ライフサイエンスコーパス: DNA damage response

1 protein in the Fanconi anemia pathway of the DNA damage response.

2 d inflammation and activation of ATM and the DNA damage response.

3 )-1 and PARP-2 play an essential role in the DNA damage response.

4 mor suppressor and a master regulator of the DNA damage response.

5 programs at different stages of the cellular DNA damage response.

6 , C1QBP is, thus, an important player in the DNA damage response.

7 anscription and replication that trigger the DNA damage response.

8 which formed complexes with PARP1 during the DNA damage response.

9 es both survival and efficient repair during DNA damage response.

10 f DNA double strand breaks and activation of DNA damage response.

11 involved in transcription regulation and the DNA damage response.

12 NA-dependent protein kinase activity and the DNA damage response.

13 s of newly synthesized DNA and activation of DNA damage response.

14 gly, L1a and L5a failed to activate cellular DNA damage response.

15 istinct linkages play important roles in the DNA damage response.

16 omatin-associated protein that regulates the DNA damage response.

17 in maintenance of genomic stability and the DNA damage response.

18 s FoxM1 and PLK1, proteins implicated in the DNA damage response.

19 n status of multiple factors involved in the DNA damage response.

20 RecF and RecO have distinct functions in the DNA damage response.

21 nase controls cell cycle transitions and the DNA damage response.

22 ases play a central role in coordinating the DNA damage response.

23 recruitment of MRE11 to DSBs and impairs the DNA damage response.

24 itize cancer cells to MET inhibitors through DNA damage response.

25 ited, NOTCH1 expression is maintained during DNA damage response.

26 on, DNA replication, the cell cycle, and the DNA damage response.

27 sets of mutations in different components of DNA damage response.

28 induces replication stress and activates the DNA damage response.

29 to high levels of Akt3, by inactivating the DNA damage response.

30 level of regulation in the induction of the DNA damage response.

31 event ongoing transcription from eliciting a DNA damage response.

32 sion, whereas ATR is an apical kinase in the DNA-damage response.

33 by end-joining in the absence of a canonical DNA-damage response.

34 ATR functions as a master regulator of the DNA-damage response.

35 utcome in cancer patients through IR-induced DNA damage responses.

36 er than CPDs, are the trigger for UV-induced DNA damage responses.

37 ocesses such as inflammation, apoptosis, and DNA damage responses.

38 genic loci, and associated with antiviral or DNA damage responses.

39 determined their respective contributions to DNA damage responses.

40 sensor kinases responsible for orchestrating DNA damage responses.

41 sidues compromised viability, fertility, and DNA-damage responses.

42 enesis, the role of regulated development of DNA damage responses 1 (REDD1), a negative regulator of

43 heckpoint signaling and that SMCHD1 mediates DNA damage response activation upstream of ATM phosphory

44 t, thereby contributing to tumorigenesis and DNA damage response activation.

45 riation may be due to differences in how the DNA damage response affects cell cycle progression.

46 , we visualized and quantified the extent of DNA damage response after (177)Lu-DOTATATE therapy using

47 The DNA damage response after kidney injury induces cell cyc

48 CSs), capsule synthesis, osmotic stress, and DNA-damage response, among other categories.

49 e after INCENP silencing due to induction of DNA damage response and activation of the p53-p21 axis.

50 is required for optimal chemotherapy induced DNA damage response and apoptosis in GBM cells.

51 form the provirus or act as a target of the DNA damage response and become circularized.

52 anisation associated with the recruitment of DNA damage response and chromatin remodellers.

53 Dual targeting of the DNA damage response and glucose transport synergisticall

54 n SMG7 plays critical roles in regulation of DNA damage response and nonsense-mediated mRNA decay (NM

55 e prevailing model is that activation of the DNA damage response and protease-mediated degradation of

56 Here, we determine if PVs in DNA damage response and repair (DDRR) genes are enriched

57 k repair genes, as well as downregulation of DNA damage response and repair genes, in two independent

58 Here, we investigate the impact of DNA damage response and repair on 3D genome folding usin

59 eatments targeting oncogenic drivers and the DNA damage response and repair pathway warrant further p

60 otherapy in cancer through the inhibition of DNA damage response and repair.

61 S-1 cDNA transfection led to the reversal of DNA damage response and restoration of cell growth.

62 tion on key nuclear proteins involved in the DNA damage response and revealed cross-talk between cyto

63 sia mutated (ATM) is the initial step in the DNA damage response and subsequent cell cycle arrest; ho

64 ssory factor HPF1, which is specific for the DNA damage response and switches the amino acid specific

65 pha-MutLalpha complex serves as a sensor for DNA damage response and that HDAC6 disrupts the MutSalph

66 iological pathways related to growth arrest, DNA damage response and the lysosomal pathway.

