ライフサイエンスコーパス: PARP1

1 PARP1 also has a major role in DNA damage response (DDR)

2 PARP1 also transformed TERT-immortalized melanocytes exp

3 PARP1 and NSD2 have been found to be recruited to DNA do

4 PARP1 and PARP2 dual inhibitors, such as olaparib, have

5 PARP1 binds RNA and its depletion results in increased e

6 PARP1 coordinates BER and relies on the upstream 8-oxogu

7 PARP1 deficiency was also associated with a modulation o

8 PARP1 depletion impacted both the synthesis of nascent m

9 PARP1 inhibition, silencing, or genetic deletion abrogat

10 PARP1 is a DNA repair gene critical for chemotherapy res

11 PARP1 is an abundant nuclear protein with many pleiotrop

12 PARP1 pY907 increases PARP1 enzymatic activity and reduc

13 PARP1 regulates gene expression by numerous mechanisms,

14 PARP1, the most abundant isoform, regulates the expressi

15 PARP1-dependent poly-ADP-ribosylation (PARylation) parti

16 PARP1-H862D, but not PARylation-deficient PARP1-E988K, f

17 PARP1-mediated senescence rescue was accompanied by tran

18 ted with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endogenous NAD(+), low expression o

19 ensor protein poly(ADP-ribose) polymerase 1 (PARP1) and activates caspase-3 to initiate cell death.

20 r drug target poly(ADP-ribose) polymerase 1 (PARP1) and its close homologue, PARP2, are early respond

21 lyzed by human poly-ADP-ribose polymerase 1 (PARP1) and PARP2.

22 se)ylation (PARylation) by PAR polymerase 1 (PARP1) and PARylation removal by poly(ADP-ribose) glycoh

23 sociates with poly(ADP-ribose) polymerase 1 (PARP1) and stimulates its auto-poly(ADP-ribosyl)ation.

24 ating enzyme poly-(ADP-ribose) polymerase 1 (PARP1) and the deribosylating enzyme poly-(ADP-ribose) g

25 repair enzyme poly(ADP-ribose) polymerase 1 (PARP1) for the detection of cancers of the oral cavity,

26 expression of poly-ADP-ribose polymerase 1 (PARP1) gene, leading to a higher intracellular NAD(+) av

27 uclear enzyme poly(ADP-ribose) polymerase 1 (PARP1) has been shown to facilitate the lesion recogniti

28 Poly (ADP-ribose) polymerase 1 (PARP1) has emerged as an attractive target for cancer th

29 lar stresses, poly(ADP-ribose) polymerase 1 (PARP1) has vital roles in orchestrating DNA damage repai

30 silencing of poly(ADP-ribose) polymerase 1 (PARP1) inhibits PAR-mediated recruitment of FBXW7 to the

31 nuclear enzyme Poly(ADP-ribose)Polymerase 1 (PARP1) is a promising target for optical imaging of OSCC

32 chanistically, poly-ADP-ribose polymerase 1 (PARP1) represses expression of NKG2DLs.

33 ys mediated by poly(ADP)ribose polymerase 1 (PARP1) serve as backups.

34 host protein, poly(ADP-ribose) polymerase 1 (PARP1), facilitates IFNAR degradation and accelerates IA

35 ncluding PML, poly(ADP-ribose) polymerase 1 (PARP1), ligase IIIalpha, and origin recognition complex

36 ular protein, poly(ADP-ribose) polymerase 1 (PARP1), plays a critical role in mediating IAV HA-induce

37 that targets poly[ADP ribose] polymerase 1 (PARP1), the expression of which has been found to be muc

38 ge regulator, poly(ADP-ribose) polymerase 1 (PARP1), was discovered.

39 his reaction, poly(ADP-ribose) polymerase 1 (PARP1), were discovered more than 50 years ago.

40 y[adenosine diphosphate-ribose]polymerase 1 (PARP1), which is a nuclear enzyme that is overexpressed

41 y catalysed by poly-ADP-ribose polymerase 1 (PARP1), whose role in gene transcription modulation has

42 m stalling at poly(ADP-ribose) polymerase 1 (PARP1)-DNA complexes trapped by PARP inhibitors, thereby

43 egulation of poly [ADP-ribose] polymerase 1 (PARP1).

