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1 ation, promoted apoptosis, and augmented the DNA damage response.
2 survival of infected cells in response to a DNA damage response.
3 olves Rad3, a master kinase coordinating the DNA damage response.
4 relies on neither HBoV1 replication nor the DNA damage response.
5 L1, but also those required for the cellular DNA damage response.
6 tance of m(6)A in the ultraviolet-responsive DNA damage response.
7 ata identified a novel 53BP1-TIRR complex in DNA damage response.
8 oupling transcription with mRNA splicing and DNA damage response.
9 differentiation, and survival as well as the DNA damage response.
10 identified histone serine ADPr marks in the DNA damage response.
11 regulation of histone acetylation during the DNA damage response.
12 nduced by short telomeres, which trigger the DNA damage response.
13 , the function of the primary cilium and the DNA damage response.
14 e deposition of histone marks as part of the DNA damage response.
15 cruited to the site of DNA-DSBs via an early DNA damage response.
16 in preventing the L1 retrotransposon-induced DNA damage response.
17 cipates in programmed cell death in the UV-B DNA damage response.
18 y p53-dependent enhancer activity during the DNA damage response.
19 cancer subclass through a hormone dependent DNA damage response.
20 erved feature of the multifaceted eukaryotic DNA damage response.
21 reased level of Rad53p triggers an efficient DNA damage response.
22 ucial for coordinating an efficient cellular DNA damage response.
23 blish a pathway of autophagy specific to the DNA damage response.
24 gulator of ADP-ribosylation signaling in the DNA damage response.
25 dogenous triplex structures evoking a robust DNA damage response.
26 lated these abnormalities with dysfunctional DNA damage response.
27 P51 is the DUB for H2AK13,15ub and regulates DNA damage response.
28 echanism to repress spurious activation of a DNA damage response.
29 tudies to understand the role of this PPI in DNA damage response.
30 and elevated levels of H2AK15ub and impairs DNA damage response.
31 stablished roles in epigenetic regulation in DNA damage response.
32 n dependent on oxidative stress, rather than DNA damage response.
33 mplex relationship between autophagy and the DNA damage response.
34 B, deubiquitylates H2AK13,15ub and regulates DNA damage response.
35 f their previously characterized role in the DNA damage response.
36 we found that O-GlcNAcylation is induced by DNA damage response.
37 or DNA-damaging agents and inhibitors of the DNA damage response.
38 ducing replication stress and activating the DNA damage response.
39 hich is important for efficiently activating DNA damage response.
40 c replication are known to induce a cellular DNA damage response.
41 al event that mediates the first wave of the DNA damage response.
42 yeast, dNTP pools expand drastically during DNA damage response.
43 ng and histone deacetylation) complex in the DNA damage response.
44 to form the triple T complex that regulates DNA damage response.
45 ssion during B lymphocyte activation and the DNA damage response.
46 er mechanism how Plk1 antagonizes p53 during DNA damage response.
47 el roles for these and other proteins in the DNA damage response.
48 n the absence of p53 activity induced by the DNA damage response.
49 is essential for mitotic checkpoints and the DNA damage response.
50 tin modification plays a crucial role in the DNA damage response.
51 es in transcription, pre-mRNA processing and DNA damage response.
52 ylated H2A histone family member X)-mediated DNA-damage response.
53 late gene expression and participates in the DNA-damage response.
54 al kinase that orchestrates the multifaceted DNA-damage response.
55 carboplatin, does not kill cells through the DNA-damage response.
56 ity or diminishing its protein levels in the DNA-damage response.
57 limits cell-cycle progression by suppressing DNA damage responses.
58 Cs through G4 stabilization and promotion of DNA damage responses.
59 important for protecting infected cells from DNA damage responses.
60 we have explored how the centrosome controls DNA damage responses.
61 proteins participate in the same pathway of DNA damage responses.
62 DNA lesions (DNA-Pt) and trigger pleiotropic DNA damage responses.
63 with methylated histones and plays a role in DNA damage responses.
64 of the Protein Regulated in Development and DNA Damage Response 1 (REDD1) in diabetes-induced retina
65 related protein regulated in development and DNA damage responses 1 (REDD1) is significantly overexpr
66 We also investigated the contribution of the DNA damage response, a pathway activated by HCMV and imp
67 DNA damage, replicative stress activates the DNA damage response, a signaling cascade allowing cell c
71 zymes is an important factor in the cellular DNA damage response and has gained much attention for it
74 localize to telomeres but fail to repress a DNA damage response and inappropriate repair by A-NHEJ.
