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1 cision repair was blocked by an inhibitor of polyADP ribose polymerase.
2 e consisting of caspase-3 and -7 and cleaved poly(ADP)-ribose polymerase.
3 ch, in turn, activates the DNA repair enzyme poly(ADP)-ribose polymerase.
4 zed human cells to olaparib, an inhibitor of poly(ADP-ribose) polymerase.
5 tential pharmaceutical target tankyrase 1, a poly(ADP-ribose) polymerase.
6 hondria, caspase 3 activity, and cleavage of poly(ADP-ribose) polymerase.
7 caspase-3 and cleaved the caspase substrate poly(ADP-ribose) polymerase.
8 f apoptotic mediators, such as caspase-3 and poly(ADP-ribose) polymerase.
9 ncreased the expression of apoptotic cleaved poly(ADP-ribose) polymerase.
10 ious enzyme families, including sirtuins and poly(ADP-ribose) polymerases.
11 HR, but confers sensitivity to inhibition of poly(ADP-ribose) polymerases.
12 e polymers, thereby reversing the effects of poly(ADP-ribose) polymerases.
13 endent enzymes, including sirtuins, CD38 and poly(ADP-ribose) polymerases.
14 erases, including a subset commonly known as poly(ADP-ribose) polymerases.
15 eference as caspase-3, is better at cleaving poly(ADP ribose) polymerase 1 (PARP) and Hsp90 cochapero
16 nents of the topoisomerase IIbeta (TOP2beta)/poly(ADP ribose) polymerase 1 (PARP1) complex are necess
17 ingly, mtp53 depletion profoundly influenced poly(ADP ribose) polymerase 1 (PARP1) localization, with
18 ion, Rev1-deficiency is associated with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endo
19 ing, whereas DNA repair pathways mediated by poly(ADP)ribose polymerase 1 (PARP1) serve as backups.
20 ing evidence shows that chromatin-associated poly(ADP-ribose) polymerase 1 (PARP-1) and its enzymatic
21 E4orf4 associates with the DNA damage sensor poly(ADP-ribose) polymerase 1 (PARP-1) and that the asso
22 role for NEDD8 in regulating the activity of poly(ADP-ribose) polymerase 1 (PARP-1) in response to ox
28 ins DNA-dependent protein kinase (DNA-PK) or poly(ADP-ribose) polymerase 1 (PARP-1) prevented the DNA
29 B and SP1 bind to a composite element in the poly(ADP-ribose) polymerase 1 (PARP-1) promoter in a mut
30 ite and promote the rapid proteolysis of the poly(ADP-ribose) polymerase 1 (PARP-1), but the mechanis
32 ivates the central DNA damage sensor protein poly(ADP-ribose) polymerase 1 (PARP1) and activates casp
34 ically, we found that ZBTB24 associates with poly(ADP-ribose) polymerase 1 (PARP1) and stimulates its
37 investigated the regulation of mitochondrial poly(ADP-ribose) polymerase 1 (PARP1) by the cyclic aden
39 ation of caspase 3 and caspase 9, along with poly(ADP-ribose) polymerase 1 (PARP1) cleavage, which is
40 -molecule inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP1) for the detection
42 response to a variety of cellular stresses, poly(ADP-ribose) polymerase 1 (PARP1) has vital roles in
43 er checkpoint kinase 1 (CHK1) inhibitors and poly(ADP-ribose) polymerase 1 (PARP1) inhibitors interac
47 n Xenopus egg extract assays, we showed that poly(ADP-ribose) polymerase 1 (PARP1) is modified by SUM
48 poly(ADP-ribosyl)ation mediated primarily by poly(ADP-ribose) polymerase 1 (PARP1) is responsible for
50 ity in identifying ADP-ribosylation sites on Poly(ADP-ribose) Polymerase 1 (PARP1) with mass spectrom
51 h increased expression of DNA ligase 3alpha, poly(ADP-ribose) polymerase 1 (PARP1), and X-ray repair
52 Here, we have found that a host protein, poly(ADP-ribose) polymerase 1 (PARP1), facilitates IFNAR
53 -ribose (PAR) chains, primarily catalyzed by poly(ADP-ribose) polymerase 1 (PARP1), is crucial for ce
54 y also contain other factors, including PML, poly(ADP-ribose) polymerase 1 (PARP1), ligase IIIalpha,
56 ng these, an important DNA damage regulator, poly(ADP-ribose) polymerase 1 (PARP1), was discovered.
