ライフサイエンスコーパス: PARP

1 PARP catalysed ADP-ribosylation is a post-translational

2 PARP inhibition and the D226 mutation impair HuR's PARyl

3 PARP inhibitors (PARPi) benefit only a fraction of breas

4 PARP inhibitors (PARPi), a cancer therapy targeting poly

5 PARP-1 stabilizes Sox2 binding to nucleosomes at subopti

6 PARP-1-dependent Sox2-binding sites reside in euchromati

7 PARP-2 has a modular architecture composed of a C-termin

8 PARP-inhibitor-induced multinucleated cells fail clonoge

9 lement in the poly(ADP-ribose) polymerase 1 (PARP-1) promoter in a mutually exclusive manner and regu

10 ent tumours to poly-ADP-ribose polymerase-1 (PARP) inhibitors.

11 nd identified poly(ADP-ribose) polymerase-1 (PARP-1) as an LXR-associated factor.

12 caspase-3 and poly ADP ribose polymerase-1 (PARP-1) cleavage) and was reversed by a pan-caspase inhi

13 regulation of poly(ADP-ribose) polymerase-1 (PARP-1) expression by MKP-1.

14 ses (MMPs) and poly-ADP-ribose-polymerase-1 (PARP-1) in diabetic kidney remodeling remains mostly obs

15 edominantly synthesized by PAR polymerase-1 (PARP-1) in genome maintenance.

16 responses of poly (ADP-ribose) polymerase-1 (PARP-1) to DNA damage with strand breaks are often not s

17 Moreover, adding HPF1 to in vitro PARP-1/PARP-2 reactions is necessary and sufficient for serine-

18 ked protein ADPr is the key signal in PARP-1/PARP-2-dependent processes that govern genome stability.

19 ompounds 13 and 14 were evaluated against 11 PARP isoforms to reveal that both 13 and 14 were more po

20 Poly(ADP-ribose) polymerase-2 (PARP-2) is one of three human PARP enzymes that are pote

21 o cells by activation of the STAT3/caspase-3/PARP signaling pathway.

22 nd after treatment with olaparib (n = 14), a PARP inhibitor, or iniparib (n = 11), which has no PARP

23 n cells and is recruited to DNA lesions in a PARP-1-dependent manner, but independently of PARP-1 cat

24 ([Ca(2+)]c), which was inhibited by PJ34, a PARP inhibitor, and abolished by TRPM2 knockout (TRPM2-K

25 enzymatic activity and reduces binding to a PARP inhibitor, thereby rendering cancer cells resistant

26 most likely to respond therapeutically to a PARP inhibitor.

27 otic bypass through EMI1 depletion abrogates PARP-inhibitor-induced cytotoxicity.

28 d hypotaurine metabolism were enriched after PARP inhibition in all three breast cancer cell lines.

29 te and genotype-specific sensitivity against PARP inhibition.

30 g-sensitive approach for PARPs, which allows PARP-specific ADP-ribosylation of substrates that is sui

31 nition domain of TNKS, as it is unique among PARP family members.

32 cer cells expressed high levels of MKP-1 and PARP-1 proteins, and that silencing MKP-1 or PARP-1 incr

33 d normalized ROMO1, MMPs-9, -13 and -14, and PARP-1 along with collagen biosynthesis and cross-linkin

34 levels and activity of active caspase-3 and PARP-1 in human and mouse macrophages during ingestion o

35 L, Bax/Bcl-2, cyto-c, cleaved caspase-3, and PARP in a dose-dependent manner, which indicates AMC ind

36 uces apoptosis by activating caspase 3/7 and PARP cleavage, and its longer exposure causes increase i

37 strate a synthetic lethality between ADT and PARP inhibition in vivo.

38 hway in vivo, thus inhibition of both AR and PARP is required for effective treatment of high risk pr

39 age, ataxia-telangiectasia mutated (ATM) and PARP-1, were induced.

40 s of pancreatitis and pancreatic cancer, and PARP inhibition has been proposed as a valuable strategy

41 levels and enhanced cleavage of Caspases and PARP.