44 on, increased poly(ADP-ribose) polymerase-1 (PARP1) activity, single-cell somatic mutations, and ulti

45 Poly (ADP-ribose) polymerase-1 (PARP1) is a highly conserved enzyme focused on the self-

46 n inhibitor of poly-ADP-ribose polymerase-1 (PARP1).

47 oteins, poly-ADP-ribose polymerases 1 and 2 (PARP1/2) and histone PARylation factor 1.

48 enefit from a dual HER3-EGFR inhibitor and a PARP1 inhibitor.

49 These findings outline a PARP1-dependent mechanism required for LTP generation, w

50 DNA breaks recruit and activate PARP1/2, which deposit poly-ADP-ribose (PAR) to recruit

51 ization of G-quadruplex structures activates PARP1 and leads to accelerated aging in Caenorhabditis e

52 nuclear localization of TyrRS that activates PARP1.

53 used persistent PARP1 foci without affecting PARP1 exchange.

54 regulators, including HDAC3, Rev-erb-alpha, PARP1 and SIRT1.

55 Although PARP1 and XRCC1 are implicated in the SSB repair pathway

56 p53 gain-of-function mutant 273H and PARP1 interact with replication forks and could serve as

57 hypersensitivity to DNA-damaging agents and PARP1/2 inhibitors.

58 est that the combination of chemotherapy and PARP1 inhibition may benefit the carriers of rs1805407 i

59 ntext is controlled by XPC itself, DDB2, and PARP1.

60 nthetic lethality between XRN2 depletion and PARP1 inhibition.

61 g between DNA methyltransferases (DNMTs) and PARP1.

62 active site formed by residues from HPF1 and PARP1 or PARP2 .

63 ed assays show selective PARG inhibition and PARP1 hyperPARylation.

64 PARPi possess both PARP1 inhibition and PARP1 trapping activities.

65 ARP1 is crucial for DNA damage-initiated and PARP1-conferred PAR production.

66 ining (alt-NHEJ) components-XRCC1, LIG3, and PARP1-suppresses stress-induced TNR mutagenesis, in cont

67 The combination of c-Met and PARP1 inhibitors synergized to suppress the growth of br

68 ed ROS, but increased mRNA levels of p27 and PARP1; all compatible with enhanced cell survival.

69 Staining of p53 and PARP1 in breast cancer TMAs and comparison with the TCGA

70 e cisplatin increased protein PARylation and PARP1 shRNA knock-down returned PRPP towards normal, and

71 These results indicate that mtp53 R273H and PARP1 interact with replicating DNA and should be consid

72 s and that the interaction between Sam68 and PARP1 is crucial for DNA damage-initiated and PARP1-conf

73 Two genes, SMARCB1 and PARP1, whose modulation by SAHA and RMD is predicted to

74 e sensitive to Trop2-targeting therapies and PARP1 inhibition.

75 e expression, four methylation variables and PARP1 SNP rs1805407.

76 istent with concurrent depletion of XRN2 and PARP1 promoting cell death, XRN2-deficient fibroblast an

77 tic or DNA repair pathways (including APBA3, PARP1 and RAB11).

78 Whereas the writers (e.g. ARTD1/PARP1) and erasers (e.g. PARG, ARH3) of poly-ADP-ribosyl

79 ime, we report the ability of NAM to augment PARP1 activation, induced by RSV, and its associated ant

80 Without RAP1 and TRF2(B), PARP1 and SLX4 HR factors promote rapid telomere resecti

81 damage response proteins and directly binds PARP1 and Ku70/Ku80.

82 The zinc-finger in ZBTB24 binds PARP1-associated poly(ADP-ribose) chains and mediates th

83 esidues of target substrates, including both PARP1 itself and histones.

84 PARPi possess both PARP1 inhibition and PARP1 trapping activities.

85 stead resulted in more motility of DNA-bound PARP1 molecules.

86 so facilitated the dissociation of DNA-bound PARP1.

