ライフサイエンスコーパス: PARP1

1 PARP1 also transformed TERT-immortalized melanocytes exp

2 PARP1 and PAR are integral players in the early DNA dama

3 PARP1 binds to and modifies PAP by poly(ADP-ribosyl)atio

4 PARP1 deficiency does not restore HR in Brca2(ko/ko) cel

5 PARP1 deficiency was also associated with a modulation o

6 PARP1 inhibition or depletion led to a decrease in LMP1-

7 PARP1 inhibition resulted in the accumulation of the rep

8 PARP1 inhibition, silencing, or genetic deletion abrogat

9 PARP1 pY907 increases PARP1 enzymatic activity and reduc

10 PARP1 regulates gene expression by numerous mechanisms,

11 PARP1 was recruited to DNA damage within condensed chrom

12 PARP1, the most abundant isoform, regulates the expressi

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

14 PARP1-mediated senescence rescue was accompanied by tran

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

16 EJ proteins, poly-(ADP-ribose) polymerase 1 (PARP1) and DNA ligase IIIalpha, were increased in the BC

17 reover, CHFR ubiquitinates PAR polymerase 1 (PARP1) and regulates chromatin-associated PARP1 in vivo.

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

19 , we identify poly(ADP-ribose) polymerase 1 (PARP1) as a previously unidentified and critical mediato

20 mitochondrial poly(ADP-ribose) polymerase 1 (PARP1) by the cyclic adenosine monophosphate (cAMP)/prot

21 Poly(ADP-ribose) (PAR) polymerase 1 (PARP1) catalyzes the poly(ADP-ribosyl)ation (PARylation)

22 ta (TOP2beta)/poly(ADP ribose) polymerase 1 (PARP1) complex are necessary for NR-mediated SWI/SNF-dep

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

24 Poly(ADP-ribose) polymerase 1 (PARP1) inhibitors were recently shown to have potential

25 Poly(ADP-ribose) polymerase 1 (PARP1) interacts genetically with the DNA-dependent prot

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

27 e showed that poly(ADP-ribose) polymerase 1 (PARP1) is modified by SUMO2/3 at mitotic centromeres and

28 primarily by poly(ADP-ribose) polymerase 1 (PARP1) is responsible for the rapid decondensation of ch

29 ly influenced poly(ADP ribose) polymerase 1 (PARP1) localization, with increased cytoplasmic and decr

30 at the enzyme poly(ADP-ribose) polymerase 1 (PARP1) modifies PAP and regulates its activity both in v

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

32 tion sites on Poly(ADP-ribose) Polymerase 1 (PARP1) with mass spectrometry and discuss a structure-ba

33 igase 3alpha, poly(ADP-ribose) polymerase 1 (PARP1), and X-ray repair cross-complementing protein 1 (

34 catalyzed by poly(ADP-ribose) polymerase 1 (PARP1), is crucial for cellular responses to DNA damage.

35 eta-catenin, poly (ADP-ribose) polymerase 1 (PARP1), or enhancer of zeste homolog 2 (EZH2) suppressed

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

37 dependent on poly (ADP-ribose) polymerase 1 (PARP1), which ADP ribosylates KDM4D after damage.

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

39 ase 1 (APE1), poly(ADP-ribose) polymerase 1 (PARP1), X-ray repair cross-complementing protein 1 (XRCC

40 damage sensor poly-ADP ribose polymerase 1 (PARP1).

41 bosylation of poly(ADP-ribose) polymerase 1 (PARP1).

42 ted mainly by poly(ADP-ribose) polymerase 1 (PARP1).

43 y initiated by poly ADP-ribose polymerase 1 (PARP1).

44 Poly(ADP-ribose) polymerase 1 (PARP1, also known as ARTD1) is an abundant nuclear enzym

45 uclear enzyme poly(ADP-ribose) polymerase-1 (PARP1) causes neuron death in brain hypoxia/ischemia by

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

47 activation of poly(ADP-ribose) polymerase-1 (PARP1).

48 c target genes such as caspase 3, caspase 7, PARP1, and Apaf-1 and activates their expression after D

49 SIRT7 is recruited in a PARP1-dependent manner to sites of DNA damage, where it

50 eading to inhibition of polyadenylation in a PARP1-dependent manner.

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

52 chondroitin sulfate proteoglycans activates PARP1, resulting in the accumulation of poly(ADP-ribose)

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

54 In contrast, although PARP1 also seemed to facilitate the association of UHRF1

55 s essential for efficient interactions among PARP1, IKKgamma, and PIASy, the modifications of IKKgamm

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

57 The novel mutation targets, CHEK2 and PARP1, were further screened in expanded DLBCL cohorts,

58 damage response targets ATM, ATR, CHK1, and PARP1 were upregulated in GSCs, and CHK1 was preferentia

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

60 ced DNA damage occurs by PARP1-dependent and PARP1-independent sub-pathways of BER.