75 ng CDT1/ORC1, p21/p27, and PHLPP1 to trigger DNA damage response and induce growth arrest at the G2/M
76 t contributes to transcriptional regulation, DNA damage response and limits heterochromatin spreading
77 py-number alterations (CNAs) associated with DNA damage response and modulation of DNA editing/repair
78 NEK1 is essential for the ionizing radiation DNA damage response and priming of the ATR kinase and of
79 nerating novel mechanistic inhibitors of the DNA damage response and repair (DDR) pathways by focusin
80 The alterations affected pathways regulating DNA damage response and repair, transcription and chroma
82 that the cell cycle critically regulates the DNA damage response and survival of intestinal stem cell
84 gle-stranded telomere DNA to prevent illicit DNA damage responses and to enhance telomerase-mediated
85 r ataxias, indicating an association between DNA damage-response and repair pathways and the age at o
86 d by phosphorylation of p53, activation of a DNA-damage response and cell cycle arrest in G1 phase, f
87 KK family, plays a critical role in the cell DNA-damage response and is an attractive anticancer drug
89 lleviated RSV-induced replication stress and DNA damage response, and consequently attenuating cellul
90 ration, dedifferentiation, activation of the DNA damage response, and gene signatures of aggressive H
91 d CDK4/6 blockade on cell-cycle progression, DNA damage response, and immune-modulation and may provi
92 processes including nutrient sensing and the DNA damage response, and implicated Vts1 in de novo gene
94 (6)A modification in the ultraviolet-induced DNA damage response, and our findings collectively suppo
95 ogene expression levels, retained functional DNA damage responses, and acquired chromatin changes tha
97 g DSB repair, which led to DSB accumulation, DNA damage responses, and early replication arrest in HG
98 ly demonstrate that Pml NBs are critical for DNA damage responses, and suggest that Pml NB disruption
99 dified chemotherapy approaches targeting the DNA damage response, angiogenesis inhibitors, immune che
100 is involved in major cellular events such as DNA damage response, apoptosis and p53-mediated growth-a
103 tations in ATM kinase, a master regulator of DNA damage responses, are found in many cancers, but the
104 e results highlight cIAP2 as a player in the DNA damage response as a posttranscriptional regulator o
105 a-telangiectasia mutated (ATM) regulates the DNA damage response as well as DNA double-strand break r
106 is directly involved in the transcriptional DNA damage response as well as in the cell death pathway
107 ce, a condition associated with an activated DNA damage response, as p19(Arf)-/- MEFs do not senesce
108 rmore, XAB2 mediates specific aspects of the DNA damage response associated with end resection profic
109 o single-stranded telomeric DNA, eliciting a DNA damage response at telomeres that promote inappropri
110 arrest due to activation of the p53-mediated DNA damage response at the neonatal stage, which reduces
111 eplication defects that result in persistent DNA damage responses at telomeres, leading to the engage
112 regulation, including DNA synthesis (NPAT), DNA damage response (ATM), mitosis (PMF1, CENPN and MAD1
113 of a single-strand annealing protein [DdrB (DNA damage response B)] in complex with a partially anne
115 now known to play key roles not only in the DNA damage response but also in regulating numerous mole
116 Ube2w does not have an essential role in the DNA damage response, but is deleterious in the absence o
117 arrest specific cell cycle phases nor elicit DNA damage response, but rather induce an irreversible,
118 1 also participates in gene silencing during DNA damage response, but the precise downstream function
119 pluripotent stem cells also display a robust DNA damage response, but the stability of their genome i
120 tenuated drug-induced activation of cellular DNA damage response by evading G2/M arrest in cancer cel
121 ere, we investigate roles of nuclear PPIs in DNA damage response by sequestering specific PPIs with t
122 c-1 interactions with the following genes in DNA damage response: C34F6.1, him-3 (ortholog of HORMAD1
128 mon translatome identified components of the DNA damage response, consistent with a role for the tran
130 ere, we show that the complete disruption of DNA damage response (DDR) adaptor proteins in ETI cells
131 xpression results in sustained activation of DNA damage response (DDR) after platinum treatment.