42 , RADX inactivation confers chemotherapy and PARP inhibitor resistance to cancer cells with reduced B

43 itizes ovarian cancer cells to cisplatin and PARP inhibitor (olaparib) while overexpression of USP13

44 dy shows PKC/NOX-mediated ROS generation and PARP-1 activation as an important mechanism in Zn(2+)-in

45 ent for serine-specific ADPr of histones and PARP-1 itself.

46 at treatment with a combination of c-Met and PARP inhibitors may benefit patients whose tumors show h

47 her alteration of miR-194-dependent MMPs and PARP-1 causes renal fibrosis in diabetes kidney, and whe

48 d increased sensitivity to both platinum and PARP inhibitor chemotherapy compared to Trp53 (-/-).

49 f MYC-regulated homologous recombination and PARP-mediated DNA repair yields potent synthetic lethali

50 e crossroads of histone ADP-ribosylation and PARP-1 automodification.

51 by pharmacological inhibitors of ROS/RNS and PARP.

52 predicting sensitivity to platinum salts and PARP inhibitors, the data regarding somatic mutation for

53 and confer resistance to platinum salts and PARP inhibitors.

54 biochemical hallmarks of apoptosis, such as PARP-1 and procaspase-3 cleavage.

55 ins mediated by PARP family members, such as PARP-1.

56 y ADP-ribosyltransferases, commonly known as PARPs, but it can also be added by other enzymes, includ

57 TM small-molecule inhibitors that attenuated PARP cleavage by inhibiting gamma-H2AX, which in turn in

58 Automodified PARP-1 then recruits repair factors to DNA damage sites.

59 Response to olaparib depended on a basal PARP enzymatic activity, but did not correlate with PARP

60 g, providing a clear functional link between PARP-1, ADP-ribosylation, and NELF.

61 We show that latonduine can inhibit both PARP-3 and -16 and that this is necessary for CFTR corre

62 ve free PARP-1 while retaining the DNA-bound PARP-1, we demonstrate a direct recruitment of the endog

63 PJ34 and UPF1069 are broad PARP inhibitors; PJ34 inserts a flexible moiety into hyd

64 ated cisplatin resistance can be bypassed by PARP-1 inhibition.

65 thetic lethality in BRCA2 deficient cells by PARP inhibition.

66 ational modification of proteins mediated by PARP family members, such as PARP-1.

67 ogenic transcription factor, is PARylated by PARP-1 on three amino acids in a conserved regulatory do

68 dulation of the level of its ribosylation by PARP-16.

69 PN cells to synthetic lethality triggered by PARP inhibitors.

70 Furthermore, chemical PARP inhibitors improve axon regeneration when administe

71 nd persistent PARP-1 residency on chromatin (PARP-1 trapping).

72 ition of Bax, cleaved caspase 3, and cleaved PARP expression.

73 a1-42, p-Tau, cleaved caspase-3, and cleaved PARP proteins.

74 We profiled 10 clinical PARP inhibitors and commonly used research tools for the

75 The combined PARP of all risk factors was 52.7% (95% CI, 49.1%-56.3%)

76 esults may provide a rationale for combining PARP and EZH2 inhibition as a therapeutic strategy for B

77 Carnosol showed comparative PARP inhibitory effects at 100 microM compared to carnos

78 ing the RAD51D-XRCC2 interaction and confers PARP inhibitor sensitivity.

79 sly discovered by our group and a congeneric PARP inhibitor, a library of derivatives was synthesized

80 or each cell line, we monitored constitutive PARP activation, spontaneous DNA damage by alkaline come

81 Conversely, PARPs, which add poly(ADP-ribose) to proteins, inhibit a

82 This review covers PARP imaging from the very first imaging agents up to th

83 ns from those of PARP-1, the other major DDR-PARP, and highlights the specialization of the multi-dom

84 DDR-PARPs detect DNA strand breaks, leading to a dramatic in

85 ion of the multi-domain architectures of DDR-PARPs.

