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1 XRCC1, requiring a minimum chain length of 7 ADP-ribose units in the oligo(ADP-ribose) ligand for a s
4 in from hepatitis E virus (HEV) serves as an ADP-ribose-protein hydrolase for mono-ADP-ribose (MAR) a
5 -oxadiazole analog in complex with Sirt2 and ADP-ribose reveals its orientation in a still unexplored
6 tor 1 (HPF1) is required for PARP1 to attach ADP-ribose groups onto the hydroxyl oxygen of the Ser re
7 t cleave the glycosidic bonds either between ADP-ribose units or between the protein proximal ADP-rib
8 arily conserved structural domains that bind ADP-ribose derivatives and are found in proteins with di
10 deletion of Parp1 rescued normal cerebellar ADP-ribose levels and reduced the loss of cerebellar neu
11 recipitation method using well-characterized ADP-ribose binding domains to provide the first genome-w
14 oronaviruses encode a macrodomain containing ADP-ribose-1"-phosphatase (ADRP) activity within the N t
17 Paneth cells in the ISC niche secrete cyclic ADP ribose that triggers SIRT1 activity and mTORC1 signa
18 ne dinucleotide phosphate (NAADP) and cyclic ADP-ribose (cADPR) are Ca(2+)-mobilizing messengers impo
20 Br-cADPr), a competitive inhibitor of cyclic ADP-ribose (cADPr) signaling that partially relieves DAM
21 ThcD) fragmentation methods when determining ADP-ribose acceptor sites within complex cellular sample
22 allowing access to products such as dimeric ADP-ribose, which has been detected but never isolated f
25 CHIKV nsP3 macrodomain is able to hydrolyze ADP-ribose groups from mono(ADP-ribosyl)ated proteins.
27 trinsic NADase activity-cleaving NAD(+) into ADP-ribose (ADPR), cyclic ADPR, and nicotinamide, with n
30 The latter involves the synthesis of long ADP-ribose chains that have specific properties due to t
33 nslationally, either attached singly as mono(ADP-ribose) (MAR) or in polymeric chains as poly(ADP-rib
34 as an ADP-ribose-protein hydrolase for mono-ADP-ribose (MAR) and poly(ADP-ribose) (PAR) chain remova
35 lation refers to the addition of one or more ADP-ribose units onto proteins post-translationally.
38 The modification of serines by molecules of ADP-ribose plays an important role in signaling that the
39 ted ARH1, the possible unbinding pathways of ADP-ribose from non-phosphorylated and phosphorylated AR
40 abolishes DNA damage-stimulated polymers of ADP-ribose (PAR) production and the PAR-dependent NF-kap
42 Ps) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate
45 stem from the physicochemical properties of ADP-ribose, which as a post-translational modification i
46 polymeric chains (poly-ADP-ribosylation) of ADP-ribose are conjugated to proteins by ADP-ribosyltran
47 gical processes through covalent transfer of ADP-ribose from the oxidized form of nicotinamide adenin
48 catalytic fragment show that the transfer of ADP-ribose to toxin takes place by a predominantly intra
50 in length of 7 ADP-ribose units in the oligo(ADP-ribose) ligand for a stable interaction with XRCC1.
53 Maintenance therapy with olaparib, a poly ADP ribose polymerase inhibitor given post-platinum ther
54 l-cycle, apoptotic genes, caspase-3 and poly ADP ribose polymerase-1 (PARP-1) cleavage) and was rever
55 ADAMTS-4 directly cleaved and degraded poly ADP ribose polymerase-1 (a key molecule in DNA repair an
60 ant channel (C1008-->A) or silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN trans
61 pathways demonstrated the activation of poly ADP-ribose polymerase-dependent cell death in bok-defici
63 eficient cancers are hypersensitive to Poly (ADP ribose)-polymerase (PARP) inhibitors, but can acquir
77 egulation of glucose transporter-1 and poly (ADP-ribose) polymerase cleavage while preserving tumor t
79 urpose Data suggest that DNA damage by poly (ADP-ribose) polymerase inhibition and/or reduced vascula
83 oncomitant with an increase in cleaved poly (ADP-ribose) polymerase 1 (P < 0.05), indicative of apopt
85 xpression of caspase-3, higher cleaved poly (ADP-ribose) polymerase levels (p < 0.007), and a higher
86 rpose To determine whether cotargeting poly (ADP-ribose) polymerase-1 plus androgen receptor is super
87 served in all eukaryotic cells include poly (ADP-ribose) polymerases (PARPs), sirtuins, AMP-activated
88 e-8, and caspase-9 activation and less poly (ADP-ribose) polymerase cleavage compared with WT livers
89 Rucaparib is an inhibitor of nuclear poly (ADP-ribose) polymerases (inhibition of PARP-1 > PARP-2 >
