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1 elastatin-like 2 (TRPM2), via stimulation of poly-ADP-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 tential pharmaceutical target tankyrase 1, a poly(ADP-ribose) polymerase.
5 hondria, caspase 3 activity, and cleavage of poly(ADP-ribose) polymerase.
6 caspase-3 and cleaved the caspase substrate poly(ADP-ribose) polymerase.
7 f apoptotic mediators, such as caspase-3 and poly(ADP-ribose) polymerase.
8 ncreased the expression of apoptotic cleaved poly(ADP-ribose) polymerase.
9 zed human cells to olaparib, an inhibitor of poly(ADP-ribose) polymerase.
10 release, caspase 3 activity, and cleavage of poly (ADP-ribose) polymerase.
11 HR, but confers sensitivity to inhibition of poly(ADP-ribose) polymerases.
12 ious enzyme families, including sirtuins and poly(ADP-ribose) polymerases.
13 ide together with velaparib, an inhibitor of poly (ADP ribose) polymerase 1, is increased by up to 10
14 005) concomitant with an increase in cleaved poly (ADP-ribose) polymerase 1 (P < 0.05), indicative of
17 langiectasia mutated (ATM), but dependent on poly (ADP-ribose) polymerase 1 (PARP1), which ADP ribosy
18 lementing protein 1, DNA polymerase beta, or poly (ADP-ribose) polymerase 1 activity, all of which fa
19 oughput screens identified multiple clinical poly (ADP-ribose) polymerase 1 and 2 (PARP1/2) inhibitor
25 eference as caspase-3, is better at cleaving poly(ADP ribose) polymerase 1 (PARP) and Hsp90 cochapero
26 nents of the topoisomerase IIbeta (TOP2beta)/poly(ADP ribose) polymerase 1 (PARP1) complex are necess
27 ingly, mtp53 depletion profoundly influenced poly(ADP ribose) polymerase 1 (PARP1) localization, with
28 ion, Rev1-deficiency is associated with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endo
29 ing, whereas DNA repair pathways mediated by poly(ADP)ribose polymerase 1 (PARP1) serve as backups.
31 ins DNA-dependent protein kinase (DNA-PK) or poly(ADP-ribose) polymerase 1 (PARP-1) prevented the DNA
32 B and SP1 bind to a composite element in the poly(ADP-ribose) polymerase 1 (PARP-1) promoter in a mut
35 investigated the regulation of mitochondrial poly(ADP-ribose) polymerase 1 (PARP1) by the cyclic aden
37 ation of caspase 3 and caspase 9, along with poly(ADP-ribose) polymerase 1 (PARP1) cleavage, which is
41 n Xenopus egg extract assays, we showed that poly(ADP-ribose) polymerase 1 (PARP1) is modified by SUM
42 poly(ADP-ribosyl)ation mediated primarily by poly(ADP-ribose) polymerase 1 (PARP1) is responsible for
44 ity in identifying ADP-ribosylation sites on Poly(ADP-ribose) Polymerase 1 (PARP1) with mass spectrom
45 h increased expression of DNA ligase 3alpha, poly(ADP-ribose) polymerase 1 (PARP1), and X-ray repair
46 -ribose (PAR) chains, primarily catalyzed by poly(ADP-ribose) polymerase 1 (PARP1), is crucial for ce
47 apurinic/apyrimidinic endonuclease 1 (APE1), poly(ADP-ribose) polymerase 1 (PARP1), X-ray repair cros
51 , we found that recruitment was dependent on poly(ADP-ribose) polymerase 1 activity as well as Kdm4b
52 oskeleton while promoting the degradation of poly(ADP-ribose) polymerase 1, an inhibitor of osteoclas
53 hat the SNAT2 ER-alpha-ERE complex contained poly(ADP-ribose) polymerase 1, Lupus Ku autoantigen prot
57 Here, we demonstrate that the nuclear enzyme Poly(ADP-ribose)Polymerase 1 (PARP1) is a promising targ
58 e, lack of hepatocyte HMGB1 led to excessive poly(ADP-ribose)polymerase 1 activation, exhausting nico