86 Jun N-terminal kinase 1/2 (JNK1/2) decreased PARP-1 ubiquitination while increasing total PARP-1 prot

87 moted PARP-1 ubiquitination, which decreased PARP-1 protein levels.

88 Moreover, depleting PARP-1 or RIPK1, key mediators of parthanatos and necrop

89 otential to develop compounds with different PARP family member specificity profiles for optimal anti

90 ling of the PARP3-active site with different PARP inhibitors also highlights the potential to develop

91 f DNA damage that are gauged by differential PARP activation regulating protein assembly at the damag

92 ll death that was inhibited by PJ34 and DPQ, PARP inhibitors, 2-APB, a TRPM2 channel inhibitor, and p

93 t recruitment of the endogenous or exogenous PARP-1 to the UV-lesion site in vivo after local irradia

94 lteration of MMPs-9, -13 and -14 expression, PARP-1, HIF1alpha, and increased collagen biosynthesis a

95 In fact, PARP-1 interacted with both LXRalpha and LXRbeta.

96 Here we find PARP inhibition to compromise replication fork stability

97 neration agent following olaparib, the first PARP inhibitor approved for cancer therapy.

98 ivity in mediating dioxin toxicity following PARP activation.

99 Interestingly, the NTR is not essential for PARP-2 localization to sites of DNA damage.

100 robust NAD(+) analog-sensitive approach for PARPs, which allows PARP-specific ADP-ribosylation of su

101 onation technique to selectively remove free PARP-1 while retaining the DNA-bound PARP-1, we demonstr

102 as synthesized to discover the first dual G4/PARP ligand.

103 -ribose) polymerases (inhibition of PARP-1 > PARP-2 > PARP-3), following a similar drug, Olaparib.

104 polymerases (inhibition of PARP-1 > PARP-2 > PARP-3), following a similar drug, Olaparib.

105 hich has restricted our understanding of how PARP-2 is specialized toward specific repair pathways.

106 Overall, our work reveals how PARP blockade, either by hyperthermia or small-molecule

107 Mechanistic understanding how PARP inhibition induces cytotoxicity in HR-deficient can

108 polymerase-2 (PARP-2) is one of three human PARP enzymes that are potently activated during the cell

109 t SCO6735 possesses the ability to hydrolyze PARP-dependent protein ADP-ribosylation.

110 lso contribute to the synthetic viability if PARP is inhibited before BRCA2 loss.

111 enhanced Annexin V staining and cleavage in PARP protein.

112 t O-linked protein ADPr is the key signal in PARP-1/PARP-2-dependent processes that govern genome sta

113 esults demonstrate how a fundamental step in PARP-1-dependent ADP-ribosylation signaling is regulated

114 artate to isoaspartate isomerization include PARPs, enzymes known to ribosylate aspartate residues in

115 with genotoxic chemotherapeutics, including PARP inhibitors, and nongenotoxic activation of p53.

116 hat NAD(+) loss is attributable to increased PARP activity in thymus and liver, as cotreatment with d

117 the molecular mechanisms used by individual PARPs to mediate their responses to cellular signals.

118 Furthermore, Zn(2+)-induced PARP-1 stimulation, increase in the [Ca(2+)]c and cell d

119 s possess two other DNA strand break-induced PARP enzymes, PARP2 and PARP3, for which the roles are u

120 ability of the latonduine analogs to inhibit PARP-16 and their ability to correct F508del-CFTR traffi

121 ith IC50 = 0.079 muM), as well as inhibiting PARP-modulated PARylation and cell proliferation in MDA-

122 in clinical trials, such as mTOR inhibitors, PARP inhibitors, and CDK4/6 inhibitors.

123 Interestingly, PARP-1 catalytic activity drops precipitously during the

124 bearing promoters, thus triggering NF-kappaB/PARP-1-dependent transcription of antimicrobial peptides

125 ession of JNK1/2 activity by MKP-1 maintains PARP-1 levels and suggests that MKP-1-mediated cisplatin

126 earch tools for their inhibition of multiple PARP enzymes.