61 g between DNA methyltransferases (DNMTs) and PARP1.

62 in telomere maintenance, including hPOT1 and PARP1.

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

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

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

66 st the involvement of CtIP, FEN1, MRE11, and PARP1 in mitochondrial MMEJ.

67 s demonstrated by experiments where PARG and PARP1 are simultaneously silenced.

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

69 two DNA damage response proteins, SIRT1 and PARP1, that are each consumers of nicotinamide adenine d

70 ken DT40 cells, we demonstrate that TDP1 and PARP1 are epistatic for the repair of Top1cc.

71 By generating TDP1 and PARP1 double-knockout lymphoma chicken DT40 cells, we de

72 analysis of lung tissue isolated from WT and PARP1 KO mice.

73 It has been shown that XRCC1 and PARP1 are involved in the repair of base lesions and SSB

74 of APE1 interaction with Polbeta, XRCC1 and PARP1 is revealed to be modulated by BER intermediates t

75 ment of the Polbeta complexes with XRCC1 and PARP1, while having no detectable influence on the prote

76 -pathway of BER that requires both XRCC1 and PARP1.

77 ins, including histone H1 (HON1), XRCC1, and PARP1, participate in a 'backup' (b)NHEJ process.

78 ns between the APE1-Polbeta, APE1-TDP1, APE1-PARP1 and Polbeta-TDP1 pairs have been detected and char

79 Comparing the target profiles of ARTD1 (PARP1) and ARTD2 (PARP2) in nuclear extracts highlighted

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

81 s of dihydrodibenzo[b,e]-oxepin compounds as PARP1 inhibitors.

82 1 (PARP1) and regulates chromatin-associated PARP1 in vivo.

83 ted by treatment with a clinically available PARP1 inhibitor.

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

85 we uncovered a cooperative interplay between PARP1 and UHRF1 in the accumulation of the heterochromat

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

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

88 so facilitated the dissociation of DNA-bound PARP1.

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

90 through the regulation of PARP1 activity by PARP1 phosphorylation.

91 the XPC-RAD23B are poly(ADP-ribosyl)ated by PARP1.

92 that poly(ADP-ribose) synthesis catalysed by PARP1 at the sites of unrepaired SBs activates ARF trans

93 Poly-ADP-ribosylation, catalyzed by PARP1, is a post-translational modification playing a pr

94 arget of poly(ADP-ribosyl)ation catalyzed by PARP1, which can be regarded as a universal regulator of

95 neuronal survival similar to those caused by PARP1 activation.

96 HEJ is the displacement of the Ku complex by PARP1.

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

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

99 s during BMP signaling can be neutralized by PARP1, as demonstrated by experiments where PARG and PAR

100 The repair of induced DNA damage occurs by PARP1-dependent and PARP1-independent sub-pathways of BE

101 al domain of PARP1, and TDP1 is PARylated by PARP1.

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

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

104 tion, and promotes interaction with cellular PARP1.

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

106 These data define PARP1 as a critical mediator of chromosomal translocatio

107 Together, these data illustrate a direct PARP1-mediated hypoxic signaling pathway involving NAD(+

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

109 cultures was mitigated by deletion of either PARP1 or Bnip3, indicating that both factors are involve

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

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

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

113 Finally, PARP1 inhibition also reduced both ionizing radiation-ge

114 ofound and prolonged G(2)/M arrest following PARP1/2 inhibitor treatment.

115 The molecular basis for PARP1 inhibitor function is complex, and appears to depe

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

117 rmation, demonstrating an essential role for PARP1 activity in LMP1-induced gene expression and cellu

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

119 The emitted signal was specific for PARP1 expression and, most importantly, PARPi-FL can be

120 rotein-induced NAD(+) depletion results from PARP1-independent excessive protein ADP-ribosylations.

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

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

123 nd enhanced pharmacodynamic endpoints (e.g., PARP1 hyperactivation, gammaH2AX, and ATP depletion).

124 either involved known melanoma genes (e.g., PARP1, CDKN2A) or cosegregated with melanoma (duplicatio

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

126 Together, this report identifies PARP1 as a novel modulator of two UHRF1-regulated hetero

127 This work identifies PARP1 as a key component driving the repair of trapped T

128 essing of mRNA precursors, and also identify PARP1 as a regulator of polyadenylation during thermal s

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

130 nisms of axon growth inhibition and identify PARP1 as an effective target to promote axon regeneratio

131 for the generation of radial chromosomes in PARP1 inhibitor-treated Brca1-deficient cells.