59 teady state levels of two ALT NHEJ proteins, poly-(ADP-ribose) polymerase 1 (PARP1) and DNA ligase II
60 iated by the nuclear ADP-ribosylating enzyme poly-(ADP-ribose) polymerase 1 (PARP1) and the deribosyl
62 yl)ation (PARylation) is mainly catalysed by poly-ADP-ribose polymerase 1 (PARP1), whose role in gene
63 PET imaging strategy for DLBCL that targets poly[ADP ribose] polymerase 1 (PARP1), the expression of
65 thodologies for studying robust responses of poly (ADP-ribose) polymerase-1 (PARP-1) to DNA damage wi
67 ent of targeted agents such as inhibitors of poly (ADP-ribose) polymerase-1 and mTOR and immunomodula
68 Purpose To determine whether cotargeting poly (ADP-ribose) polymerase-1 plus androgen receptor is
71 1/cell-cycle, apoptotic genes, caspase-3 and poly ADP ribose polymerase-1 (PARP-1) cleavage) and was
72 large Ca(2+) and Na(+) influx, activation of poly(ADP ribose) polymerase-1 (PARP-1), and delayed Ca(2
73 ecting parthanatos, monitored by cleavage of poly(ADP ribose)polymerase-1 (PARP-1), or necroptosis, a
75 ze nuclear LXRalpha complexes and identified poly(ADP-ribose) polymerase-1 (PARP-1) as an LXR-associa
83 PAH-PASMCs have increased the activation of poly(ADP-ribose) polymerase-1 (PARP-1), a critical enzym
84 poly(ADP-ribosyl)ation (i.e., PARylation) of poly(ADP-ribose) polymerase-1 (PARP-1), a multifunctiona
86 yrin repeat-containing protein that mediates poly(ADP-ribose) polymerase-1 (PARP-1)-dependent transcr
89 he DNA-dependent protein kinase (DNA-PK) and Poly(ADP-ribose) polymerase-1 (PARP1) are critical enzym
90 physiological activity of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP1) causes neuron deat
93 is able to recruit the transcription factors poly(ADP-ribose) polymerase-1 and splicing factor prolin
96 repair; we found that salidroside activated poly(ADP-ribose)polymerase-1 (PARP-1), a component of th
100 (miRs), matrix metalloproteinases (MMPs) and poly-ADP-ribose-polymerase-1 (PARP-1) in diabetic kidney
106 and RAD50 as suppressors and 53BP1, DDB1 and poly(ADP)ribose polymerase 3 (PARP3) as promoters of chr
108 caspase-9 and caspase-3 and the cleavage of poly (ADP-ribose) polymerase; (5) upregulating pancreati
110 increase in caspase-3, cytochrome c release, poly(ADP-ribose) polymerase activation, down-regulation
113 lies of enzymes consume NAD(+) as substrate: poly(ADP-ribose) polymerases, ADP-ribosyl cyclases (CD38
115 these conditions correlates with cleavage of poly(ADP-ribose) polymerase, an indicator of apoptosis.
118 is (p53, Fas, and MST1), DNA damage control (poly(ADP)-ribose polymerase and ataxia telangiectasia mu
119 1-XPF endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap format
120 P-ribose) (pADPr) can be rapidly produced by poly(ADP-ribose) polymerases and degraded by poly(ADP-ri
122 creased levels of apoptotic markers, cleaved poly (ADP-ribose) polymerase, and caspase-3 and -8 (P <
123 tivation of caspase-8, caspase-9, caspase-3, poly (ADP-ribose) polymerase, and downregulation of Mcl-
125 ase and cleavage of caspases 3, 8, and 9 and poly(ADP ribose) polymerase, and suppressed survivin, my
126 Western blotting for the cleaved fragment of poly(ADP-ribose) polymerase, and the active isoform of c
127 y reduced cleavage of caspase-3, -8, and -9, poly(ADP-ribose) polymerase, and the externalization of
128 ntrols the activities of sirtuins, mono- and poly-(ADP-ribose) polymerases, and NAD nucleosidase.