90 we have characterized the mechanism of poly (ADP-ribose) binding by XRCC1 and examined its importance
91 s were tested for inhibitory effect of poly (ADP-ribose) polymerase (PARP) activity in vitro and in v
93 ogies for studying robust responses of poly (ADP-ribose) polymerase-1 (PARP-1) to DNA damage with str
94 ctasia mutated (ATM), but dependent on poly (ADP-ribose) polymerase 1 (PARP1), which ADP ribosylates
95 ing protein 1, DNA polymerase beta, or poly (ADP-ribose) polymerase 1 activity, all of which fail to
98 omoting stabilization of a new target, poly (ADP-ribose) glycohydrolase (PARG) mRNA, by binding a uni
99 sub-nuclear PCNA foci, suggesting that poly (ADP-ribose) promotes XRCC1 recruitment both at single-st
100 These data support the hypothesis that poly (ADP-ribose) synthesis promotes XRCC1 recruitment at DNA
101 t approval of olaparib (Lynparza), the poly (ADP-ribose) polymerase (PARP) inhibitor for treating tum
102 Durable and long-term responses to the poly (ADP-ribose) polymerase inhibitor olaparib are observed i
103 1 is required for selective binding to poly (ADP-ribose) at low levels of ADP-ribosylation, and promo
104 y PML-RARA) are extremely sensitive to poly (ADP-ribose) polymerase (PARP) inhibition, in part owing
105 ential marker of long-term response to poly (ADP-ribose) polymerase inhibition and that restoration o
109 alpha-ketoglutarate or treatment with a poly(ADP ribose) polymerase inhibitor protects reductive carb
110 nd cleavage of caspases 3, 8, and 9 and poly(ADP ribose) polymerase, and suppressed survivin, myeloid
111 , mtp53 depletion profoundly influenced poly(ADP ribose) polymerase 1 (PARP1) localization, with incr
113 Ca(2+) and Na(+) influx, activation of poly(ADP ribose) polymerase-1 (PARP-1), and delayed Ca(2+) de
114 g parthanatos, monitored by cleavage of poly(ADP ribose)polymerase-1 (PARP-1), or necroptosis, assess
115 of the topoisomerase IIbeta (TOP2beta)/poly(ADP ribose) polymerase 1 (PARP1) complex are necessary f
127 uced cleavage of caspase-3, -8, and -9, poly(ADP-ribose) polymerase, and the externalization of phosp
129 We report results for veliparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, combined with c
132 provides further evidence that use of a poly(ADP-ribose) polymerase inhibitor in the maintenance trea
134 ent of the chemotherapeutic Olaparib, a poly(ADP-ribose) polymerase inhibitor, in live cells and with
138 demonstrate the involvement of Alc1, a poly(ADP-ribose)- and ATP-dependent remodeler, in the chromat
139 he difficulty associated with accessing poly(ADP-ribose) (PAR) in a homogeneous form has been an impe
142 hydrolase for mono-ADP-ribose (MAR) and poly(ADP-ribose) (PAR) chain removal (de-MARylation and de-PA
143 -1 overexpression stimulates PARP-1 and poly(ADP-ribose) (PAR) protein expression and cisplatin resis
145 geneous responses to platinum drugs and poly(ADP-ribose) polymerase (PARP) inhibitors in clinical tri
146 tumors to DNA cross-linking agents and poly(ADP-ribose) polymerase (PARP) inhibitors, we sought to i
149 initially respond well to platinum and poly(ADP-ribose) polymerase inhibitor (PARPi) therapy; howeve
153 nic/apyrimidinic endonuclease 1 (APE1), poly(ADP-ribose) polymerase 1 (PARP1), X-ray repair cross-com
159 Following DNA double-strand breaks, poly(ADP-ribose) (PAR) is quickly and heavily synthesized to
160 reaks and disruption of this pathway by Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) is toxi
161 ADP-ribosyl)ation mediated primarily by poly(ADP-ribose) polymerase 1 (PARP1) is responsible for the
162 se (PAR) chains, primarily catalyzed by poly(ADP-ribose) polymerase 1 (PARP1), is crucial for cellula
164 dification, is immediately catalyzed by poly(ADP-ribose) polymerases (PARPs) at DNA lesions, which fa
165 translational modification catalyzed by poly(ADP-ribose) polymerases (PARPs) that mediate EBV replica
167 ted by caspase-3/7 activity and cleaved poly(ADP-ribose) polymerase, in different cell lines that sup
168 he SNAT2 ER-alpha-ERE complex contained poly(ADP-ribose) polymerase 1, Lupus Ku autoantigen protein p
171 inhibition of the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation with
173 ological activity of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP1) causes neuron death in
175 we demonstrate that the nuclear enzyme Poly(ADP-ribose)Polymerase 1 (PARP1) is a promising target fo