87 matory cytokines/chemokines are abolished by PARP1 ablation or inhibition, or blocked in D226A HuR-ex

88 ration of damaged DNA which was augmented by PARP1 inhibition.

89 ruited to DNA double-strand breaks (DSBs) by PARP1 at an early time point, which requires its interac

90 PARylation of EZH2 by PARP1 then induces PRC2 complex dissociation and EZH2 do

91 nale for targeting therapy-resistant LSCs by PARP1 inhibition, which renders them amenable to control

92 showed that this PTM is specifically made by PARP1/HPF1 and PARP2/HPF1 complexes.

93 XRCC1 recruitment is promoted by PARP1, an enzyme that is activated following DNA damage

94 laxation at DNA damage sites is regulated by PARP1 enzymatic activity.

95 n oxidative stress or alkylating DNA damage, PARP1 interacts with and attaches poly-ADP-ribose (PAR)

96 cells from patients with NGPS have defective PARP1 activity and impaired repair of oxidative lesions.

97 PARP1-H862D, but not PARylation-deficient PARP1-E988K, formed stable PARP1 foci upon activation.

98 ersistent PARP1 foci are formed by different PARP1 molecules that are continuously recruited to and e

99 N activity, resulting in activation of EGFR, PARP1, and caspases and inhibition of p53 and NFkappaB.

100 s of ADP-ribosylation, synthesized by either PARP1 or PARP2, are sufficient for XRCC1 recruitment fol

101 Surprisingly, we show that either PARP1 or PARP2 are sufficient for near-normal XRCC1 recr

102 nzymatic activity of PARP1 without eliciting PARP1 trapping or cGAS-STING activation.

103 P signaling, whereas silencing of endogenous PARP1 enhances signaling and BMP-induced differentiation

104 py showed altered localization of endogenous PARP1 upon transient IAV HA expression or during IAV inf

105 XRN2-deficient cells also showed enhanced PARP1 activity.

106 rom nSIRT1OE mice, the NAD+-consuming enzyme PARP1 was deactivated and the major deacetylated protein

107 orescent PARP inhibitor targeting the enzyme PARP1/2, can delineate oral cancer and accurately identi

108 uced expression of several core BER enzymes (PARP1, LIG3 and POLbeta).

109 e we show that, in response to LPS exposure, PARP1 interacts with the adenylateuridylate-rich element

110 rveillance via the transcriptional co-factor PARP1.

111 Repair factors, PARP1 and PCNA, were immediately recruited to the site o

112 The fluorescent PARP1 inhibitor can also detect oral carcinoma in a pati

113 D(eff) for PARP1, as derived by our approach, is 6x greater than fo

114 mmune response and reveal a new function for PARP1 during influenza virus infection.IMPORTANCE Influe

115 identified H862 as a potential regulator for PARP1 exchange.

116 e PARylation factor 1 (HPF1) is required for PARP1 to attach ADP-ribose groups onto the hydroxyl oxyg

117 l oncogene MITF, highlighting a new role for PARP1 in melanomagenesis.

118 tin and thus offers a therapeutic window for PARP1 inhibitor treatment in UBQLN4-overexpressing tumor

119 cancers, cell death mechanism switches from PARP1 hyperactivation-mediated programmed necrosis with

120 actionable molecular addiction to functional PARP1 signaling was preserved in models that were profic

121 Furthermore, PARP1 inhibitors act synergistically with chemotherapy i

122 y adds OGG1 to the list of BER factors, e.g. PARP1, as potential targets for cancer treatment.

123 2L1 and MCL1, and the DNA damage repair gene PARP1, identifying both expected and uncharacterized buf

124 Higher PARP1 protein levels and PAR proteins were detected in m

125 ele (rs3219090[G]) is correlated with higher PARP1 levels.

126 and decay, adding a new dimension as to how PARP1 regulates gene expression.

127 and our results support recently identified PARP1, POT1, ATM, and MPHOSPH6 loci.

128 We identified PARP1 as an interacting partner for IAV HA through mass

129 or normal neurological function and identify PARP1 as a therapeutic target in DNA strand break repair

130 Our findings thus identify PARP1 trapping as a major contributor of the immunomodul

131 e half-lives were significantly decreased in PARP1-depleted cells.