57 e major enzyme that catalyses this reaction, poly(ADP-ribose) polymerase 1 (PARP1), were discovered m
58 apurinic/apyrimidinic endonuclease 1 (APE1), poly(ADP-ribose) polymerase 1 (PARP1), X-ray repair cros
59 protects replication forks from stalling at poly(ADP-ribose) polymerase 1 (PARP1)-DNA complexes trap
63 , we found that recruitment was dependent on poly(ADP-ribose) polymerase 1 activity as well as Kdm4b
64 to and irreversibly inhibits the activity of poly(ADP-ribose) polymerase 1, an important anticancer t
65 oskeleton while promoting the degradation of poly(ADP-ribose) polymerase 1, an inhibitor of osteoclas
66 hat the SNAT2 ER-alpha-ERE complex contained poly(ADP-ribose) polymerase 1, Lupus Ku autoantigen prot
70 Here, we demonstrate that the nuclear enzyme Poly(ADP-ribose)Polymerase 1 (PARP1) is a promising targ
71 e, lack of hepatocyte HMGB1 led to excessive poly(ADP-ribose)polymerase 1 activation, exhausting nico
72 ion of caspases 3, 7, 8, and 9 and inhibited poly(ADP-ribose)polymerase 1 cleavage and DNA fragmentat
74 large Ca(2+) and Na(+) influx, activation of poly(ADP ribose) polymerase-1 (PARP-1), and delayed Ca(2
75 ecting parthanatos, monitored by cleavage of poly(ADP ribose)polymerase-1 (PARP-1), or necroptosis, a
76 combination of LuTate and the small molecule Poly(ADP-ribose) polymerase-1 (PARP) inhibitor, talazopa
79 ze nuclear LXRalpha complexes and identified poly(ADP-ribose) polymerase-1 (PARP-1) as an LXR-associa
90 PAH-PASMCs have increased the activation of poly(ADP-ribose) polymerase-1 (PARP-1), a critical enzym
91 poly(ADP-ribosyl)ation (i.e., PARylation) of poly(ADP-ribose) polymerase-1 (PARP-1), a multifunctiona
93 yrin repeat-containing protein that mediates poly(ADP-ribose) polymerase-1 (PARP-1)-dependent transcr
96 of DNA damage, neuroinflammation, increased poly(ADP-ribose) polymerase-1 (PARP1) activity, single-c
97 actors necessary for iPSC generation, namely poly(ADP-ribose) polymerase-1 (Parp1) and ten-eleven tra
98 he DNA-dependent protein kinase (DNA-PK) and Poly(ADP-ribose) polymerase-1 (PARP1) are critical enzym
99 physiological activity of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP1) causes neuron deat
103 is able to recruit the transcription factors poly(ADP-ribose) polymerase-1 and splicing factor prolin
107 repair; we found that salidroside activated poly(ADP-ribose)polymerase-1 (PARP-1), a component of th
111 e L1 endonuclease trigger the recruitment of poly(ADP-ribose) polymerase 2 (PARP2) to L1 integration
115 and RAD50 as suppressors and 53BP1, DDB1 and poly(ADP)ribose polymerase 3 (PARP3) as promoters of chr
118 involved in apoptosis (cleaved caspase-3 and poly(ADP-ribose)polymerase), acetylation of tumor suppre
119 increase in caspase-3, cytochrome c release, poly(ADP-ribose) polymerase activation, down-regulation
121 lies of enzymes consume NAD(+) as substrate: poly(ADP-ribose) polymerases, ADP-ribosyl cyclases (CD38
123 these conditions correlates with cleavage of poly(ADP-ribose) polymerase, an indicator of apoptosis.
