ライフサイエンスコーパス: poly ADP-ribose polymerase

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

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

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

4 appears to involve the catalytic activity of poly (ADP-ribose) polymerase.

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

6 tive cells and the cleavage of caspase-3 and poly (ADP-ribose) polymerase.

7 erases, including a subset commonly known as poly(ADP-ribose) polymerases.

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

9 endent enzymes, including sirtuins, CD38 and poly(ADP-ribose) polymerases.

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

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

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

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

14 -2, MCP-3, CXCL9, CXCL10, CXCL5, ENRAGE, and poly (ADP-ribose) polymerase 1.

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

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

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

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

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

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

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

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

23 E4orf4 associates with the DNA damage sensor poly(ADP-ribose) polymerase 1 (PARP-1) and that the asso

24 role for NEDD8 in regulating the activity of poly(ADP-ribose) polymerase 1 (PARP-1) in response to ox

25 The success of poly(ADP-ribose) polymerase 1 (PARP-1) inhibitors in can

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

27 Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzy

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

29 ite and promote the rapid proteolysis of the poly(ADP-ribose) polymerase 1 (PARP-1), but the mechanis

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

31 ivates the central DNA damage sensor protein poly(ADP-ribose) polymerase 1 (PARP1) and activates casp

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

33 ically, we found that ZBTB24 associates with poly(ADP-ribose) polymerase 1 (PARP1) and stimulates its

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

35 -molecule inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP1) for the detection

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

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

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

39 Furthermore, inhibition or silencing of poly(ADP-ribose) polymerase 1 (PARP1) inhibits PAR-media

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

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

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

43 Here, we have found that a host protein, poly(ADP-ribose) polymerase 1 (PARP1), facilitates IFNAR

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

45 y also contain other factors, including PML, poly(ADP-ribose) polymerase 1 (PARP1), ligase IIIalpha,

46 Here, we report that a cellular protein, poly(ADP-ribose) polymerase 1 (PARP1), plays a critical

47 ng these, an important DNA damage regulator, poly(ADP-ribose) polymerase 1 (PARP1), was discovered.

48 e major enzyme that catalyses this reaction, poly(ADP-ribose) polymerase 1 (PARP1), were discovered m

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

50 protects replication forks from stalling at poly(ADP-ribose) polymerase 1 (PARP1)-DNA complexes trap

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

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

53 to and irreversibly inhibits the activity of poly(ADP-ribose) polymerase 1, an important anticancer t

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

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

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

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

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

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

60 ty for protein PARylation catalyzed by human poly-ADP-ribose polymerase 1 (PARP1) and PARP2.

61 50 nM PSKalpha exhibited lower expression of poly-ADP-ribose polymerase 1 (PARP1) gene, leading to a

62 Mechanistically, poly-ADP-ribose polymerase 1 (PARP1) represses expressio

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

64 Inhibitors of poly-ADP-ribose polymerase 1 (PARPi) are highly effectiv

65 bes the accumulation of three test proteins, poly-ADP-ribose polymerases 1 and 2 (PARP1/2) and histon

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

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

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

69 motes cytotoxicity in a process dependent on poly (ADP-ribose) polymerase-1 (PARP-1); a NAD(+)-consum

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

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

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

73 1/cell-cycle, apoptotic genes, caspase-3 and poly ADP ribose polymerase-1 (PARP-1) cleavage) and was

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

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

76 combination of LuTate and the small molecule Poly(ADP-ribose) polymerase-1 (PARP) inhibitor, talazopa

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

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

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

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

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

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

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

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

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

86 of DNA damage, neuroinflammation, increased poly(ADP-ribose) polymerase-1 (PARP1) activity, single-c

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

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

89 DP-ribose) in cerebellar neurons, supporting poly(ADP-ribose) polymerase-1 upregulation.

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

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

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

93 ion 2 homologs) and SIRT1 is an inhibitor of poly-ADP-ribose polymerase-1 (PARP1).

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

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

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

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

98 presenilin-1-associated protein to attenuate poly ADP-ribose polymerase activation and mitochondrial

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

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

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

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

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

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

105 1-XPF endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap format

106 at includes elevated CD38 NADase and reduced poly(ADP-ribose) polymerase and SIRT1 activities, respec

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

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

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

110 of NAD(+)-converting enzymes, such as CD38, poly-ADP-ribose polymerases, and sirtuins (SIRTs).

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

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

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

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

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

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

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

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

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

120 s are exquisitely sensitive to inhibition of poly(ADP-ribose) polymerase has ushered in a new era of

121 2 mutant channel (C1008-->A) or silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN

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

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

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

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

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

127 Veliparib, a poly (ADP ribose) polymerase inhibitor, potentiated stan

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

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

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

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

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

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

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

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

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

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

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

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

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

141 ard in three steps to produce veliparib 1, a poly(ADP-ribose) polymerase inhibitor.

142 tion forks is a prominent mechanism of PARP (Poly(ADP-ribose) Polymerase) inhibitor (PARPi) resistanc

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

144 Poly (ADP-ribose) polymerase inhibitors combined with im

145 4K20me0 is required for HR and resistance to poly (ADP-ribose) polymerase inhibitors.

