ライフサイエンスコーパス: poly ADP-ribose

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

2 catalytic efficiency for protein-conjugated poly(ADP-ribose).

3 Poly(ADP-ribose) a dynamic and reversible posttranslatio

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

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

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

7 ng meiosis, beyond its enzymatic activity in poly(ADP-ribose) catabolism.

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

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

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

11 This facilitates the poly(ADP-ribose)-dependent assembly of the LIG4/XRCC4 co

12 oxidative lesions and a conserved N-terminal poly(ADP-ribose)-dependent recruitment motif, with later

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 We recently identified that poly (ADP) ribose glycohydrolase (PARG) is a strong cand

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

17 Poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glycohydrolase (PARG) are key enzymes i

18 lymerase 1 (PARP1) and PARylation removal by poly(ADP-ribose) glycohydrolase (PARG) critically regula

19 ved from patient biopsies are sensitive to a poly(ADP-ribose) glycohydrolase (PARG) inhibitor.

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

21 ed by ADP-ribose transferases and removed by poly(ADP-ribose) glycohydrolase (PARG), which plays impo

22 ns, ZBTB24 protects them from degradation by poly(ADP-ribose) glycohydrolase (PARG).

23 polymers show increased resistance to human poly(ADP-ribose) glycohydrolase-mediated degradation.

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

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

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

27 Blocking poly-ADP-ribose gylcohydrolase also enhanced this associ

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

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

30 ponses, leading to elevated DNA breakage and poly(ADP-ribose) induction that cannot be rescued by cat

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

32 -strand break repair; a process regulated by poly(ADP-ribose) metabolism.

33 ed synthesis of mono(ADP-ribose) (mADPr) and poly(ADP-ribose) (pADPr) conjugates by pADPr polymerase

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

35 G1 and the ZnF domain of SIRT1 interact with poly-ADP ribose (PAR) in response to DNA damage, and are

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

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

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

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

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

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

42 4orf4 is expressed alone, it associates with poly(ADP-ribose) (PAR) chains and is recruited to DNA da

43 l challenges including the complexity of the poly(ADP-ribose) (PAR) chains, low abundance of the modi

44 Through its ability to bind the ends of poly(ADP-ribose) (PAR) chains, the function of the histo

45 requently mutated in human cancers, binds to poly(ADP-ribose) (PAR) immediately following DNA damage

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

47 Poly(ADP-ribose) (PAR) is a nucleic acid-like protein mo

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

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

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

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

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

53 ll nucleolar RNAs (snoRNAs) as activators of poly(ADP-ribose) (PAR) synthesis, demonstrating that thi

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

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

56 bose monomers or polymers, commonly known as poly(ADP-ribose) (PAR), modulate the activities of the m

57 ranslational modification by the addition of poly(ADP-ribose) (PAR), which promotes protein recruitme

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

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

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

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

62 1/cell-cycle, apoptotic genes, caspase-3 and poly ADP ribose polymerase-1 (PARP-1) cleavage) and was

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

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

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

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

67 2 mutant channel (C1008-->A) or silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 50 nM PSKalpha exhibited lower expression of poly-ADP-ribose polymerase 1 (PARP1) gene, leading to a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 -2, MCP-3, CXCL9, CXCL10, CXCL5, ENRAGE, and poly (ADP-ribose) polymerase 1.

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

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

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

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

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

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

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

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

128 4K20me0 is required for HR and resistance to poly (ADP-ribose) polymerase inhibitors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 9 rendered GLS(high) cells vulnerable to the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 1-XPF endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap format

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

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

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

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

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

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

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

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

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

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

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

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

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

229 2-positive disease, bone stabilizing agents, poly(ADP-ribose) polymerase inhibitors for BRCA mutation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 And its derived poly-ADP-ribose polymers show increased resistance to hu

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

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

296 ) to modify numerous proteins with mono- and poly(ADP-ribose) signals that are important for the subs

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