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1 trations required to maximally activate auto-poly(ADP-ribosylation).
2 ng to the lesions where it catalyses protein poly(ADP-ribosylation).
3 CTCF participate in DNA damage response via poly(ADP-ribosylation).
4 r sumoylation), or nucleotides (for example, poly(ADP-ribosyl)ation).
5 may be regulated via mechanisms governed by polyADP-ribosylation.
6 ver, histone phosphorylation is modulated by poly(ADP-)ribosylation.
7 osylate aspartate residues in the process of poly(ADP-ribosyl)ation.
8 ARG activity regulates the extent of in vivo poly(ADP-ribosyl)ation.
9 and is consumed in lysine deacetylation and poly(ADP-ribosyl)ation.
10 n of Mre11 foci coincide with these areas of poly(ADP-ribosyl)ation.
11 these agents had opposite effects on protein poly(ADP-ribosyl)ation.
12 econdensation are similar to the kinetics of poly(ADP-ribosyl)ation.
13 32P]beta NAD+ resulted in its time-dependent poly(ADP-ribosyl)ation.
14 mere function in human cells is regulated by poly(ADP-ribosyl)ation.
15 e next examined p53 as a covalent target for poly(ADP-ribosyl)ation.
16 associating with them or by catalyzing their poly(ADP-ribosyl)ation.
17 ction to maintain CtIP abundance and promote poly(ADP-ribosyl)ation.
18 sm, and potential pathogenic roles for hyper-poly(ADP-ribosyl)ation.
19 DP-ribose) chains to enhance PARP1-dependent poly(ADP-ribosyl)ation.
20 such as ubiquitination, palmitoylation, and poly(ADP-ribosyl)ation.
21 plicing, but its function can be modified by poly(ADP-ribosyl)ation.
22 chitecture of the genome may be modulated by poly(ADP-ribosyl)ation.
23 ribose-ribose glycosidic bond formed during poly(ADP-ribosyl)ation.
24 polymerase 1 (PARP1) and stimulates its auto-poly(ADP-ribosyl)ation.
25 mportant cellular processes are regulated by poly(ADP-ribosyl)ation.
26 localize to the sites of DNA-damage-induced poly(ADP-ribosyl)ation.
27 otif is also required for post-translational poly(ADP-ribosyl)ation.
32 binding domain of WRN strongly inhibits the poly(ADP-ribosyl)ation activity in H2O2-treated control
34 t ADP-ribosyl transferase (ARTs) enzyme with Poly(ADP-ribosyl)ation activity that is triggered by DNA
35 tecture that couples DNA damage detection to poly(ADP-ribosyl)ation activity through a poorly underst
37 ss-of-function, which caused increased Hrp38 poly(ADP-ribosyl)ation, also resulted in the rough-eye p
38 P-ribose may not be unique to PARPs and that poly(ADP-ribosylation), an established nuclear activity,
39 RP +/+ fibroblasts showed the early burst of poly(ADP-ribosyl)ation and a rapid apoptotic response wh
40 s a dual function being involved both in the poly(ADP-ribosyl)ation and being a constituent of the NA
41 t RPA directly binds activated PARP2 through poly(ADP-ribosyl)ation and can protect single-strand L1
42 ), that modifies various nuclear proteins by poly(ADP-ribosyl)ation and functions as a key enzyme in
43 ow PARG activity controls reversible protein poly(ADP-ribosyl)ation and potentially of how the defect
44 odels, under hypoxic conditions, we detected poly(ADP-ribosyl)ation and reduced activity of GAPDH; in
45 ular nucleases of this type are inhibited by poly(ADP-ribosyl)ation and suggested that subsequent cle
49 ies through aberrant crosstalk between CTCF, poly(ADP-ribosyl)ation, and DNA methylation may be a gen
50 These data implicate intra-mitochondrial poly(ADP-ribosylation) as an important therapeutic targe
51 ic activity is required for PARP-1-dependent poly(ADP-ribosyl)ation at the promoters of commonly regu
57 clearly shows that XPC-RAD23B is a target of poly(ADP-ribosyl)ation catalyzed by PARP1, which can be
59 Therefore, our results suggest that Hrp38 poly(ADP-ribosyl)ation controls eye pattern formation vi
63 uce Wnt/beta-catenin signaling by preventing poly(ADP-ribosyl)ation-dependent AXIN degradation, there