132 mportantly, these effects were suppressed in PARP1-null TNBC cells, suggesting that this phenotype re

133 A six-gene model, including PARP1, EP300, KDM5C, SMARCB1, and UHRF1 matched this pat

134 Disruption of multiple proteins, including PARP1 and CHD4, leads to the same end point of replicati

135 n of specific DNA repair proteins, including PARP1.

136 PARP1 pY907 increases PARP1 enzymatic activity and reduces binding to a PARP i

137 PARPi) extend the lifetime of damage-induced PARP1/2 foci, referred to as 'trapping'.

138 Thus, Erk-induced PARP1 activation mediated IEG expression implicated in l

139 matin of cerebral neurons caused Erk-induced PARP1 activation, rendering transcription factors and pr

140 A stimulation induced PARP1 binding to phosphorylated Erk2 in the chromatin of

141 is crucial to reset oxidative-stress-induced PARP1 activity.

142 breast cancer 1) prevents it from inhibiting PARP1 [poly(adenosine diphosphate-ribose) polymerase], a

143 1 demonstrated excellent potency (inhibiting PARP1 enzyme activity with IC50 = 0.079 muM), as well as

144 7 demonstrates excellent potency, inhibiting PARP1 and PARP2 enzyme activity with Ki = 1.2 and 0.87 n

145 s epigenetics of the PARP1 complex, inhibits PARP1 activity, and is synergistic with olaparib in TNBC

146 Olaparib inhibits PARP1/2 enzymatic activity and traps PARP1 on DNA at sin

147 nd PBX1, recruits PARP1/ARTD1, and initiates PARP1-mediated eviction of H1 from the chromatin fiber.

148 dification and the enzymes that catalyze it (PARP1, PARP2, tankyrase 1, and tankyrase 2) function to

149 In human primary melanocytes, PARP1 promoted cell proliferation and rescued BRAF(V600E

150 e TALE TF MEIS recruits the histone modifier PARP1/ARTD1 at promoters to decompact chromatin and acti

151 Finally, we show that a small molecule PARP1 degrader blocks the enzymatic activity of PARP1 wi

152 inducing 1D diffusion of otherwise nonmotile PARP1, while excess APE1 also facilitated the dissociati

153 iguingly, myeloid deletion of PARP2, but not PARP1, increases the population of immature myeloid cell

154 ancer bone metastasis through PARP2, but not PARP1, specifically in the myeloid lineage, but not in t

155 Notably, PARP1 was crucial for the robust replication of IAV, whi

156 Notably, a novel PARP1 inhibitor from TCM has been identified from the na

157 Nuclear PARP1 protein levels were higher in HER3-EGFR-high TNBCs

158 These results suggest that the abundance of PARP1 pY907 may predict tumor resistance to PARP inhibit

159 also be regulated by the opposing actions of PARP1 and PARG.

160 A synthetase (TyrRS)-dependent activation of PARP1.

161 iven H3K27 trimethylation, and activation of PARP1.

162 The catalytic activity of PARP1 is not required for the initial complex formation

163 P1 degrader blocks the enzymatic activity of PARP1 without eliciting PARP1 trapping or cGAS-STING act

164 sociated genes Rip1 and Rip3 The activity of PARP1, which mediates BER, cell death, and inflammation,

165 V and NAM have emerged as potent agonists of PARP1 through inhibition of SIRT1.

166 to follow the real-time dynamic behavior of PARP1 in the absence and presence of AP endonuclease (AP

167 Moreover, a predominant binding of PARP1 to single-strand DNA breaks, occluding its Erk bin

168 s interaction with the DNA-binding domain of PARP1.