132 e-induced damage to the mitochondrial DNA in PARP1-depleted cells was found to be more robust compare

133 on, mitochondrial biogenesis was enhanced in PARP1-depleted cells, including mitochondrial DNA copy n

134 or to promote radial chromosome formation in PARP1 inhibitor-treated Brca1-deficient cells.

135 ccumulation in vitro and in vivo resulted in PARP1 overactivation and dopaminergic cell toxicity via

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

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

138 covalently bind DNMTs into DNA and increase PARP1 tightly bound into chromatin.

139 n our simulations, we observe that increased PARP1 activity may be able to trigger SIRT1-induced circ

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

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

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

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

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

145 1 demonstrated excellent potency (inhibiting PARP1 enzyme activity with IC50 = 0.079 muM), as well as

146 7 demonstrates excellent potency, inhibiting PARP1 and PARP2 enzyme activity with Ki = 1.2 and 0.87 n

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

148 NAD hydrolase activity in the two isoforms (PARP1, PARP2) that are highly expressed in leaves.

149 romoting tumorigenesis in thymocytes lacking PARP1 and DNA-PKcs.

150 KA activators enhanced, the oxidant-mediated PARP1 activation.

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

152 Our data show that intra-mitochondrial PARP1 interacts with a key mitochondrial-specific DNA ba

153 onclude that the activation of mitochondrial PARP1 is an early, active participant in oxidant-induced

154 In summary, we conclude that mitochondrial PARP1, in opposite to nuclear PARP1, exerts a negative e

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

156 mediate platinum sensitivity, also modulated PARP1/2 sensitivity.

157 n-spliced TyrRS catalytic null reveals a new PARP1- and NAD(+)-dependent dimension to the physiologic

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

159 Direct normoxic PARP1 activation by a DNA alkylating agent enhanced Bnip

160 mitochondrial oxidant production and nuclear PARP1 activation (by 6 hours).

161 mitochondrial PARP1, in opposite to nuclear PARP1, exerts a negative effect on several mitochondrial

162 Inhibition of PARP1, or abrogation of PARP1 expression, also suppressed the expression of LMP1

163 The absence of PARP1 led to reduced accumulation of H4K20me3 onto peric

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

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

166 al DNA damage, and concomitant activation of PARP1 in the mitochondria.

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

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

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

170 ciency as a clinically relevant biomarker of PARP1/2 inhibitor sensitivity.

171 Pharmacological blockade of PARP1 enzymatic activity impairs XRCC1-dependent repair

172 ed wild-type A549 cells or cells depleted of PARP1.

173 TDP1 directly binds the C-terminal domain of PARP1, and TDP1 is PARylated by PARP1.

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

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

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

177 pproaches, we have analyzed the influence of PARP1 and PAR synthesis on the interaction of XPC-RAD23B

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

179 Inhibition of PARP1 through gene deletion or drug inhibition reversed

180 Inhibition of PARP1, or abrogation of PARP1 expression, also suppresse

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

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

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

184 sensitivity to small-molecule inhibitors of PARP1.

185 Small-molecule inhibitors of PARP1/2, such as olaparib, have been proposed to serve a

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

187 nal poly(ADP-ribose)-mediated interaction of PARP1 with the E3 ubiquitin ligase UHRF1 (also known as

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

189 pidly, pathway choice and the involvement of PARP1 are highly dependent on the types of lesion induce

190 ological inhibition of PARP and knockdown of PARP1 induced the expression of EZH2, which resulted in

191 Knockdown of PARP1 or PARP2 (but not PARP3 and PARP4) not only increa

192 ents confirmed that the expression levels of PARP1 and DNA ligase IIIalpha correlated with the sensit

193 Thus, the expression levels of PARP1 and DNA ligase IIIalpha serve as biomarkers to ide

194 Although a mitochondrial localization of PARP1 has been suggested, its role in the maintenance of

195 ary cells and tissues indicates that loss of PARP1 increases in vivo radiosensitivity and genomic ins

196 harmacological inhibition or genetic loss of PARP1 markedly facilitates axon regeneration over nonper

197 hesized that Bnip3 is a critical mediator of PARP1-induced mitochondrial dysfunction and neuron death

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

199 as significantly affected in the presence of PARP1.

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

201 acilitate the lesion-specific recruitment of PARP1 and IKKgamma and, ultimately, the concomitant recr

202 ptor/cAMP/PKA axis through the regulation of PARP1 activity by PARP1 phosphorylation.

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

204 This study demonstrates a critical role of PARP1 in mediating SMC loss in patients with HGPS and el

205 entifies for the first time a direct role of PARP1 in regulating the expression and function of EZH2.