65 er nuclear proteins, p53 undergoes extensive poly(ADP-ribosyl)ation early during the apoptotic progra
69 Here, we report that HMGN1 affects the self-poly(ADP-ribosyl)ation (i.e., PARylation) of poly(ADP-ri
70 activity and provided evidence for a role of poly(ADP ribosyl)ation in Stat-mediated transcriptional
71 nerve immunohistochemistry revealed enhanced poly(ADP-ribosyl)ation in all experimental groups manife
72 n this review, we discuss recent findings on poly(ADP-ribosyl)ation in DNA damage response as well as
75 nuclease (CME) DNAS1L3 and its inhibition by poly(ADP-ribosyl)ation in the DNA degradation that accom
76 in somatic tissues, much less is known about poly(ADP-ribosyl)ation in the germline, where DNA double
78 pendent endonuclease DNAS1L3 is inhibited by poly(ADP-ribosyl)ation in vitro, and its activation duri
80 ATP or release certain nuclear proteins from poly(ADP-ribosyl)ation-induced inhibition, both of which
99 this mobilization is largely independent of poly(ADP-ribosyl)ation, it cannot solely explain the chr
100 n) was at least 100-fold lower than in trans-poly(ADP-ribosylation) (K(a) = 1400 versus 3-15, respect
102 These results suggest that p65 NF-kappaB poly(ADP-ribosyl)ation may be a critical determinant for
103 in ligases, our results suggest that protein poly(ADP-ribosyl)ation may be a general mechanism to tar
108 Cells devoid of TIM fail to support the poly(ADP-ribosyl)ation necessary for backing up the cano
112 ro and in vivo data support a model in which poly(ADP-ribosyl)ation of DDB2 suppresses DDB2 ubiquityl
113 t2(+), and pathogen-dependent changes in the poly(ADP-ribosyl)ation of discrete proteins were also ob
114 DNA fragmentation and resulted in persistent poly(ADP-ribosyl)ation of DNAS1L3; it did not, however,
116 In conclusion, these data indicate that poly(ADP-ribosyl)ation of GAPDH and the subsequent inhib
117 inhibition was found to be a consequence of poly(ADP-ribosyl)ation of GAPDH by poly(ADP-ribose) poly
121 o-activators of PARP-1 auto-modification and poly(ADP-ribosyl)ation of histone H1 in the absence of f
127 ss, PARP-1 itself becomes activated, but the poly(ADP-ribosyl)ation of other cellular proteins is sev
130 1 confirmed our conclusion that the covalent poly(ADP-ribosyl)ation of p53 results in the transcripti
132 m was poly(ADP-ribosyl)ated, suggesting that poly(ADP-ribosyl)ation of PCNA may regulate its function
133 NF-kappaB sites and showed that TNF induced poly(ADP-ribosyl)ation of RelA when bound to the Phex pr
134 by and binds to DNA breaks and catalyzes the poly(ADP-ribosyl)ation of several substrates involved in
135 ts showed that Parg null mutation does cause poly(ADP-ribosyl)ation of Squid and hrp38 protein, as we
137 d by binding to nicked DNA, PARP-1 catalyzes poly(ADP-ribosyl)ation of the acceptor proteins and itse
138 d by binding to nicked DNA, PARP-1 catalyzes poly(ADP-ribosyl)ation of the acceptor proteins using NA
139 ation in proximal tubules after IRI leads to poly(ADP-ribosyl)ation of the key glycolytic enzyme glyc
142 ction (PARP-1 action) or by the formation of poly(ADP-ribosyl)ation of topoisomerase I (PARP-1/NAD ac
145 at binding factor 2 (TRF2) and is capable of poly(ADP-ribosyl)ation of TRF2, which affects binding of
148 NuMA promotes transcription by limiting the polyADP-ribosylation of RNA polymerase II, increasing it
151 ed SSB level, gamma-H2AX foci formation, and poly(ADP-ribosylation) of PARP-1, which were associated
153 ose from NAD to histone H1 (defined as trans-poly(ADP-ribosylation)) or to PARP I (defined as auto-po
154 p50 was not an efficient covalent target for poly(ADP-ribosyl)ation, our results are consistent with
156 ns of oxidative stress and energy depletion, poly(ADP-ribosylation) paradoxically contributes to mito
157 eins to tankyrase 1 usually results in their poly(ADP-ribosyl)ation (PARsylation) and can lead to ubi