125 is (p53, Fas, and MST1), DNA damage control (poly(ADP)-ribose polymerase and ataxia telangiectasia mu
126 1-XPF endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap format
127 at includes elevated CD38 NADase and reduced poly(ADP-ribose) polymerase and SIRT1 activities, respec
128 P-ribose) (pADPr) can be rapidly produced by poly(ADP-ribose) polymerases and degraded by poly(ADP-ri
129 ase and cleavage of caspases 3, 8, and 9 and poly(ADP ribose) polymerase, and suppressed survivin, my
130 Western blotting for the cleaved fragment of poly(ADP-ribose) polymerase, and the active isoform of c
131 y reduced cleavage of caspase-3, -8, and -9, poly(ADP-ribose) polymerase, and the externalization of
132 hibitors (PARPi), a cancer therapy targeting poly(ADP-ribose) polymerase, are the first clinically ap
133 ed to modulation of Bax, Bcl2, caspase-9 and poly(ADP-ribose) polymerase as well as Reactive Oxygen S
134 f the DNA damage marker gammaH2AX as well as poly(ADP-ribose) polymerase cleavage were elevated in SM
135 poptosis, as assessed by caspase-3 activity, poly(ADP-ribose) polymerase cleavage, phosphatidylserine
137 h the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppres
141 s are exquisitely sensitive to inhibition of poly(ADP-ribose) polymerase has ushered in a new era of
143 eflected by caspase-3/7 activity and cleaved poly(ADP-ribose) polymerase, in different cell lines tha
145 ability, hypersensitivity to DNA damage, and poly(ADP-ribose) polymerase inhibition associated with A
146 rate alpha-ketoglutarate or treatment with a poly(ADP ribose) polymerase inhibitor protects reductive
147 tions initially respond well to platinum and poly(ADP-ribose) polymerase inhibitor (PARPi) therapy; h
149 IEL3 provides further evidence that use of a poly(ADP-ribose) polymerase inhibitor in the maintenance
155 gagement of the chemotherapeutic Olaparib, a poly(ADP-ribose) polymerase inhibitor, in live cells and
156 cells with mutant p53 were resistant to the poly(ADP-ribose) polymerase inhibitor, veliparib (2-[(2R
160 tion forks is a prominent mechanism of PARP (Poly(ADP-ribose) Polymerase) inhibitor (PARPi) resistanc
162 uely responsible for cellular sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi) in BRCA1-
165 t samples, RITA, AF, and Onc-1 sensitized to poly(ADP-ribose) polymerase inhibitors both in vitro and
166 2-positive disease, bone stabilizing agents, poly(ADP-ribose) polymerase inhibitors for BRCA mutation
168 rt expansion of the treatment indication for poly(ADP-ribose) polymerase inhibitors to include patien
169 nt kinases 4 and 6, angiogenesis inhibitors, poly(ADP-ribose) polymerase inhibitors, as well as chemo
176 ated that, besides direct cytotoxic effects, poly(ADP ribose) polymerase (PARP) inhibitors (PARPis) e
178 w that ATAD5-depleted cells are sensitive to poly(ADP)ribose polymerase (PARP) inhibitors and that th
179 l series of tetrahydropyridophthlazinones as poly(ADP-ribose) polymerase (PARP) 1 and 2 inhibitors.
180 modification is catalyzed mainly by nuclear poly(ADP-ribose) polymerase (PARP) 1 in response to DNA
181 t its chromatin accumulation was enhanced in poly(ADP-ribose) polymerase (PARP) 1(-/-) compared with
182 nM), we observed loss of CIPs and increased poly(ADP-ribose) polymerase (PARP) activation [also obse
186 emonstrate that concurrent administration of poly(ADP-ribose) polymerase (PARP) and WEE1 inhibitors i
187 n BC3 and BCBL1 PEL cells but did not induce poly(ADP-ribose) polymerase (PARP) cleavage in virus-neg
188 hylation, induction of autophagy, and robust poly(ADP-ribose) polymerase (PARP) cleavage indicative o
190 vidence is provided that the activity of the poly(ADP-ribose) polymerase (Parp) enzyme is required fo
194 e a critical function of some members of the poly(ADP-ribose) polymerase (PARP) family in clearance o
197 ld, leading the way for the discovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and
201 ly(ADP-ribosyl)ated and that mutation of the poly(ADP-ribose) polymerase (Parp) gene impairs their fu
203 highly toxic DNA strand breaks that trigger poly(ADP-ribose) polymerase (Parp) hyperactivation, cell
206 t led to the automated radiosynthesis of the poly(ADP-ribose) polymerase (PARP) inhibitor [(18)F]olap
208 ion of BRCA2, could help select patients for poly(ADP-ribose) polymerase (PARP) inhibitor or platinum
