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1 egy: a cyclic phosphodiesterase that acts on adenosine diphosphate-ribose 1"-2" cyclic phosphate (App
2 isolated terminals, we tested 8-bromo-cyclic adenosine diphosphate ribose (8Br-cADPr), a competitive
3 ribosyltransferases catalyze the transfer of adenosine diphosphate ribose (ADP-ribose) from nicotinam
4 brane protein that converts NAD primarily to adenosine diphosphate ribose (ADPR) and a small amount o
8 where, involves the release of mitochondrial adenosine diphosphate ribose (ADPR) or nicotinamide aden
10 ous substrates (e.g. lipopolysaccharides and adenosine diphosphate ribose (ADPr)) challenged this per
12 this strategy should be applicable to cyclic adenosine diphosphate ribose and nicotinic acid adenine
13 PM2 channels were activated by intracellular adenosine diphosphate-ribose and blocked by flufenamic a
15 f two potent Ca(2+) releasing agents: cyclic adenosine diphosphate ribose (cADPR) from nicotinamide a
16 of the calcium-mobilizing metabolite, cyclic adenosine diphosphate ribose (cADPR), from nicotinamide
18 osal mast cells through an IL-13-CD38-cyclic adenosine diphosphate ribose (cADPR)-dependent process.
23 sitol 1,4,5-trisphosphate (IP(3)) and cyclic adenosine diphosphate-ribose (cADPR) are second messenge
25 ng agents sphingosine-1-phosphate and cyclic adenosine diphosphate ribose exhibited weaker ABA-stimul
26 ial growth factor, 3-nitrotyrosine, and poly(adenosine diphosphate ribose) expression in lung tissue.
27 is a calcium-permeable channel activated by adenosine diphosphate ribose metabolites and oxidative s
29 ROS), 3-nitrotyrosine (marker of RNS), poly(adenosine diphosphate-ribose) (PAR, marker of PARP activ
31 of caspase-2 and caspase-3, cleavage of poly(adenosine diphosphate-ribose) (poly(ADP-ribose)) polymer
32 accompanied by caspase-3 activation and poly-adenosine diphosphate ribose polymerase (PARP) cleavage
33 tibody that blocks angiogenesis) and/or poly-adenosine diphosphate ribose polymerase (PARP) inhibitor
34 age during transplantation can activate poly-adenosine diphosphate ribose polymerase (PARP) resulting
36 rgery, radiation, and therapies such as poly-adenosine diphosphate ribose polymerase inhibitors for B
37 on stress, a defect accentuated by poly-ADP (adenosine diphosphate) ribose polymerase inhibitors.
39 rial dysfunction, caspase cleavage, and poly adenosine diphosphate-ribose polymerase (PARP) degradati
40 ing for imbalances in subsequent use of poly adenosine diphosphate-ribose polymerase inhibitors and o
41 by caspase-8, -9, and -3 and PARP (poly-ADP [adenosine diphosphate]-ribose polymerase) cleavage and d
44 st cancer (TNBC) cells are sensitive to poly(adenosine diphosphate ribose) polymerase (PARP) inhibito
45 NBC has rationalized clinical trials of poly(adenosine diphosphate ribose) polymerase (PARP) inhibito
47 stigated PARPi-FL, an exogenous nuclear poly(adenosine diphosphate ribose) polymerase (PARP1)-targete
48 o human skin indicated that PARPi-FL, a poly(adenosine diphosphate ribose) polymerase 1 (PARP1) inhib
49 p53 interacting with and delivering the poly(adenosine diphosphate ribose) polymerase 1 (PARP1)/Ku70
50 wn or putative radiosensitizers such as poly(adenosine diphosphate ribose) polymerase and mammalian-t
51 ired IHHs displayed caspase activation, poly(adenosine diphosphate ribose) polymerase cleavage, and a
52 ngs (hormonal treatments, chemotherapy, poly(adenosine diphosphate ribose) polymerase inhibitors, rad
53 In cells deficient in the telomeric poly(adenosine diphosphate ribose) polymerase tankyrase 1, si
54 noblots demonstrated adaphostin induced poly(adenosine diphosphate-ribose) polymerase (PARP) cleavage
55 ected by caspases-3 and -8 cleavage and poly(adenosine diphosphate-ribose) polymerase (PARP) degradat
57 a rational target for therapy based on poly(adenosine diphosphate-ribose) polymerase (PARP) inhibiti
58 repair, are associated with response to poly(adenosine diphosphate-ribose) polymerase (PARP) inhibiti