169 nism(s) underlying the protective effects of PARP1 inhibition in colitis and the cell types in which

170 inence because it determines the efficacy of PARP1 inhibitory drugs (PARPi) in BRCA1-deficient cancer

171 In contrast to PARG, ectopic expression of PARP1 suppresses BMP signaling, whereas silencing of end

172 iated that the immunomodulatory functions of PARP1 inhibitors (PARPi) underlie their clinical activit

173 We tested the direct impact of PARP1 and PARylation on mRNA stability and decay.

174 PARylation enhanced the impact of PARP1 depletion.

175 A expression, exemplifying the importance of PARP1 for IAV-induced reduction of IFNAR1.

176 IL-1 signaling-dependent, but independent of PARP1, which also functions downstream of NLRP3 and regu

177 tform to begin to tease out the influence of PARP1 at each step of RNA biogenesis and decay to fine-t

178 DNA repair protein, leading to inhibition of PARP1 auto-ADP-ribosylation and defective repair of oxid

179 s, and adhesion molecules, and inhibition of PARP1 enzymatic activity reduced or ameliorated autoimmu

180 Inhibition of PARP1 in BRCA-mutated cancers has been observed to be cl

181 Genetic or pharmacologic inhibition of PARP1 induces NKG2DLs on the LSC surface but not on heal

182 Knockdown or inhibition of PARP1 rescued IFNAR1 levels upon IAV infection or HA exp

183 The inhibition of PARP1 sensitizes LSCs to immunotherapy, highlighting its

184 ankyrase inhibitor and a potent inhibitor of PARP1 in vitro and in cells, whereas IWR1 and AZ-6102 ar

185 ib and niraparib are selective inhibitors of PARP1 and PARP2; olaparib, rucaparib, and talazoparib ar

186 nd talazoparib are more potent inhibitors of PARP1 but are less selective.

187 nd suggests that blocking the interaction of PARP1 with HuR could be a strategy to treat inflammation

188 ce microscopy to examine the interactions of PARP1 with common DNA repair intermediates.

189 be used to quantify the expression levels of PARP1 and to detect oral, oropharyngeal and oesophageal

190 Moreover, auto-PARylation of PARP1 allowed the protein to switch its damage search st

191 nity to explore the therapeutic potential of PARP1 inhibition via G-quadruplex DNA targeting.

192 arib did not significantly alter the rate of PARP1 dissociation from DNA, but instead resulted in mor

193 cover a role for MUC1-C in the regulation of PARP1 and identify a therapeutic strategy for enhancing

194 e therapeutic approach for the regulation of PARP1 expression.

195 NEPC displays a significant up-regulation of PARP1, and PARP inhibitors significantly delay tumor gro

196 Thus, we uncover ZBTB24 as a regulator of PARP1-dependent NHEJ and class-switch recombination, pro

197 analyses of the NAD+ interacting residues of PARP1 showed that PARP1 can be physically trapped at DNA

198 icacy, increasing amplitude and retention of PARP1 directly at laser-induced DNA damage sites.

199 provide the first direct comparative role of PARP1 and PARylation in RNA stability and decay, adding

200 Given the highly important role of PARP1 in DNA repair and cancer intervention, this struct

201 dvances in our understanding of the roles of PARP1 in cellular processes such as DNA repair, gene tra

202 e and switches the amino acid specificity of PARP1 and PARP2 from aspartate or glutamate to serine re

203 that switches the amino acid specificity of PARP1 and PARP2 from aspartate or glutamate to serine(9,

204 In conclusion, GEMA-guided targeting of PARP1 resulted in dual cellular synthetic lethality in q

205 chment of PCNA persisted longer than that of PARP1.

206 ings disclose a molecular mechanism based on PARP1-Erk synergism, which may underlie this phenomenon.

207 of RSV with NAM, exerts additive effects on PARP1 activation.

208 utations, particularly given their impact on PARP1 and ATR inhibitors.

209 esulted from an on-target effect of PARPi on PARP1.

210 was not caused by suppression of sirtuins or PARP1, and 4) phosphorylation of several proteins TLR4 s

211 Olaparib treatment or PARP1/2 deletion promotes osteoclast differentiation and

212 Our PARP1-targeted PET imaging approach may be an attractive

213 Upon DNA damage, binding of PARylated PARP1 by the macro domain induces a conformational chang

214 ate the ALC1 ATPase independent of PARylated PARP1, and alter the dynamics of ALC1 recruitment at DNA

215 Its engagement with PARylated PARP1 activates ALC1 at sites of DNA damage, but the und

216 ream effector of PAR, also caused persistent PARP1 foci without affecting PARP1 exchange.