127 nhibitor, or iniparib (n = 11), which has no PARP inhibitory activity.

128 More generally, acquisition of PARP inhibitors and cisplatin resistance is associated w

129 These actions of PARP-1 occur independently of its poly(ADP-ribosyl) tran

130 Our biochemical and structural analysis of PARP inhibitor potencies establishes a molecular basis f

131 ark for experimental design in assessment of PARP inhibitor effects.

132 DNA damage-induced hyper-automodification of PARP-1.

133 Despite the availability of PARP inhibitors for cancer therapy, a biomarker to clear

134 on the biochemistry and molecular biology of PARP-1 in DNA damage detection and repair, the mechanist

135 readily detectable by analyzing cleavage of PARP and caspase-7.

136 tivation of caspase-9 and -3 and cleavage of PARP in tumor cells compared to normal cells.

137 Notably, concentrations of PARP inhibitor >1000-fold higher than the IC50 were requ

138 Both depletion of PARP-1 and inhibition of PARP-1 activity augmented LXR l

139 lly considered the key DNA-binding domain of PARP-2, we report here that all three domains of PARP-2

140 The multiple domains of PARP-1 are organized upon detecting DNA damage, creating

141 -2, we report here that all three domains of PARP-2 collectively contribute to interaction with DNA d

142 ural insights into the functional domains of PARP-2, which has restricted our understanding of how PA

143 rovide insight into the cytotoxic effects of PARP inhibition, and point at combination therapies to p

144 ograft models, expanding use and efficacy of PARP inhibitors for human cancer therapy.

145 Our study differentiates the functions of PARP-2 domains from those of PARP-1, the other major DDR

146 Targeted molecular imaging of PARP using fluorescent or radiolabeled tags has followed

147 ARP-1-dependent manner, but independently of PARP-1 catalytic ADP-ribosylation activity.

148 Notably, the pharmacologic inhibition of PARP activity restored cisplatin sensitivity in MKP-1 ov

149 In contrast, inhibition of PARP by PARPi attenuates alkylating DNA damage-induced E

150 poly (ADP-ribose) polymerases (inhibition of PARP-1 > PARP-2 > PARP-3), following a similar drug, Ola

151 Both depletion of PARP-1 and inhibition of PARP-1 activity augmented LXR ligand-induced ABCA1 expre

152 Depletion or inhibition of PARP-1 or mutation of the ADP-ribosylation sites on NELF

153 Depletion or chemical inhibition of PARP-1, or mutation of the PARylation sites on C/EBPbeta

154 r cells responsive to combined inhibition of PARP/PI3K, with concomitantly induced DNA damage accumul

155 s efficiently as pharmacologic inhibitors of PARP (PARPi), producing comparable delay in DNA repair,

156 th which we characterized the interaction of PARP-1 with UV-damaged DNA in vivo and in vitro.

157 Here, we discuss current knowledge of PARP inhibitors and potential ways to maximize their cli

158 denosine diphosphate-ribose) (PAR, marker of PARP activation) and IL-6, in the bronchoalveolar lavage

159 implicate Charon as an essential mediator of PARP-1-dependent transcription in the innate immune path

160 Until now, numbers of PARP inhibitors have been reported and used for breast c

161 Up-regulation of PARP-1 by FASN in turn increases Ku protein recruitment

162 1 (HPF1), a recently identified regulator of PARP-1.

163 eated cells are found in vivo in remnants of PARP inhibitor-treated Brca2(-/-);p53(-/-) and Brca1(-/-

164 he functions of PARP-2 domains from those of PARP-1, the other major DDR-PARP, and highlights the spe

165 e global and local structural transitions of PARP-1 that are associated with DNA damage detection and

166 w, we summarize the current understanding of PARP functions in these two dismal pathologies and discu

167 Furthermore, upregulation of PARP activity is essential for the survival of prostate

168 linical mechanistic rationale for the use of PARP and ATR inhibitors to improve treatment of ATM-muta

169 rovide a preclinical rational for the use of PARP inhibitors in ATM-affected human CLL.ATM and TP53 m

170 e results extend the potential usefulness of PARP inhibitors in the treatment setting beyond BRCA mut

171 ometrial cancers, the therapeutic utility of PARP inhibitors is limited in this disease.