59 t for patients who have progressed on a poly(adenosine diphosphate-ribose) polymerase (PARP) inhibito
60 ient epithelial ovarian cancer (EOC) to poly(adenosine diphosphate-ribose) polymerase (PARP) inhibito
62 ated the effects of a novel ultrapotent poly(adenosine diphosphate-ribose) polymerase (PARP) inhibito
63 Few prospective studies have compared poly(adenosine diphosphate-ribose) polymerase (PARP) inhibito
64 patients, 13 (33.3%) were eligible for poly(adenosine diphosphate-ribose) polymerase (PARP) inhibito
65 1/2 alterations are eligible to receive poly(adenosine diphosphate-ribose) polymerase (PARP) inhibito
67 ding DNA fragmentation and cleavage of poly (adenosine diphosphate-ribose) polymerase (PARP), as well
68 ankyrins and to the catalytic domain of poly(adenosine diphosphate-ribose) polymerase (PARP), was ide
71 the human bax promoter and found that poly (adenosine diphosphate-ribose) polymerase 1 recruited the
73 C-alpha, phospho-PKC-beta1, and cleaved poly(adenosine diphosphate-ribose) polymerase in post-CP/Rep
74 HR) as measured by hypersensitivity to poly (adenosine diphosphate-ribose) polymerase inhibition and
75 high tidal volume ventilation plus the poly-(adenosine diphosphate-ribose) polymerase inhibitor 3-ami
76 e another complementary determinant of poly (adenosine diphosphate-ribose) polymerase inhibitor effic
77 onsistent with the association between poly (adenosine diphosphate-ribose) polymerase inhibitor effic
78 of 1% to 3% of patients treated with a poly(adenosine diphosphate-ribose) polymerase inhibitor for h
79 asibility and toxicity of combining the poly(adenosine diphosphate-ribose) polymerase inhibitor olapa
80 e II prospective clinical trial of the poly-(adenosine diphosphate-ribose) polymerase inhibitor olapa
82 ympiA trial compared 1 year of the oral poly(adenosine diphosphate-ribose) polymerase inhibitor, olap
83 First-line maintenance therapy with poly(adenosine diphosphate-ribose) polymerase inhibitors (PAR
85 among patients with cancer treated with poly(adenosine diphosphate-ribose) polymerase inhibitors and
86 dent kinase 4 or 6 (CDK4/6) inhibitors, poly(adenosine diphosphate-ribose) polymerase inhibitors, and
87 nstability in response to radiation and poly(adenosine diphosphate-ribose) polymerase inhibitors, com
89 ospho-PKC-alpha, phospho-PKC-beta1, and poly(adenosine diphosphate-ribose) polymerase were quantified
90 actor, caspase 3, caspase 8, caspase 9, poly(adenosine diphosphate-ribose) polymerase, B-cell lymphom
91 ble, and some of these targets, such as poly(adenosine diphosphate-ribose) polymerase, Wee1, and Auro
92 -FTT) is a PET radiotracer for imaging poly (adenosine diphosphate-ribose) polymerase-1 (PARP-1), an
93 te homolog 2 (EZH2) directly methylates poly(adenosine diphosphate-ribose) polymerase-1 (PARP-1), an
97 r 1) prevents it from inhibiting PARP1 [poly(adenosine diphosphate-ribose) polymerase], a critical DN
98 luorthanatrace (FTT) depicts activated poly (adenosine diphosphate-ribose)polymerase (PARP) expressio
100 ed forms of caspases-2 and -3, bax, and poly-adenosine diphosphate-ribose-polymerase (PARP) by Wester
101 ATR), DNA-dependent protein kinase, and poly[adenosine diphosphate ribose] polymerase (PARP) 1/2.
102 ), enhanced cell death (caspase 3/7 and poly[adenosine diphosphate-ribose] polymerase activity, chrom
103 from targeted therapies, such as PARP (poly [adenosine diphosphate-ribose] polymerase) inhibitors.
104 m the past 5 years, with an emphasis on poly[adenosine diphosphate ribose]polymerase-1 as an imaging
105 of PARPi-FL, a fluorescent inhibitor of poly[adenosine diphosphate-ribose]polymerase 1 (PARP1), which
107 an essential substrate for sirtuins and poly(adenosine diphosphate-ribose) polymerases (PARPs), which
110 infection through the synthesis of a cyclic adenosine diphosphate ribose signalling molecule, which
111 Poly(ADP-ribose) (PAR) is a homopolymer of adenosine diphosphate ribose that is added to proteins a
112 entification of an unexpected molecule, poly(adenosine diphosphate ribose), that may be implicated in