129 hibitors (PARPi), a cancer therapy targeting poly(ADP-ribose) polymerase, are the first clinically ap
130 ed to modulation of Bax, Bcl2, caspase-9 and poly(ADP-ribose) polymerase as well as Reactive Oxygen S
131 caspase-8, and caspase-9 activation and less poly (ADP-ribose) polymerase cleavage compared with WT l
132 downregulation of glucose transporter-1 and poly (ADP-ribose) polymerase cleavage while preserving t
133 anism of cell death, involving apoptosis via poly (ADP-ribose) polymerase cleavage-independent of cas
134 P] followed by progressive ATP depletion and Poly ADP Ribose Polymerase cleavage, (2) increased vacuo
136 f the DNA damage marker gammaH2AX as well as poly(ADP-ribose) polymerase cleavage were elevated in SM
137 poptosis, as assessed by caspase-3 activity, poly(ADP-ribose) polymerase cleavage, phosphatidylserine
138 hout chilling) and more than 60% cleavage of poly-ADP ribose polymerase (compared to less than 5% in
139 h the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes to TCDD suppres
140 eath pathways demonstrated the activation of poly ADP-ribose polymerase-dependent cell death in bok-d
144 2 mutant channel (C1008-->A) or silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN
146 eflected by caspase-3/7 activity and cleaved poly(ADP-ribose) polymerase, in different cell lines tha
148 a potential marker of long-term response to poly (ADP-ribose) polymerase inhibition and that restora
149 Purpose Data suggest that DNA damage by poly (ADP-ribose) polymerase inhibition and/or reduced v
151 ability, hypersensitivity to DNA damage, and poly(ADP-ribose) polymerase inhibition associated with A
153 rpose Durable and long-term responses to the poly (ADP-ribose) polymerase inhibitor olaparib are obse
157 mor-derived DNA were resistant to platin- or poly ADP ribose polymerase inhibitor-based chemotherapy.
158 rate alpha-ketoglutarate or treatment with a poly(ADP ribose) polymerase inhibitor protects reductive
159 tions initially respond well to platinum and poly(ADP-ribose) polymerase inhibitor (PARPi) therapy; h
161 IEL3 provides further evidence that use of a poly(ADP-ribose) polymerase inhibitor in the maintenance
166 gagement of the chemotherapeutic Olaparib, a poly(ADP-ribose) polymerase inhibitor, in live cells and
167 cells with mutant p53 were resistant to the poly(ADP-ribose) polymerase inhibitor, veliparib (2-[(2R
171 d treatments such as antiangiogenic drugs or poly (ADP-ribose) polymerase inhibitors offer potential
173 lethality anticancer therapeutics, including poly ADP-ribose polymerase inhibitors for BRCA1- and BRC
174 uely responsible for cellular sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi) in BRCA1-
177 overexpression of caspase-3, higher cleaved poly (ADP-ribose) polymerase levels (p < 0.007), and a h
178 HR-deficient cancers are hypersensitive to Poly (ADP ribose)-polymerase (PARP) inhibitors, but can
180 emicals were tested for inhibitory effect of poly (ADP-ribose) polymerase (PARP) activity in vitro an
185 oded by PML-RARA) are extremely sensitive to poly (ADP-ribose) polymerase (PARP) inhibition, in part
187 recent approval of olaparib (Lynparza), the poly (ADP-ribose) polymerase (PARP) inhibitor for treati
188 tudies suggested impressive potential when a poly (ADP-ribose) polymerase (PARP) inhibitor is given f
189 izes cancer cells to DNA damaging agents, to Poly (ADP-ribose) polymerase (PARP) inhibitors and cross
197 the sensitivity of BRCA1-deficient cells to poly ADP ribose polymerase (PARP) inhibition is partiall
198 /NF45-depleted HeLa cells displayed elevated poly ADP-ribose polymerase (PARP) cleavage and susceptib
201 l series of tetrahydropyridophthlazinones as poly(ADP-ribose) polymerase (PARP) 1 and 2 inhibitors.