176 k we identify a physical and functional poly(ADP-ribose)-mediated interaction of PARP1 with the E3 ub
177 clear LXRalpha complexes and identified poly(ADP-ribose) polymerase-1 (PARP-1) as an LXR-associated f
179 chromatin accumulation was enhanced in poly(ADP-ribose) polymerase (PARP) 1(-/-) compared with wild-
180 drugs that block DNA repair, including poly(ADP-ribose) polymerase (PARP) inhibitors, fail due to la
181 and BCBL1 PEL cells but did not induce poly(ADP-ribose) polymerase (PARP) cleavage in virus-negative
182 we show that the loss of TCDD-inducible poly(ADP-ribose) polymerase (Tiparp), an ADP-ribosyltransfera
183 epressor (Ahrr/AhRR) and TCDD-inducible poly(ADP-ribose)polymerase (Tiparp/TiPARP) by AhR ligands wer
185 cells and decreases the level of intact poly(ADP-ribose) polymerase, which is indicative of apoptosis
186 ibose (iso-ADPr), the smallest internal poly(ADP-ribose) (PAR) structural unit, binds between the WWE
189 repeat-containing protein that mediates poly(ADP-ribose) polymerase-1 (PARP-1)-dependent transcriptio
190 tigated the regulation of mitochondrial poly(ADP-ribose) polymerase 1 (PARP1) by the cyclic adenosine
195 DNA damage response by the synthesis of poly(ADP-ribose) (PAR) is mediated mainly by poly(ADP-ribose)
197 Over 50 years ago, the discovery of poly(ADP-ribose) (PAR) set a new field of science in motion-t
198 PARP1, resulting in the accumulation of poly(ADP-ribose) in the cell body and axon and limited axonal
199 Our results indicate that regulation of poly(ADP-ribose) levels is a critical function of the DLK reg
200 ide insight into why clinical trials of poly(ADP-ribose) polymerase (PARP) inhibitors, which require
203 eton while promoting the degradation of poly(ADP-ribose) polymerase 1, an inhibitor of osteoclastogen
206 rn blotting for the cleaved fragment of poly(ADP-ribose) polymerase, and the active isoform of caspas
207 mages DNA and causes hyperactivation of poly(ADP-ribose) polymerase, resulting in extensive NAD(+)/AT
208 This work focuses on the regulation of poly(ADP-ribose) polymerase-1 (PARP-1) expression by MKP-1.
211 PNKP and implicates hyperactivation of poly(ADP-ribose) polymerase/s as a cause of cerebellar ataxia
212 l the mechanisms by which inhibition of poly(ADP-ribose) polymerases (PARPs) elicits clinical benefit
213 ng to the tankyrase (Tnks) subfamily of poly(ADP-ribose) polymerases (PARPs) have recently been shown
214 ecursors, exercise regimens, or loss of poly(ADP-ribose) polymerases yet surprisingly do not exhibit
217 n identifying ADP-ribosylation sites on Poly(ADP-ribose) Polymerase 1 (PARP1) with mass spectrometry
219 endonuclease in cooperation with PARP1 poly(ADP-ribose) polymerase and RPA The novel gap formation s
220 we show that the anti-apoptotic protein poly(ADP-ribose) polymerase (PARP)14 promotes aerobic glycoly
222 rinsic regulators of axon regeneration: poly(ADP-ribose) glycohodrolases (PARGs) and poly(ADP-ribose)
224 and cleavage of the caspase 3 substrate poly(ADP-ribose) polymerase were inhibited in E. faecalis-inf
225 of enzymes consume NAD(+) as substrate: poly(ADP-ribose) polymerases, ADP-ribosyl cyclases (CD38 and
227 ors (PARPi), a cancer therapy targeting poly(ADP-ribose) polymerase, are the first clinically approve
229 opus egg extract assays, we showed that poly(ADP-ribose) polymerase 1 (PARP1) is modified by SUMO2/3
231 Prior work has established that the poly(ADP-ribose) polymerase (PARP) enzyme Tankyrase (TNKS) an
233 eading the way for the discovery of the poly(ADP-ribose) polymerase (PARP) family of enzymes and the
235 ents melphalan and cisplatin and to the poly(ADP-ribose) polymerase (PARP) inhibitor veliparib (ABT-8
236 the present study we observed that the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and ve
238 SP1 bind to a composite element in the poly(ADP-ribose) polymerase 1 (PARP-1) promoter in a mutually
240 Resolution at telomeres requires the poly(ADP-ribose) polymerase tankyrase 1, but the mechanism th
241 istone variant macroH2A1.1 binds to the poly(ADP-ribose) polymerase tankyrase 1, preventing it from l
244 inity that depends on the length of the poly(ADP-ribose) strand and competes with DNA for protein bin
245 gets are the tankyrase proteins (TNKS), poly(ADP-ribose) polymerases (PARP) that regulate Wnt signali
246 ases the binding of the macro domain to poly(ADP-ribose) and stimulates the de-PARylation activity.