206 The positive role of PARP1 in regulation of various nuclear DNA transactions

207 Here we investigated the role of PARP1 in the repair of the mitochondrial DNA in the base

208 , and appears to depend on the dual roles of PARP1 in DNA damage repair and transcriptional regulatio

209 ulation stimulates a powerful suppression of PARP1 and consequently triggers an activation of the err

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

211 , particularly in ongoing clinical trials of PARP1/2 inhibitors and other agents that trigger replica

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

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

214 logous end-joining (A-NHEJ), which relies on PARP1 and LIG3.

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

216 vely monitors interactions between PARylated PARP1 and XRCC1.

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

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

219 we define the effects that PARP1, PARylated PARP1, and PAR have on RECQL5 and WRN, using both in vit

220 WRN have differential responses to PARylated PARP1 and PAR.

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

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

223 The PAR polymerase PARP1 binds to damaged chromatin and synthesizes PAR cha

224 Olaparib pretreatment, PARP1 knockdown or Parp1 heterozygosity of Brca2(cko/ko)

225 elicases), DNA repair/replication processes (PARP1, MSH2, Ku, DNA-PKcs, MCM proteins, PCNA and DNA Po

226 Hypoxia produced PARP1-dependent depletion of nicotinamide adenine dinucl

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

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

229 nant PKA directly phosphorylated recombinant PARP1 on serines 465 (in the automodification domain) an

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

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

232 he basic domain of TRF2 (TRF2(B)) to repress PARP1 and SLX4 localization to telomeres.

233 amage may require XRCC1 but does not require PARP1 activity.

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

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

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

237 mitotic SUMOylation, we analyzed SUMOylated PARP1-specific binding proteins.

238 ICH) as an interaction partner of SUMOylated PARP1 in Xenopus egg extract.

239 Propranolol also suppressed PARP1 activation in peripheral blood leukocytes during b

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

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

242 TDP1-PARP1 complexes, in turn recruit X-ray repair cross-comp

243 arms of the circadian regulation and 2) that PARP1 is a major consumer of NAD during the DNA damage r

244 Chromatin immunoprecipitation confirmed that PARP1 inhibition led to H3K27me3 deposition at EZH2 targ

245 In conclusion, our results demonstrate that PARP1 and PAR actively, and in some instances differenti

246 Furthermore, we define the effects that PARP1, PARylated PARP1, and PAR have on RECQL5 and WRN,

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

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

249 Here we show that PARP1 plays a critical role in this process.

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

251 On the other hand, we showed that PARP1 controls the UHRF1-mediated ubiquitination of DNMT

252 Collectively, our results suggest that PARP1 imaging with PARPi-FL can enhance the detection of

253 This study suggests that PARP1/2 inhibitors as a monotherapy could represent a no

254 The PARP1-associated DNA repair pathway was extensively comp

255 drolase (PARG) to completely disassemble the PARP1-XRCC1 complex without assistance from a mono(ADP-r

256 ith the free radical scavenger Tempol or the PARP1 inhibitor 3-aminobenzamide attenuated irradiation-

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

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

259 vity in vitro nor it sensitized cells to the PARP1 inhibitor olaparib.

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

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

262 bitory histone modification H3K27me3 through PARP1 activation.

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

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

265 pharmacologic PARP inhibitors as well as to PARP1-targeting siRNAs by initiating a DNA damage respon

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

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

268 ncer cells appear to develop a dependency to PARP1, becoming susceptible to PARP inhibitor-induced ap

269 proteins in the nucleus, providing a path to PARP1 activation other than DNA damage.

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

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

272 tion was sufficient to confer sensitivity to PARP1/2 inhibition, suppression of DNA repair via homolo

273 re known previously to confer sensitivity to PARP1/2 inhibition.

274 to establishing Ku-BRG1 binding and TOP2beta/PARP1 recruitment by nuclear receptor transactivation, w

275 Indeed, in clinical trials, PARP1/2 inhibitors elicit sustained antitumor responses

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

277 ing pathways are causally connected to TyrRS-PARP1-NAD(+) collaboration.

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 LMP1) and PAR levels that was dependent upon PARP1.

281 that TRPM2 is activated by irradiation, via PARP1 activation, and contributes to irreversible loss o

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

283 Therefore, we asked whether PARP1 inhibition could prevent chromosomal translocation

284 Here we investigated whether PARP1 and PARP2 were also involved in B-NHEJ in Arabidop

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

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

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

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

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

292 scaffold and unique binding interaction with PARP1 protein.

293 , through its constitutive interactions with PARP1 and IKKgamma, functions to facilitate the lesion-s

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

295 ate that LRP16 constitutively interacts with PARP1 and IKKgamma.

296 art of its role in DDR, Filia interacts with PARP1 and stimulates its enzymatic activity.

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

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

299 Although the XRCC1-PARP1 complex is relevant to the proposed therapeutic me

300 rated that 7 genes (FEN1, RFC5, EXO1, XRCC5, PARP1, POLR2F, and GTF2H3) that were relatively up-regul