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1 gative regulation by poly(ADP-ribosyl)ation (PARylation).
2 th or without PARP-1 poly(ADP-ribosyl)ation (PARylation).
3 te by posttranslationally modulating protein PARylation.
4 s, loss of HMGN1 protein reduces PARP-1 self-PARylation.
7 spectrometry and Western blotting, Parp1 and PARylation activity were intensively detected in induced
9 alization of RECQL5 and WRN, suggesting that PARylation acts as a fine-tuning mechanism to coordinate
10 9 muM), as well as inhibiting PARP-modulated PARylation and cell proliferation in MDA-MB-436 cells (B
12 ith a strand break, and this results in self-PARylation and PARylation of other chromatin proteins.
13 1 (Parp1) catalyzes poly(ADP-ribosylation) (PARylation) and induces replication networks involved in
15 increase in protein poly(ADP-ribosyl)ation (PARylation), and was blocked by pharmacological inhibiti
16 (e.g. PARG, ARH3) of poly-ADP-ribosylation (PARylation) are relatively well described, the enzymes i
17 e) (PAR) polymerase 1 (PARP1) activation and PARylation at DNA damage sites, PAR-dependent recruitmen
19 ntrast, although Adprt1b was dispensable for PARylation at DSBs, Adprt1a and, to a lesser extent, Adp
20 er low energy laser-induced DNA damage, less PARylation at lesion sites was observed in Hmgn1(-/-) th
21 lation (PARylation) at genomic damage sites, PARylation at telomeres is mainly dependent on tankyrase
23 unlike PARP1-mediated Poly-ADP-Ribosylation (PARylation) at genomic damage sites, PARylation at telom
24 n of Parp1 and pharmacological inhibition of PARylation both reduced the efficiency of iPSC generatio
25 tic investigations indicated that inhibiting PARylation by either hyperthermia or PARPi induced letha
26 ly adenosine diphosphate (ADP)-ribosylation (PARylation) by poly ADP-ribose (PAR) polymerases (PARPs)
27 Our results provide direct evidence that PARylation can control processing of mRNA precursors, an
31 ates both Drosophila Axin and APC2, but that PARylation does not globally regulate APC2 protein level
32 plored the model that disruption in cellular PARylation, driven by LMP1 expression, subsequently prom
34 we detail the mechanisms that drive cellular PARylation during latent EBV infection and the effects o
36 iglio et al. (2017) demonstrate that histone PARylation factor 1 (HPF1) is required for PARP1 to atta
37 serine ADPr is strictly dependent on histone PARylation factor 1 (HPF1), a recently identified regula
39 biology, physiology, and pathophysiology of PARylation, focusing on the activity of PARP-1, the most
44 ge response localized to telomeres, inhibits PARylation in cells, and has an antiproliferative effect
45 elium discoideum to uncover a novel role for PARylation in regulating nonhomologous end joining (NHEJ
50 venting demethylation of H3K4me3 through the PARylation, inhibition, and exclusion of the histone dem
58 se and other recent findings suggesting that PARylation may be the critical event that mediates the f
59 he decrease in PARG levels enhances the auto-PARylation-mediated inhibition of PARP, thereby avoiding
61 ARP1 enzyme activity, poly-ADP-ribosylation (PARylation), nor did inhibition of SUMOylation of PARP1
62 nhibition and the D226 mutation impair HuR's PARylation, nucleocytoplasmic shuttling and mRNA binding
69 Purified HMGN1 was able to stimulate self-PARylation of purified PARP-1, and in experiments with c
71 cilitating SSBR at damaged telomeres through PARylation of TRF1, thereby protecting genome stability
72 fects the self-poly(ADP-ribosyl)ation (i.e., PARylation) of poly(ADP-ribose) polymerase-1 (PARP-1), a
73 PARP1) catalyzes the poly(ADP-ribosyl)ation (PARylation) of proteins, a posttranslational modificatio
74 ring latent EBV infection and the effects of PARylation on host gene expression and cellular function
75 oss of SUMOylation increased PARP1-dependent PARylation on isolated chromosomes, indicating SUMOylati
77 yers in the early DNA damage response, since PARylation orchestrates the recruitment of repair protei
81 difications, such as poly(ADP-ribosyl)ation (PARylation), regulate chromatin-modifying enzymes, ultim
82 e) (PAR) chain removal (de-MARylation and de-PARylation, respectively) from mono- and poly(ADP)-ribos
83 cal inhibition of PARP-1, or mutation of the PARylation sites on C/EBPbeta, enhances these early adip
85 and in experiments with cell extracts, self-PARylation was greater in Hmgn1(+/+) than in Hmgn1(-/-)
86 alyze massive protein poly ADP-ribosylation (PARylation) within seconds after the induction of DNA si
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