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

147 Poly(ADP ribose) polymerase inhibitors (PARPi) have effi

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

149 Poly(ADP-ribose) polymerase inhibitors (PARPi) selective

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

151 t samples, RITA, AF, and Onc-1 sensitized to poly(ADP-ribose) polymerase inhibitors both in vitro and

152 2-positive disease, bone stabilizing agents, poly(ADP-ribose) polymerase inhibitors for BRCA mutation

153 rt expansion of the treatment indication for poly(ADP-ribose) polymerase inhibitors to include patien

154 nt kinases 4 and 6, angiogenesis inhibitors, poly(ADP-ribose) polymerase inhibitors, as well as chemo

155 cancer (mCRPC) and may confer sensitivity to poly(ADP-ribose) polymerase inhibitors.

156 and sensitizes cells to DNA crosslinkers and poly(ADP-ribose) polymerase inhibitors.

157 d DNA damage-repair-targeting agents such as poly(ADP-ribose)-polymerase inhibitors.

158 their sensitivity to DNA damaging agents and poly-(ADP)-ribose polymerase inhibitors (PARPis).

159 Poly-(ADP-ribose) polymerase inhibitors (PARPi) selectiv

160 The success of poly-ADP ribose polymerase inhibitors in the treatment o

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

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

163 In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently acti

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

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

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

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

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

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

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

171 Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi), i

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

173 displayed synergistic cytotoxicity with the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib a

174 The poly (ADP-ribose) polymerase (PARP) inhibitor olaparib i

175 rminant that elicits therapeutic response to poly (ADP-Ribose) polymerase (PARP) inhibitor.

176 Poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib

177 (BRCA) mutations that confer sensitivity to poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis),

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

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

180 Targeted therapies such as poly (ADP-ribose) polymerase (PARP) inhibitors have emer

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

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

183 atment with immune checkpoint inhibitors and poly (ADP-ribose) polymerase (PARP) inhibitors in a vari

184 ion (HR) and renders cells hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors used to t

185 eclinical work, we found that combination of poly (ADP-ribose) polymerase (PARP) inhibitors with drug

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

187 HR deficient show a significant response to poly (ADP-ribose) polymerase (PARP) inhibitors; patients

188 Poly (ADP-ribose) polymerase (PARP) is the best-known el

189 Poly (ADP-ribose) polymerase (PARP) plays a significant

190 er an exquisite sensitivity to inhibitors of poly (ADP-ribose) polymerase (PARP) that are being teste

191 nd other molecular targets available such as poly (ADP-ribose) polymerase (PARP), epidermal growth fa

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

193 rs of the base excision repair (BER) protein poly (ADP-ribose) polymerase (PARP).

194 caspase activity and accompanied full-length poly ADP ribose polymerase (PARP) cleavage.

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

196 ated that, besides direct cytotoxic effects, poly(ADP ribose) polymerase (PARP) inhibitors (PARPis) e

197 w that ATAD5-depleted cells are sensitive to poly(ADP)ribose polymerase (PARP) inhibitors and that th

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

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

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

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

202 Poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose)

203 emonstrate that concurrent administration of poly(ADP-ribose) polymerase (PARP) and WEE1 inhibitors i

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

205 hylation, induction of autophagy, and robust poly(ADP-ribose) polymerase (PARP) cleavage indicative o

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

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

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

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

210 Inhibitors of poly(ADP-ribose) polymerase (PARP) have demonstrated eff

211 Synthetic lethality between poly(ADP-ribose) polymerase (PARP) inhibition and BRCA d

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

213 t led to the automated radiosynthesis of the poly(ADP-ribose) polymerase (PARP) inhibitor [(18)F]olap

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

215 ion of BRCA2, could help select patients for poly(ADP-ribose) polymerase (PARP) inhibitor or platinum

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

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

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

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

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

221 9 rendered GLS(high) cells vulnerable to the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib,

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

223 understanding acquired tumour resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and other

224 RCA2-mutated breast cancers are sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors and platin

225 Poly(ADP-ribose) polymerase (PARP) inhibitors are increa

226 Bevacizumab and maintenance poly(ADP-ribose) polymerase (PARP) inhibitors both signi

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

228 Poly(ADP-ribose) polymerase (PARP) inhibitors have shown

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

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

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

232 ression levels show increased sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors, especiall

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

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

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

236 (T-ALL) cells exhibit a high sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors.

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

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

239 ian cancer but also creates vulnerability to poly(ADP-ribose) polymerase (PARP) inhibitors.

240 Poly(ADP-ribose) Polymerase (PARP) is a family of enzyme

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

242 Poly(ADP-ribose) polymerase (PARP) superfamily members c

243 Human tankyrase-1 (TNKS) is a member of the poly(ADP-ribose) polymerase (PARP) superfamily of protei

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

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

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

247 er at their C termini: ZAPL (long) encodes a poly(ADP-ribose) polymerase (PARP)-like domain that is m

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

249 damage by inhibiting the DNA repair protein poly(ADP-ribose) polymerase (PARP).

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

251 e minutes) through mechanisms that depend on poly(ADP-ribose) polymerases (PARP) and the catalytic su

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

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

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

255 vity of ATM-mutant cells to topotecan or the poly-(ADP-ribose) polymerase (PARP) inhibitor olaparib r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 It forms DNA adducts, thereby activating poly(ADP-ribose) polymerases (PARPs) to initiate DNA rep

278 posttranslational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) using NAD(+) as ADP

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

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

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

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

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

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

288 ecently been suggested to be a target of the poly (ADP-ribose) polymerases Tankyrase 1, and we have f

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

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

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

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

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

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

295 ian log-fold change (suppression) of cleaved poly (ADP-ribose) polymerase was greater with palbocicli

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

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

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

299 DNA damage was associated with activation of poly(ADP-ribose) polymerase, which led to consumption of

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