161 RP-1 inhibitor) also prevented mitochondrial poly(ADP-ribosyl)ation (PARylation) and ROS formation.
164 Proteomic analyses uncover a new role for poly(ADP-ribosyl)ation (PARylation) in regulating the ch
172 se) (PAR) polymerase 1 (PARP1) catalyzes the poly(ADP-ribosyl)ation (PARylation) of proteins, a postt
175 , was associated with an increase in protein poly(ADP-ribosyl)ation (PARylation), and was blocked by
177 Posttranslational modifications, such as poly(ADP-ribosyl)ation (PARylation), regulate chromatin-
180 f different repair pathways to block histone polyADP-ribosylation (PARylation), a known effect of che
181 ected repair (HDR) through the inhibition of polyADP-ribosylation (PARylation), in which cGAMP reduce
183 y(ADP-ribose) polymerase 1 (Parp1) catalyzes poly(ADP-ribosylation) (PARylation) and induces replicat
184 we found that WS cells are deficient in the poly(ADP-ribosyl)ation pathway after they are treated wi
188 ave focused on the signaling role of PARP in poly(ADP-ribosyl)ation rather than any role that can be
189 syl)ation of p53 is a time-dependent protein-poly(ADP-ribosyl)ation reaction and that the addition of
190 consistent with the conclusion that the auto-poly(ADP-ribosyl)ation reaction catalyzed by PARP-1 faci
191 PARP, this domain is capable of catalyzing a poly(ADP-ribosyl)ation reaction; thus, the 193-kD protei
192 In contrast to p53, a positive acceptor in poly(ADP-ribosyl)ation reactions, E2F-1 was not poly(ADP
193 st-translational modification of proteins by poly(ADP-ribosyl)ation regulates many cellular pathways
194 Taken together, these findings suggest that poly(ADP-ribosyl)ation regulates the interaction between
195 etected defense-associated expression of the poly(ADP-ribosyl)ation-related genes PARG2 and NUDT7 and
196 p38 represses Nanos translation, whereas its poly(ADP-ribosyl)ation relieves the repression effect, a
198 Additionally, DDB2 itself was targeted by poly(ADP-ribosyl)ation, resulting in increased protein s
200 for PARP I and catalyze preferentially trans-poly(ADP- ribosylation), thereby opening the possibility
201 be due to the suppression of topoisomerase I poly(ADP-ribosyl)ation through the competition with NAD
202 integrity, and uncontrolled accumulation of poly(ADP-ribosyl)ation triggers a poly(ADP-ribose) (PAR)
203 of PARP I toward dcDNA or dsDNA in the auto-poly(ADP-ribosylation) was at least 100-fold lower than
204 ribosylation)) or to PARP I (defined as auto-poly(ADP-ribosylation)) was studied with respect to the
205 nduced decrease in activity of GAPDH and its poly(ADP-ribosyl)ation were prevented by overexpression
206 To this end, the presence of PARP-1 and poly(ADP-ribosylation) were verified within mitochondria
207 rt oligomers predominate early during hetero-poly(ADP-ribosyl)ation, whereas longer ADP-ribose chains
208 cts of H2O2 can be overcome by inhibitors of poly(ADP)-ribosylation, which also preserve cellular ATP
209 ted with a decrease in the extent of DNAS1L3 poly(ADP-ribosyl)ation, which likely releases DNAS1L3 fr
210 in is rapidly modified by tankyrase-mediated poly(ADP-ribosyl)ation, which promotes the proteolysis o