217 findings uncovered the nature of persistent PARP1 foci and identified NAD+ interacting residues invo

218 Thus, we propose that the persistent PARP1 foci are formed by different PARP1 molecules that

219 ase c-Met associates with and phosphorylates PARP1 at Tyr907 (PARP1 pTyr907 or pY907).

220 DNA repair/replication (Ku70-Ku80, DNA-PKcs, PARP1, MCM2-7, PCNA, RPA1) and RNA metabolism (RNA helic

221 d that uptake was confined to proliferating, PARP1-expressing cells.

222 und that LMP1 activates the cellular protein PARP1, leading to a decrease in a repressive histone mod

223 Breaks in DNA strands recruit the protein PARP1 and its paralogue PARP2 to modify histones and oth

224 Rapid PARP1-dependent BRN2 association with sites of DNA damag

225 sociates with chromatin-bound PBX1, recruits PARP1/ARTD1, and initiates PARP1-mediated eviction of H1

226 lly those containing macroH2A1, can regulate PARP1 function through a novel mechanism that promotes b

227 ese data offer insight into Banf1-regulated, PARP1-directed repair of oxidative lesions.

228 Moreover, RECQ1 regulates PARP1 auto-(ADP-ribosyl)ation and the choice between lon

229 e pioneer transcription factor Sox2 requires PARP1 to bind to a subset of its recognition motifs, whi

230 an SDH-targeting molecule that induced RIP1/PARP1-mediated necroptosis and inhibited tumor growth.

231 l of combining niraparib, a highly selective PARP1/2 inhibitor, with anti-PD-1 immune checkpoint inhi

232 In patient-derived OSCC specimens, PARP1 expression was increased 7.8 +/- 2.6-fold when com

233 ylation-deficient PARP1-E988K, formed stable PARP1 foci upon activation.

234 ecruited at NSD2-regulated genes, suggesting PARP1 regulates NSD2 localization and H3K36me2 balance.

235 optical imaging agent to specifically target PARP1 expression, which was demonstrated to be higher in

236 man histological tissues, the probes target, PARP1, was highly expressed in DIPG compared to normal b

237 Therefore, targeting PARP1 activity may be an effective treatment for EBV-ass

238 mature mRNA, albeit to a lesser extent than PARP1 KD.

239 We demonstrate that PARP1 is required for HR by modulating nucleosome densit

240 We demonstrate that PARP1 regulates NSD2 via PARylation upon oxidative stres

241 Unexpectedly, we found that PARP1 exchanges rapidly at DNA damage sites even in the

242 These results indicate that PARP1 promotes IAV replication by controlling viral HA-i

243 AFM volume analysis indicates that PARP1 binds to DNA at nicks, abasic (AP) sites, and ends

244 These experiments revealed that PARP1 conducted damage search mostly through 3D diffusio

245 Here, we show that PARP1 plays an additional DDB2-independent direct role i

246 D+ interacting residues of PARP1 showed that PARP1 can be physically trapped at DNA damage sites, and

247 in nonsense-mediated decay, suggesting that PARP1 might be involved in mRNA stability.

248 The PARP1 inhibitor could serve as the basis of a rapid and

249 The PARP1-associated DNA repair pathway was extensively comp

250 ed NAD+ interacting residues involved in the PARP1 exchange.

251 ed by a 23-nucleotide G-rich sequence in the PARP1 promoter.

252 ted poly(ADP-ribose) chains and mediates the PARP1-dependent recruitment of ZBTB24 to DNA breaks.

253 targeting MUC1-C disrupts epigenetics of the PARP1 complex, inhibits PARP1 activity, and is synergist

254 We find that the presence of the PARP1 protein with uncompromised DNA-binding activities

255 s a approximately 100-kb region spanning the PARP1 gene.