172 plausible approach to expand the utility of PARP inhibitors to endometrioid endometrial cancers in a

173 oss species, and that chemical inhibition of PARPs can elicit axon regeneration.

174 and functional understanding of the role of PARPs in different biological processes has grown consid

175 Leung introduces the various roles of PARPs and the regulation of ADP-ribosylation of protein

176 New findings on the diverse roles of PARPs in chromatin regulation, transcription, RNA biolog

177 One PARP inhibitor, olaparib (Lynparza, AstraZeneca), was re

178 PARP-1 proteins, and that silencing MKP-1 or PARP-1 increased cisplatin sensitivity in resistant cell

179 ath was not dependent on either caspase-3 or PARP-1 cleavage, but cleavage of caspase-1 was detected

180 Combinations of cisplatin or PARP inhibitors enhanced the antitumor cell effect of AT

181 dependent PD-L1 upregulation after X-rays or PARP inhibition.

182 DNA repair molecules, TET1 GADD45A, TDG, or PARP-1 decreased gene expression.

183 y, to predict response to rucaparib, an oral PARP inhibitor.

184 ion, inefficient PAR removal, and persistent PARP-1 residency on chromatin (PARP-1 trapping).

185 attenuated after genetic or pharmacological PARP inactivation, and several clinical trials have demo

186 tly sensitive to poly-ADP-ribose polymerase (PARP) inhibitors olaparib and BMN673.

187 r exacerbated by poly-ADP ribose polymerase (PARP) inhibitors.

188 analogs inhibit poly-ADP ribose polymerase (PARP) isozymes 1, 3, and 16.

189 We found that poly(ADP-ribose) polymerase (PARP) activation distinguishes between the two damage st

190 tory effect of poly (ADP-ribose) polymerase (PARP) activity in vitro and in vivo.

191 3, cleavage of poly (ADP-Ribose) polymerase (PARP) and apoptosis.

192 bitors against poly (ADP-ribose) polymerase (PARP) are promising targeted agents currently used to tr

193 The poly(ADP-ribose) polymerase (PARP) enzymes were initially characterized as sensors of

194 iscovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and the ADP-ribosylation reactio

195 Poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) olaparib has been approved for t

196 served that the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib synergizes with GLS1 inhibitors

197 or veliparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, combined with carboplatin.

198 Olaparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, has previously shown efficacy in a phas

199 this pathway by Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) is toxic to cells with defects

200 Poly-(ADP-ribose) polymerase (PARP) inhibitors (PARPis) selectively kill BRCA1/2-defic

201 Poly(ADP-ribose) polymerase (PARP) inhibitors have activity in ovarian carcinomas wit

202 Poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as promising cancer therap

203 Poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as promising therapeutics

204 Poly (ADP-ribose) polymerase (PARP) inhibitors have shown promising results in clinica

205 pair, including poly(ADP-ribose) polymerase (PARP) inhibitors, fail due to lack of tumor-selectivity.

206 inum drugs and poly (ADP-ribose) polymerase (PARP) inhibitors.

207 ly sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors.

208 The poly(ADP-ribose) polymerase (PARP) Tankyrase (TNKS and TNKS2) is paramount to Wnt-bet

209 eracting with a poly(ADP-ribose) polymerase (PARP) tankyrase.

210 ly(adenosine diphosphate-ribose) polymerase (PARP).

211 -7, and cleaved poly(ADP-ribose) polymerase (PARP).

