF endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap format

194 f the DNA damage marker gammaH2AX as well as poly(ADP-ribose) polymerase cleavage were elevated in SM

195 ability, hypersensitivity to DNA damage, and poly(ADP-ribose) polymerase inhibition associated with A

196 tions initially respond well to platinum and poly(ADP-ribose) polymerase inhibitor (PARPi) therapy; h

197 Olaparib is a poly(ADP-ribose) polymerase inhibitor and cediranib is a

198 IEL3 provides further evidence that use of a poly(ADP-ribose) polymerase inhibitor in the maintenance

199 The poly(ADP-ribose) polymerase inhibitor olaparib has shown

200 Rucaparib, a poly(ADP-ribose) polymerase inhibitor, has anticancer ac

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

202 gagement of the chemotherapeutic Olaparib, a poly(ADP-ribose) polymerase inhibitor, in live cells and

203 cells with mutant p53 were resistant to the poly(ADP-ribose) polymerase inhibitor, veliparib (2-[(2R

204 reaks (DSBs), and increased sensitivity to a poly(ADP-ribose) polymerase inhibitor.

205 y, or had received previous treatment with a poly(ADP-ribose) polymerase inhibitor.

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

207 Although poly(ADP-ribose) polymerase inhibitors have shown promis

208 sed apoptosis characterized by caspase 3 and poly(ADP-ribose) polymerase processing, DNA cleavage, an

209 Resolution at telomeres requires the poly(ADP-ribose) polymerase tankyrase 1, but the mechani

210 the histone variant macroH2A1.1 binds to the poly(ADP-ribose) polymerase tankyrase 1, preventing it f

211 n be induced by inhibition of tankyrase 1, a poly(ADP-ribose) polymerase that is required for resolut

212 se 3 and cleavage of the caspase 3 substrate poly(ADP-ribose) polymerase were inhibited in E. faecali

213 However, poly(ADP-ribose) polymerase, a protein involved in DNA r

214 these conditions correlates with cleavage of poly(ADP-ribose) polymerase, an indicator of apoptosis.

215 Western blotting for the cleaved fragment of poly(ADP-ribose) polymerase, and the active isoform of c

216 y reduced cleavage of caspase-3, -8, and -9, poly(ADP-ribose) polymerase, and the externalization of

217 hibitors (PARPi), a cancer therapy targeting poly(ADP-ribose) polymerase, are the first clinically ap

218 eflected by caspase-3/7 activity and cleaved poly(ADP-ribose) polymerase, in different cell lines tha

219 ch damages DNA and causes hyperactivation of poly(ADP-ribose) polymerase, resulting in extensive NAD(

220 rker proteins, cleaved caspase 7 and cleaved poly(ADP-ribose) polymerase, were significantly reduced

221 This activates nuclear poly(ADP-ribose) polymerase, which inhibits GAPDH, shunt

222 ncer cells and decreases the level of intact poly(ADP-ribose) polymerase, which is indicative of apop

223 ze nuclear LXRalpha complexes and identified poly(ADP-ribose) polymerase-1 (PARP-1) as an LXR-associa

224 Poly(ADP-ribose) polymerase-1 (PARP-1) creates the postt

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

226 The nuclear protein poly(ADP-ribose) polymerase-1 (PARP-1) has a well-establ

227 Interest in nuclear imaging of poly(ADP-ribose) polymerase-1 (PARP-1) has grown in rece

228 Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant nu

229 Massive poly(ADP-ribose) formation by poly(ADP-ribose) polymerase-1 (PARP-1) triggers NAD depl

230 PAH-PASMCs have increased the activation of poly(ADP-ribose) polymerase-1 (PARP-1), a critical enzym

231 Poly(ADP-ribose) polymerase-1 (PARP-1), a ubiquitous and

232 yrin repeat-containing protein that mediates poly(ADP-ribose) polymerase-1 (PARP-1)-dependent transcr

233 IL-1, controls gene expression by activating poly(ADP-ribose) polymerase-1 (PARP-1).

234 physiological activity of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP1) causes neuron deat

235 This was linked to suppressed poly(ADP-ribose) polymerase-1 activity and was reversibl

236 Poly(ADP-ribose) polymerase-13 (PARP13/ZAP/ZC3HAV1) is a

237 Interestingly, miR-149 inhibits poly(ADP-ribose) polymerase-2 (PARP-2) and so increased

238 Poly(ADP-ribose) polymerase-2 (PARP-2) is one of three h

239 responses through its N-terminal region in a poly(ADP-ribose) polymerase-dependent manner.

240 tential pharmaceutical target tankyrase 1, a poly(ADP-ribose) polymerase.

241 hondria, caspase 3 activity, and cleavage of poly(ADP-ribose) polymerase.

242 caspase-3 and cleaved the caspase substrate poly(ADP-ribose) polymerase.

243 f apoptotic mediators, such as caspase-3 and poly(ADP-ribose) polymerase.

244 ncreased the expression of apoptotic cleaved poly(ADP-ribose) polymerase.

245 zed human cells to olaparib, an inhibitor of poly(ADP-ribose) polymerase.