202 t its chromatin accumulation was enhanced in poly(ADP-ribose) polymerase (PARP) 1(-/-) compared with
203 nM), we observed loss of CIPs and increased poly(ADP-ribose) polymerase (PARP) activation [also obse
206 n BC3 and BCBL1 PEL cells but did not induce poly(ADP-ribose) polymerase (PARP) cleavage in virus-neg
208 vidence is provided that the activity of the poly(ADP-ribose) polymerase (Parp) enzyme is required fo
212 e a critical function of some members of the poly(ADP-ribose) polymerase (PARP) family in clearance o
215 ld, leading the way for the discovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and
218 ly(ADP-ribosyl)ated and that mutation of the poly(ADP-ribose) polymerase (Parp) gene impairs their fu
219 highly toxic DNA strand breaks that trigger poly(ADP-ribose) polymerase (Parp) hyperactivation, cell
222 ng agents melphalan and cisplatin and to the poly(ADP-ribose) polymerase (PARP) inhibitor veliparib (
226 and breaks and disruption of this pathway by Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) is
229 eterogeneous responses to platinum drugs and poly(ADP-ribose) polymerase (PARP) inhibitors in clinica
230 ical trials exploiting this concept by using poly(ADP-ribose) polymerase (PARP) inhibitors in patient
231 In the present study we observed that the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib a
232 eutic drugs that block DNA repair, including poly(ADP-ribose) polymerase (PARP) inhibitors, fail due
233 tizes tumors to DNA cross-linking agents and poly(ADP-ribose) polymerase (PARP) inhibitors, we sought
235 provide insight into why clinical trials of poly(ADP-ribose) polymerase (PARP) inhibitors, which req
242 ication effected by enzymes belonging to the poly(ADP-ribose) polymerase (PARP) superfamily, mainly b
245 ed caspase 3, cleaved caspase 9, and cleaved poly(ADP-ribose) polymerase (PARP), suggesting that impa
246 ed by inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation
247 while p65NF-kappaB phosphorylation, cleaved poly(ADP-ribose) polymerase (PARP)-1, and cyclooxygenase
250 ivo, we show that the anti-apoptotic protein poly(ADP-ribose) polymerase (PARP)14 promotes aerobic gl
251 ediated apoptosis by affecting expression of poly(ADP-ribose) polymerase (PARP)14, a key regulator of
253 r targets are the tankyrase proteins (TNKS), poly(ADP-ribose) polymerases (PARP) that regulate Wnt si
255 r has been the exploitation of inhibitors of poly-(ADP-ribose) polymerase (PARP) for the treatment of
259 ty increases already in 1 hr after nsPEF and poly-ADP ribose polymerase (PARP) cleavage is detected i
262 We show that the latonduine analogs inhibit poly-ADP ribose polymerase (PARP) isozymes 1, 3, and 16.
263 t cancer associated proteins 1, 2 (BRCA1/2), Poly-ADP ribose polymerase (PARP), replication factor c2
264 eir cellular hyper-dependence on alternative poly-ADP ribose polymerase (PARP)-mediated DNA repair me
265 ith 3dSB or 3dSB-PNBS results in cleavage of poly-ADP-ribose polymerase (PARP) and caspase-9, both ma
266 cells and is catalyzed by 11 members of the poly-ADP-ribose polymerase (PARP) family of proteins (17
267 breaks (DSBs) and were modestly sensitive to poly-ADP-ribose polymerase (PARP) inhibitors olaparib an
268 otoxic alkylating agents, hyperactivation of poly-ADP-ribose polymerase (PARP) leads to cellular NAD
270 ys conserved in all eukaryotic cells include poly (ADP-ribose) polymerases (PARPs), sirtuins, AMP-act
274 al modification, is immediately catalyzed by poly(ADP-ribose) polymerases (PARPs) at DNA lesions, whi
275 unveil the mechanisms by which inhibition of poly(ADP-ribose) polymerases (PARPs) elicits clinical be
276 longing to the tankyrase (Tnks) subfamily of poly(ADP-ribose) polymerases (PARPs) have recently been
278 posttranslational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) that mediate EBV re
282 sed apoptosis characterized by caspase 3 and poly(ADP-ribose) polymerase processing, DNA cleavage, an
283 of their breakage, and to be antagonized by poly (ADP-ribose) polymerase/RECQ1-regulated restart.
284 ch damages DNA and causes hyperactivation of poly(ADP-ribose) polymerase, resulting in extensive NAD(
285 otein PNKP and implicates hyperactivation of poly(ADP-ribose) polymerase/s as a cause of cerebellar a
286 RK1 inhibition cooperates with inhibition of poly (ADP-ribose) polymerase signalling to inhibit growt
288 the histone variant macroH2A1.1 binds to the poly(ADP-ribose) polymerase tankyrase 1, preventing it f
289 n be induced by inhibition of tankyrase 1, a poly(ADP-ribose) polymerase that is required for resolut
292 tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly(ADP-ribose) polymerase (TiPARP) gene expression, de
293 ere, we show that the loss of TCDD-inducible poly(ADP-ribose) polymerase (Tiparp), an ADP-ribosyltran
294 AhR repressor (Ahrr/AhRR) and TCDD-inducible poly(ADP-ribose)polymerase (Tiparp/TiPARP) by AhR ligand
295 se 3 and cleavage of the caspase 3 substrate poly(ADP-ribose) polymerase were inhibited in E. faecali
296 rker proteins, cleaved caspase 7 and cleaved poly(ADP-ribose) polymerase, were significantly reduced
299 ncer cells and decreases the level of intact poly(ADP-ribose) polymerase, which is indicative of apop
300 AD precursors, exercise regimens, or loss of poly(ADP-ribose) polymerases yet surprisingly do not exh
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