212 ly (adenosine diphosphate-ribose)polymerase (PARP) expression and is feasible for clinical trial eval

213 oly(adenosine diphosphate-ribose)polymerase (PARP) family of enzymes is an important factor in the ce

214 ersensitive to Poly (ADP ribose)-polymerase (PARP) inhibitors, but can acquire resistance and relapse

215 oteins (TNKS), poly(ADP-ribose) polymerases (PARP) that regulate Wnt signaling by targeting Axin for

216 Poly ADP-ribose polymerases (PARPs) catalyze massive protein poly ADP-ribosylation (P

217 inhibition of poly(ADP-ribose) polymerases (PARPs) elicits clinical benefits in cancer therapy.

218 n catalyzed by poly(ADP-ribose) polymerases (PARPs) that mediate EBV replication during latency.

219 a rapid modular assembly of MC2050, a potent PARP-1 inhibitor; and gram-scale preparations.

220 point at combination therapies to potentiate PARP inhibitor treatment of HR-deficient tumours.

221 indicate that Zn(2+) induced ROS production, PARP-1 stimulation, increase in the [Ca(2+)]c and cell d

222 Silencing MKP-1 promoted PARP-1 ubiquitination, which decreased PARP-1 protein le

223 Functionally, HPF1 promotes PARP-1-dependent in trans ADP-ribosylation of histones a

224 suggesting that mitotic progression promotes PARP-inhibitor-induced cell death.

225 the population-attributable risk proportion (PARP) for breast cancer associated with clinical breast

226 ression of the apoptosis-associated proteins PARP, Bax, and caspase-3.

227 effects of G4 ligands, cancer cells recruit PARP enzymes at telomeres.

228 and CAT domains function together to recruit PARP-2 to sites of DNA breaks.

229 nd subsequent H3S10 phosphorylation recruits PARP-1 to the remodeling site independently of H2Av phos

230 sults suggest that (18)F-FTT uptake reflects PARP expression and that its radiation dosimetry profile

231 in a mutually exclusive manner and regulate PARP-1 expression.

232 e against genotoxic insults by up-regulating PARP-1 and DNA repair via NF-kappaB and SP1.

233 wever, clinical development of TNKS-specific PARP catalytic inhibitors is challenging due to off-targ

234 e found that MKP-1 overexpression stimulates PARP-1 and poly(ADP-ribose) (PAR) protein expression and

235 obtained after WI exhibit oxidative stress, PARP activation, and tissue injury, which are suppressed

236 We show that the polymeric state supports PARP activity and allows Tankyrase to effectively access

237 sistance while its downregulation suppresses PARP-1 and PAR protein expression and cisplatin resistan

238 lity allele and supports the use of targeted PARP-inhibitor therapies in ovarian cancer patients carr

239 Targeting PARP-associated DNA repair may represent a novel therape

240 ishes between the two damage states and that PARP activation is essential for rapid TRF2 recruitment

241 Finally, we demonstrated that PARP inhibitor olaparib did not significantly alter the

242 We found that PARP-1 ADP-ribosylates and inhibits negative elongation

243 greement with this hypothesis, we found that PARP-1 deficiency significantly increased the chromatin

244 Here we show that PARP-1, a nucleosome-binding protein, cooperates with in

245 We show that PARP-mediated repair pathways are upregulated in prostat

246 The PARP inhibitor AZD2461 was developed as a next-generatio

247 oach should be broadly applicable across the PARP family and has the potential to illuminate the ADP-

248 regulates HR and AR inhibition activates the PARP pathway in vivo, thus inhibition of both AR and PAR

249 nd liver, as cotreatment with dioxin and the PARP inhibitor PJ34 increased NAD(+) levels and prevente

250 Essentially, PrxII depletion hampers the PARP-dependent Axin1 degradation through tankyrase inact

251 Importantly, the PARP inhibitor 3-aminobenzamide enhanced macrophage ABCA

252 s to probe cell line-specific effects of the PARP inhibitor Veliparib and radiation on metabolism in

253 ogenous serine ADPr sites are located on the PARP-1 automodification domain.