132 meres, PHF11 was enriched as cells mounted a DNA damage response (DDR) against exposed chromosome end
133 eptibility genes encode proteins involved in DNA damage response (DDR) and are characterized by rare
135 ew the genome-protective role of the mitotic DNA damage response (DDR) and evidence suggesting that i
136 ed regeneration coincides with activation of DNA damage response (DDR) and impaired ability to differ
138 hrough resection activates the ATR-dependent DNA damage response (DDR) and is required for DSB repair
140 complex syndromes that include a compromised DNA damage response (DDR) and prominent nervous system p
141 The function of many factors involved in DNA damage response (DDR) and the cell cycle depends on
143 t mitotic arrest induces a caspase-dependent DNA damage response (DDR) at telomeres in non-apoptotic
145 The mitotic kinase Plk1 contributes to the DNA damage response (DDR) by targeting multiple factors
146 n response to this replication blockade, the DNA damage response (DDR) cell signalling network is act
147 together PTTG and PBF significantly modulate DNA damage response (DDR) genes, including p53 target ge
149 anipulation of host chromatin.IMPORTANCE The DNA damage response (DDR) is a cellular network that is
151 ature of the adenovirus genome, the cellular DNA damage response (DDR) is considered a barrier to suc
152 KSHV replication, we have determined that a DNA damage response (DDR) is directed to viral genomes b
154 Here we show that these agents activate the DNA damage response (DDR) kinases ATM and DNA-PKcs throu
157 USP7) in the regulation of the p53-dependent DNA damage response (DDR) pathway is well established.
158 to ionizing radiation (IR), cells activate a DNA damage response (DDR) pathway to re-program gene exp
159 ve DNA damage and activation of the ATR-Chk1 DNA damage response (DDR) pathway via ill-defined mechan
160 and BCLAF1 in the regulation of the cellular DNA damage response (DDR) pathway, a key pathway involve
161 ression is associated with activation of the DNA damage response (DDR) pathway, as evidenced by eleva
162 an S-phase checkpoint that acts through the DNA damage response (DDR) pathway, involving the Cds1 ki
163 irectly participate in the regulation of the DNA damage response (DDR) pathway, we challenged Plk1-ov
166 ctions at the cross-roads of three different DNA damage response (DDR) pathways involved in protectin
169 Whether intranuclear inclusions containing DNA damage response (DDR) proteins are causally linked t
170 on-exclusive markers, including constitutive DNA damage response (DDR) signaling, senescence-associat
175 rylation cascade integrates signals from the DNA damage response (DDR) towards PGC-1beta-dependent mi
176 s of mice (MVM) induces a sustained cellular DNA damage response (DDR) which the virus exploits to pr
177 s of mice (MVM) induces a sustained cellular DNA damage response (DDR) which the virus then exploits
178 E-ALI) cultures, HBoV1 infection initiates a DNA damage response (DDR), activating all three phosphat
179 te procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflamm
195 ymphocytes and that targeted manipulation of DNA damage-response (DDR) signaling pathways would allow
197 ted this approach by targeting genes for the DNA-damage response (DDR) proteins MDC1, 53BP1, RIF1 and
199 the breast epithelium unleashes a torrent of DNA damage responses (DDRs) at the telomeres, culminatin
200 ly and has been implicated in the control of DNA damage responses (DDRs) through its interactions wit
205 , induce DNA breaks and orientation-specific DNA damage responses during conflicts with replication f
206 on entails the activation of p53 through the DNA damage-response enzymes, ATM and ATR, and requires t
207 work identifies a critical chromatin-binding DNA damage response factor, ZMYM3, which modulates BRCA1
210 takes advantage of signaling pathways in the DNA damage response for efficient genome amplification i
211 mportant role in regulating the ATM mediated DNA damage response, for epithelial cell survival/self-r
212 lar senescence, as evidenced by a persistent DNA damage response (gammaH2AX and 53BP1) and the expres
213 ontain hepatocytes with a notable persistent DNA damage response (gammaH2AX, 53BP1) due to chronic in
216 he regulatory pathways implicated in the HSC DNA damage response have not been fully elucidated.