209 DNA damage, BRCA1 localization to DSBs, and poly(ADP-ribose) polymerase (PARP) inhibitor resistance.
210 ng agents melphalan and cisplatin and to the poly(ADP-ribose) polymerase (PARP) inhibitor veliparib (
214 9 rendered GLS(high) cells vulnerable to the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib,
216 and breaks and disruption of this pathway by Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) is
217 understanding acquired tumour resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and other
218 RCA2-mutated breast cancers are sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors and platin
224 eterogeneous responses to platinum drugs and poly(ADP-ribose) polymerase (PARP) inhibitors in clinica
225 ical trials exploiting this concept by using poly(ADP-ribose) polymerase (PARP) inhibitors in patient
226 In the present study we observed that the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib a
227 ression levels show increased sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors, especiall
228 eutic drugs that block DNA repair, including poly(ADP-ribose) polymerase (PARP) inhibitors, fail due
229 fold is an important structural motif of new poly(ADP-ribose) polymerase (PARP) inhibitors, playing a
230 tizes tumors to DNA cross-linking agents and poly(ADP-ribose) polymerase (PARP) inhibitors, we sought
232 provide insight into why clinical trials of poly(ADP-ribose) polymerase (PARP) inhibitors, which req
244 Human tankyrase-1 (TNKS) is a member of the poly(ADP-ribose) polymerase (PARP) superfamily of protei
245 ication effected by enzymes belonging to the poly(ADP-ribose) polymerase (PARP) superfamily, mainly b
249 ed caspase 3, cleaved caspase 9, and cleaved poly(ADP-ribose) polymerase (PARP), suggesting that impa
250 ed by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation
251 while p65NF-kappaB phosphorylation, cleaved poly(ADP-ribose) polymerase (PARP)-1, and cyclooxygenase
252 er at their C termini: ZAPL (long) encodes a poly(ADP-ribose) polymerase (PARP)-like domain that is m
258 ivo, we show that the anti-apoptotic protein poly(ADP-ribose) polymerase (PARP)14 promotes aerobic gl
259 ediated apoptosis by affecting expression of poly(ADP-ribose) polymerase (PARP)14, a key regulator of
260 e minutes) through mechanisms that depend on poly(ADP-ribose) polymerases (PARP) and the catalytic su
262 r targets are the tankyrase proteins (TNKS), poly(ADP-ribose) polymerases (PARP) that regulate Wnt si
270 al modification, is immediately catalyzed by poly(ADP-ribose) polymerases (PARPs) at DNA lesions, whi
271 unveil the mechanisms by which inhibition of poly(ADP-ribose) polymerases (PARPs) elicits clinical be
272 longing to the tankyrase (Tnks) subfamily of poly(ADP-ribose) polymerases (PARPs) have recently been
274 posttranslational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) that mediate EBV re
275 It forms DNA adducts, thereby activating poly(ADP-ribose) polymerases (PARPs) to initiate DNA rep
276 posttranslational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) using NAD(+) as ADP
281 sed apoptosis characterized by caspase 3 and poly(ADP-ribose) polymerase processing, DNA cleavage, an
282 ch damages DNA and causes hyperactivation of poly(ADP-ribose) polymerase, resulting in extensive NAD(
283 otein PNKP and implicates hyperactivation of poly(ADP-ribose) polymerase/s as a cause of cerebellar a
284 ates for several NAD-consuming enzymes (e.g. poly(ADP-ribose) polymerases, sirtuins, and others).
286 the histone variant macroH2A1.1 binds to the poly(ADP-ribose) polymerase tankyrase 1, preventing it f
287 n be induced by inhibition of tankyrase 1, a poly(ADP-ribose) polymerase that is required for resolut
290 lation of downstream effector TCDD-inducible poly(ADP-ribose) polymerase (TiPARP) during infection.
291 tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly(ADP-ribose) polymerase (TiPARP) gene expression, de
292 ere, we show that the loss of TCDD-inducible poly(ADP-ribose) polymerase (Tiparp), an ADP-ribosyltran
293 AhR repressor (Ahrr/AhRR) and TCDD-inducible poly(ADP-ribose)polymerase (Tiparp/TiPARP) by AhR ligand
294 se 3 and cleavage of the caspase 3 substrate poly(ADP-ribose) polymerase were inhibited in E. faecali
295 rker proteins, cleaved caspase 7 and cleaved poly(ADP-ribose) polymerase, were significantly reduced
298 ncer cells and decreases the level of intact poly(ADP-ribose) polymerase, which is indicative of apop
299 DNA damage was associated with activation of poly(ADP-ribose) polymerase, which led to consumption of
300 AD precursors, exercise regimens, or loss of poly(ADP-ribose) polymerases yet surprisingly do not exh