256 ing purified proteins, we also show that the PARP1-XPC complex facilitates the handover of XPC to the

257 ymerase beta at damaged telomeres, while the PARP1/2 inhibitor only has such an effect at non-telomer

258 -canonical G-quadruplex structure within the PARP1 promoter, which could serve as an alternative ther

259 orming sequence containing bulges within the PARP1 promoter.

260 ed by various PARPi closely depends on their PARP1 trapping activities.

261 In a syngeneic DLBCL mouse model, this PARP1-targeted PET imaging approach allowed us to discri

262 r blocking replication fork reversal through PARP1 inhibition or depleting UBC13 or ZRANB3 prevents t

263 Thus, PARP1 inhibition could target cancers exhibiting XRN2 fu

264 ral of these contain candidate genes (TINF2, PARP1, TERF1, ATM and POT1) with potential roles in telo

265 of immediate early genes (IEG) accessible to PARP1-bound phosphorylated Erk2.

266 e lesions promote direct binding of Banf1 to PARP1, a critical NAD(+)-dependent DNA repair protein, l

267 qMS), we found that the lncRNA BGL3 binds to PARP1 and BARD1, exhibiting unexpected roles in homologo

268 ystal structures of these compounds bound to PARP1 or PARP2.

269 tions decline, DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapid

270 and its impact on cancer cell resistance to PARP1 inhibitors.

271 show that Atm-deficient CLL is sensitive to PARP1 inhibition.

272 oliferating leukemia cells were sensitive to PARP1 inhibitors that were administered alone or in comb

273 ancer cells also demonstrated sensitivity to PARP1 inhibition.

274 malignancies, the ability of 'non-trapping' PARP1 degraders to avoid the activation of innate immune

275 nhibits PARP1/2 enzymatic activity and traps PARP1 on DNA at single-strand breaks, leading to replica

276 By measuring the half-lives of two PARP1-mRNA targets we found that the half-lives were sig

277 tes with and phosphorylates PARP1 at Tyr907 (PARP1 pTyr907 or pY907).

278 Here, we found unlike PARP1-mediated Poly-ADP-Ribosylation (PARylation) at gen

279 to the sites of DNA damage is dependent upon PARP1 activation and not dependent on ATM activation.

280 Upon recruitment via PARP1-triggered chromatin remodeling, CHD7 stimulates fu

281 IC50 = 100 pM vs TNKS2 and IC50 = 6.5 muM vs PARP1 for 14.

282 shed 'isogenic' human diploid cells in which PARP1 and/or PARP2, or PARP3 are deleted.

283 owever, the precise mechanisms through which PARP1 is activated and PAR is robustly synthesized are n

284 Co-localization of APE1 with PARP1 on DNA was found capable of inducing 1D diffusion

285 rs, UBQLN4 overexpression is associated with PARP1 inhibitor sensitivity.

286 BIR of telomeric DSBs competed with PARP1-, LIG3-, and XPF-dependent alternative nonhomologo

287 ks that have initially formed a complex with PARP1 and its binding partner XRCC1, this interaction ac

288 s BMI1 and EZH2, which formed complexes with PARP1 during the DNA damage response.

289 d ERCC1-XPF endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap

290 zymatic activity, but did not correlate with PARP1 expression.

291 )-binding site, the interaction of HPF1 with PARP1 or PARP2 is enhanced by allosteric networks that o

292 BMP pathway, Smad1 and Smad5, interact with PARP1 and can be ADP-ribosylated in vitro, whereas PARG

293 ver, we demonstrate that AR-Vs interact with PARP1 and PARP2 and are dependent upon their catalytic f

294 tensive and unique binding interactions with PARP1/2 proteins.

295 recruited to and significantly overlaps with PARP1 at DNA lesions and that the interaction between Sa

296 the known interaction of many proteins with PARP1 under steady-state conditions could have functiona

297 As HPF1 forms a joint active site with PARP1 or PARP2, our data implicate HPF1 as an important

298 Consistently, treatment with PARP1 inhibitor antagonized the anti-inflammatory effect

299 Treatment with PARP1 inhibitors, followed by transfer of polyclonal NK

300 ositively correlated with PCNA, APE1, XRCC1, PARP1, Chk1, and Chk2 across these 6 tumor tissue types;