218 SSB1 and SSB2 are crucial regulators of the DNA damage response; however, their overlapping roles du
219 een Pol epsilon and the main elements of the DNA damage response in Arabidopsis (Arabidopsis thaliana
221 ivo fate analysis of HFSCs revealed that the DNA damage response in HFSCs causes proteolysis of type
222 This is the first study to detect an acute DNA damage response in operators performing fluoroscopic
223 senescence may result from chronic, low-dose DNA damage responses in which p19(Arf) has a specific ro
224 omeric overhang of telomeres, elicits potent DNA-damage responses in melanoma cells; however, its mec
225 le-strand breaks (DSBs) activate a canonical DNA damage response, including highly conserved cell cyc
226 damage, severe hypoxia (<0.1% O2) induces a DNA damage response, including the activation of p53 and
228 unctional role of ATM kinase, which controls DNA damage responses involving several hundreds of prote
231 1 has been established well as a mediator in DNA damage response, its function in mitosis is not clea
234 recurrent functional mutations of the master DNA damage response kinase ATM, which has been shown to
236 While mTOR is known to be involved in the DNA damage response, little is actually known regarding
237 the G4 fold in vitro and in cells, induces a DNA damage response localized to telomeres, inhibits PAR
239 th a strong induction of the p53 pathway and DNA damage response, manifesting as gamma-H2A.X positivi
240 the DNA damage/repair marker, gamma-H2AX and DNA damage response marker, phosphorylated ataxia telang
241 ing that the role of p19(Arf) in the chronic DNA damage response may be partially p53-independent.
242 long these lines, we have tested whether the DNA damage response mediated by the Ataxia Telangiectasi
243 Consistent with the role of cyclin D1 in DNA damage response, ML364 also caused a decrease in hom
246 and 53BP1 foci, two factors involved in the DNA damage response network, in cells treated with small
248 orylation of Mdm2 regulates the p53-mediated DNA damage response or p53 tumor suppression in vivo.
249 d cyclin-dependent kinase 1 (CDK1) activity, DNA damage responses, or unscheduled DNA synthesis but t
250 hways that control cell proliferation (ERK), DNA-damage responses (p53), and innate immune and stress
252 nced G2 cell cycle arrest with activation of DNA damage response pathway and increased apoptosis was
253 Huwe1's critical role as a modulator of the DNA damage response pathway in the earliest steps of spe
254 induced AICD, as a result of activating the DNA damage response pathway through ATM-mediated Ser15 p
259 ts partners, notably those implicated in the DNA-damage response, preferentially localized to and act
260 ass III deacetylase SIRT1; activation of the DNA damage response prevents SIRT1 deacetylation of TopB
261 variation lies in genes that are part of the DNA damage response, previously suggested to be importan
263 cancer subclass through a hormone-dependent DNA damage response.Prostate cancer is a heterogeneous d
264 ation was associated with an accumulation of DNA damage response protein gammaH2AX, impaired downstre
266 acting protein 1 (Rint1) associates with the DNA damage response protein Rad50 during the transition
270 conserved sites disrupt its deacetylation of DNA-damage response proteins by impairing SIRT2 catalyti
273 -specific small non-coding RNAs, also termed DNA damage response RNAs (DDRNAs), have been shown to pl
274 zed the effect of H. pylori infection on the DNA damage response sensor, ATM, in gastric epithelial c
275 protein expression of key modulators of the DNA damage response.Sequestering mRNA in cytoplasmic str
276 vealed a reliance of SS tumor cells upon the DNA damage response serine/threonine protein kinase ATR.
281 used endoplasmic reticulum stress, activated DNA-damage-response signaling, and ultimately induced ap
282 has been attributed to its canonical role in DNA damage response signalling following replication for
284 gulate multiple cellular functions including DNA damage response, telomere maintenance, and Notch sig
285 ata identifies a new target for manipulating DNA damage response that could impact the development of
286 re to ultraviolet light leads to a cell-wide DNA damage response that includes a global reduction in
287 modification coincides with the ATM-mediated DNA damage response that occurs on functional telomeres
288 layed onset (days), in contrast to the acute DNA-damage responses that occur in minutes to hours.
289 and p-ATM expression, and further triggered DNA damage response through activation of ATM-p53-p21 an
290 ng enzyme that has been reported to regulate DNA-damage responses through its N-terminal region in a
292 thus identifies TRAIP as a component of the DNA damage response to replication-blocking DNA lesions.
294 NA-mRNA interaction networks involved in the DNA damage response, validating them through the identif
298 despread intron retention and markers of the DNA damage response were also observed with SMN depletio
300 hort telomeres must avoid recognition by the DNA damage response while promoting telomerase recruitme
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