254 usal women and had the largest effect on the PARP; 39.3% (95% CI, 36.6%-42.0%) of premenopausal and 2

255 y, augmented the effects of cisplatin or the PARP inhibitor olaparib, and improved the response of pl

256 Targeting the PARP DNA repair pathway extensively sensitized IDH1-muta

257 pporting this possibility, we found that the PARP inhibitor olaparib or ATR inhibitors reduced the vi

258 noprecipitation assays demonstrated that the PARP-1 protein binds and posttranslationally modifies Hu

259 mors, exhibited increased sensitivity to the PARP inhibitor olaparib as compared to MPCs transformed

260 sphomimetic Mre11 were more sensitive to the PARP inhibitor olaparib, compared with those expressing

261 cient cells and tumors were sensitive to the PARP inhibitor olaparib.

262 ed a relative increase in sensitivity to the PARP inhibitor rucaparib and slower orthotopic tumor gro

263 int to the latonduine analogs binding to the PARP nicotinamide-binding domain.

264 y compromized mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1alpha axis.

265 ian cancer, maintenance monotherapy with the PARP inhibitor olaparib significantly improves progressi

266 used a synthetic lethal interaction with the PARP-1 inhibitor olaparib.

267 The physiological roles of these PARPs remain largely unknown.

268 in toxicity, we identify NAD(+) loss through PARP activation as a novel unifying mechanism for divers

269 eficient endometrioid endometrial cancers to PARP inhibition remain controversial.

270 of BRCA proteins sensitizes cancer cells to PARP inhibition.

271 es the relative sensitivity of PDAC cells to PARP inhibitors (PARPi).

272 lts for the first time link MEIS proteins to PARP-regulated chromatin dynamics and provide a mechanis

273 lear particles and delivers active Relish to PARP-1-bearing promoters, thus triggering NF-kappaB/PARP

274 PARP1 pY907 may predict tumor resistance to PARP inhibitors, and that treatment with a combination o

275 thereby rendering cancer cells resistant to PARP inhibition.

276 graft models, including tumours resistant to PARP inhibition.

277 h c-Met expression and who do not respond to PARP inhibition alone.

278 To enhance the clinical response to PARP inhibitors (PARPis), understanding the mechanisms u

279 als have demonstrated promising responses to PARP inhibitors in pancreatic cancer patients.

280 dometrial cancer cells are not responsive to PARP inhibitor Olaparib alone, but instead show superior

281 placement of histones, which is sensitive to PARP inhibition and is transient in nature.

282 ancers, rendering these tumours sensitive to PARP inhibition.

283 air machinery, which makes them sensitive to PARP inhibitors (PARPi).

284 leukemia cells enhances their sensitivity to PARP inhibition and could provide a safe and effective c

285 ld have selective therapeutic sensitivity to PARP inhibition.

286 ell lines showed an increased sensitivity to PARP inhibitors (Figure 4C).

287 /BRCA2) also confer selective sensitivity to PARP inhibitors.

288 PARP-1 ubiquitination while increasing total PARP-1 protein levels.

289 However, developing a new type PARP inhibitor with distinctive skeleton is alternativel

290 Upon PARP inhibition, ACLY silencing promotes genomic instabi

291 cell line-independent metabolic changes upon PARP inhibition.

292 lly could be exploited therapeutically using PARP inhibitors in combination with androgen-deprivation

293 Moreover, adding HPF1 to in vitro PARP-1/PARP-2 reactions is necessary and sufficient for

294 he next steps necessary to determine whether PARP inhibitors will finally make the difference in trea

295 begun to reveal the promising ways in which PARPs may be targeted therapeutically for the treatment

296 ective cytotoxicity to V-C8 cells along with PARP inhibitory effects.

297 -selective, caspase-dependent apoptosis with PARP inhibitors and beta-lapachone.

298 Apoptosis was associated with PARP-1 cleavage and oncosis was associated with a rapid

299 /C4orf27 forms a robust protein complex with PARP-1 in cells and is recruited to DNA lesions in a PAR

300 In recent years, PARPs have been implicated in the pathogenesis of pancre