248 responsible for cellular sensitivity to poly(ADP-ribose) polymerase inhibitors (PARPi) in BRCA1-defic
250 of nuclear ATP, leading from NAD(+) to poly(ADP-ribose) to ADP-ribose to ATP, which supports the act
251 trials exploiting this concept by using poly(ADP-ribose) polymerase (PARP) inhibitors in patients wit
253 The vault-interacting domain of vault poly(ADP-ribose)-polymerase (INT) has been used as a shuttle
254 slational modification of proteins with poly(ADP-ribose) (PAR) regulates protein-protein interactions
256 erstanding the interactions of PAR with poly(ADP-ribose) glycohydrolase (PARG) and other binding prot
257 ellular hyper-dependence on alternative poly-ADP ribose polymerase (PARP)-mediated DNA repair mechani
258 Assays for DNA ladder formation and poly-ADP ribose polymerase (PARP) cleavage were performed to
260 how that the latonduine analogs inhibit poly-ADP ribose polymerase (PARP) isozymes 1, 3, and 16.
261 endent polymerization of long chains of poly-ADP ribose (PAR) onto itself in response to DNA damage a
262 chilling) and more than 60% cleavage of poly-ADP ribose polymerase (compared to less than 5% in contr
264 ), matrix metalloproteinases (MMPs) and poly-ADP-ribose-polymerase-1 (PARP-1) in diabetic kidney remo
266 ion (PARylation) is mainly catalysed by poly-ADP-ribose polymerase 1 (PARP1), whose role in gene tran
267 s and is catalyzed by 11 members of the poly-ADP-ribose polymerase (PARP) family of proteins (17 in h
268 s (DSBs) and were modestly sensitive to poly-ADP-ribose polymerase (PARP) inhibitors olaparib and BMN
273 (PARP1) and the deribosylating enzyme poly-(ADP-ribose) glycohydrolase (PARG), which dynamically reg
274 by the nuclear ADP-ribosylating enzyme poly-(ADP-ribose) polymerase 1 (PARP1) and the deribosylating
275 imaging strategy for DLBCL that targets poly[ADP ribose] polymerase 1 (PARP1), the expression of whic
277 unique loop that both excludes proteinaceous ADP-ribose acceptors and contributes to hydrolysis.
279 structure of adenosine-5-diphosphate-ribose (ADP-ribose) in complex with non-phosphorylated and phosp
280 ibosyltransferases either conjugate a single ADP-ribose to a target or generate ADP-ribose chains.
282 sor adenomatous polyposis coli (APC) and the ADP-ribose polymerase Tankyrase (Tnks) have evolutionari
284 Nevertheless, accurate assignment of the ADP-ribose acceptor site(s) within the modified proteins
285 re we describe the chemical synthesis of the ADP-ribose dimer, and we use this compound to obtain the
286 P-ribosylation refers to the transfer of the ADP-ribose group from NAD(+) to target proteins post-tra
287 d the unique fragmentation properties of the ADP-ribose moiety were used to trigger targeted fragment
289 rly effects of Wnt on Axin and find that the ADP-ribose polymerase Tankyrase (Tnks)--known to target
292 , leading from NAD(+) to poly(ADP-ribose) to ADP-ribose to ATP, which supports the activity of ATP-de
295 RS-CoV macro domain in the host response via ADP-ribose binding but also as a potential target for dr
296 ttranslational protein modification in which ADP-ribose is transferred from NAD(+) to specific accept
298 ters how the conserved Asp-20 interacts with ADP-ribose and may explain the efficient binding of the
299 s), enzymes that modify target proteins with ADP-ribose, play important roles in many of the RNA regu
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