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

247 Poly-(ADP-ribose) polymerase (PARP) inhibitors (PARPis)

248 Bax and Bak, and processing of caspases and poly-(ADP-ribose) polymerase (PARP-gamma).

249 iated by the nuclear ADP-ribosylating enzyme poly-(ADP-ribose) polymerase 1 (PARP1) and the deribosyl

250 ecting parthanatos, monitored by cleavage of poly(ADP ribose)polymerase-1 (PARP-1), or necroptosis, a

251 The enzyme poly(ADP-ribose)polymerase (PARP) has a dual function be

252 AhR repressor (Ahrr/AhRR) and TCDD-inducible poly(ADP-ribose)polymerase (Tiparp/TiPARP) by AhR ligand

253 Poly(ADP-ribose)polymerase 1 (PARP-1) is a key eukaryoti

254 Here, we demonstrate that the nuclear enzyme Poly(ADP-ribose)Polymerase 1 (PARP1) is a promising targ

255 e, lack of hepatocyte HMGB1 led to excessive poly(ADP-ribose)polymerase 1 activation, exhausting nico

256 Herein, we demonstrate that poly(ADP-ribose)polymerase-1 (PARP-1) is a genome-wide e

257 e synthesized and evaluated as inhibitors of poly(ADP-ribose)polymerase-1 (PARP-1).

258 c chromatin condensation as well as distinct poly(ADP-ribose)polymerase-1 cleavage.

259 HR-deficient cancers are hypersensitive to Poly (ADP ribose)-polymerase (PARP) inhibitors, but can

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

261 ocation from mitochondria to the nucleus and poly-(ADP-ribose)-polymerase (PARP) activation.

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

263 Poly [ADP-ribose] polymerase 1 (PARP-1) is a highly abun

264 -1) liposomes were used to deliver a PARP-1 (poly [ADP-ribose] polymerase 1) inhibitor: AZ7379.

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

266 (ATM), phosphorylated H2AX (gammaH2AX), and poly[ADP-ribose] polymerase 1 (PARP-1).

267 Poly ADP-ribose polymerases (PARPs) catalyze massive pro

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

269 ys conserved in all eukaryotic cells include poly (ADP-ribose) polymerases (PARPs), sirtuins, AMP-act

270 Poly(ADP-ribose) polymerases (PARP) attach poly(ADP-ribo

271 r targets are the tankyrase proteins (TNKS), poly(ADP-ribose) polymerases (PARP) that regulate Wnt si

272 The poly(ADP-ribose) polymerases (PARPs) are a major family

273 Poly(ADP-ribose) polymerases (PARPs) are involved in DNA

274 al modification, is immediately catalyzed by poly(ADP-ribose) polymerases (PARPs) at DNA lesions, whi

275 unveil the mechanisms by which inhibition of poly(ADP-ribose) polymerases (PARPs) elicits clinical be

276 longing to the tankyrase (Tnks) subfamily of poly(ADP-ribose) polymerases (PARPs) have recently been

277 Poly(ADP-ribose) polymerases (PARPs) synthesize and bind

278 posttranslational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) that mediate EBV re

279 Poly(ADP-ribose) polymerases (PARPs), enzymes that modif

280 poly(ADP-ribose) glycohodrolases (PARGs) and poly(ADP-ribose) polymerases (PARPs).

281 rate of tankyrases, which are members of the poly(ADP-ribose) polymerases (PARPs).

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

283 Various poly(ADP-ribose) polymerases which are notorious guardia

284 AD precursors, exercise regimens, or loss of poly(ADP-ribose) polymerases yet surprisingly do not exh

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

286 ious enzyme families, including sirtuins and poly(ADP-ribose) polymerases.

287 HR, but confers sensitivity to inhibition of poly(ADP-ribose) polymerases.

288 ntrols the activities of sirtuins, mono- and poly-(ADP-ribose) polymerases, and NAD nucleosidase.

289 es of sub-nuclear PCNA foci, suggesting that poly (ADP-ribose) promotes XRCC1 recruitment both at sin

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

291 g for ICAM-1, P-selectin, nitrotyrosine, and poly(ADP)ribose showed a positive staining in the inflam

292 n affinity that depends on the length of the poly(ADP-ribose) strand and competes with DNA for protei

293 These data support the hypothesis that poly (ADP-ribose) synthesis promotes XRCC1 recruitment a

294 Our data suggest that poly(ADP-ribose) synthesis at the sites of SBs initiates

295 We discovered that poly(ADP-ribose) synthesis catalysed by PARP1 at the sit

296 A burst of poly(ADP-ribose) synthesis initiates DNA damage response

297 CHD4-N domain binds with higher affinity to poly(ADP-ribose) than to DNA.

298 hesis of nuclear ATP, leading from NAD(+) to poly(ADP-ribose) to ADP-ribose to ATP, which supports th

299 Conversely, PARPs, which add poly(ADP-ribose) to proteins, inhibit axon regeneration

300 NuMA accumulates at sites of DNA damage in a poly[ADP-ribose]ylation-dependent manner and functionall