67 proteins have been identified in regulating DNA damage responses and cell survival following treatme

68 ubsequent P2Y(2) receptor function stimulate DNA damage responses and hepatocyte proliferation, there

69 TP and subsequent P2Y(2)R function stimulate DNA damage responses and hepatocyte proliferation, there

70 DNA breaks activate the Escherichia coli SOS DNA-damage response and error-prone DNA polymerases in a

71 ed DNA (ssDNA) intermediates, activating the DNA-damage response and handing off ssDNA to the appropr

72 al RNAPII levels as integral to the cellular DNA-damage response and open the intriguing possibility

73 Partial depletion of DarG(Mtb) triggers a DNA-damage response and sensitizes Mtb to drugs targetin

74 expression of genes involved in cell cycle, DNA damage response, and cilium function.

75 etics, splicing, immune surveillance and the DNA damage response, and highlight the rapid rise of spe

76 male sex, somatic mutations that impair the DNA damage response, and more severe pretransplant cytop

77 establishes OTUD5 as a new regulator of the DNA damage response, and provides an insight into the FA

78 emonstrated indices of metabolic activation, DNA damage response, and stress response.

79 ion of retrotransposons, the activation of a DNA damage response, and switches in the global chromati

80 ates several genes orchestrating mitosis and DNA-damage responses, and its depletion causes chromosom

81 DNA damage responses are crucial for plant growth under

82 SMC5/6 depletion triggers a CHEK2-p53 DNA damage response, as concomitant deletion of the Trp5

83 DNA-PK is a key component within the DNA damage response, as it is responsible for recognizin

84 nd PLK1 is functionally important during the DNA damage response, as we found that whereas PLK1 activ

85 nism that involves induction of a persistent DNA damage response at chromosome ends and loss of cellu

86 POT1B or BRD2 with TRF2 restores a canonical DNA damage response at telomeres, resulting in frequent

87 e about an alternative role for this NR in a DNA damage response at telomeres.

88 n of G-quadruplex DNA along with the related DNA damage response at the telomere.

89 s the potentiation of the carcinogen-induced DNA damage response, at the tumor initiation stage, to i

90 ecome dependent upon an ATR/CHK1/CDC25A/CDK2 DNA damage response axis.

91 HELLS has been implicated in the DNA damage response, but its mechanistic function in rep

92 The ATR kinase plays a key role in the DNA damage response by activating essential signaling pa

93 Sae2 functions in the DNA damage response by controlling Mre11-Rad50-Xrs2 (MRX

94 n links high expression of HSATII RNA to the DNA damage response, centered on a noncanonical function

95 l sampling provides definitive evidence that DNA damage response clones outcompete other clones when

96 n in FA is the consequence of defects in the DNA-damage response combined with chronic activation of

97 First, alpha-synuclein colocalizes with DNA damage response components within discrete foci in h

98 ysine (RPB1 K(1268)), is the focal point for DNA-damage-response coordination.

99 trols, indicating that this component of the DNA damage response could be associated with the increas

100 Mutations in genes that function in the DNA damage response (DDR) also improve phenotypes in Mec

101 ther deficiencies in other components of the DNA damage response (DDR) also result in Pol theta addic

102 n by analyzing the chromosome end (telomere) DNA damage response (DDR) and cellular apoptosis in a T-

103 -cell destruction by analyzing the telomeric DNA damage response (DDR) and cellular apoptosis in high

104 rocessing of trapped TOP2ccs, suppressed the DNA damage response (DDR) and completely protected cells

105 ells 204 open reading frames involved in the DNA damage response (DDR) and determine their impact on

106 Most importantly, we identified multiple DNA damage response (DDR) and DNA repair pathways that s

107 is achieved mainly through execution of the DNA damage response (DDR) and DNA repair pathways, knowl

108 ted acetylation plays a critical role in the DNA damage response (DDR) and embryonic stem cell develo

109 be explained by NOTCH1 ability to block the DNA damage response (DDR) and ensuing growth arrest thro

110 kinase (DNA-PK) is a critical player in the DNA damage response (DDR) and instrumental in the non-ho

111 ects the expression of genes involved in the DNA damage response (DDR) and mRNA processing.

112 ular domains mechanistically involved in the DNA damage response (DDR) and pinpointing their roles in

113 f cancer that arises owing to defects in the DNA damage response (DDR) and/or increased replication s

114 The ubiquitin system regulates the DNA damage response (DDR) by modifying histone H2A at Ly

115 ntributes to virus-induced inhibition of the DNA damage response (DDR) by reducing ATM and ATR signal

116 The DNA damage response (DDR) coordinates DNA metabolism wit

117 The downregulation of the DNA damage response (DDR) enables aggressive tumors to a

118 The DNA damage response (DDR) encompasses the cellular respo

119 derstand why BKPyV-induced activation of the DNA damage response (DDR) enhances viral titers and prev

120 Anti-cancer drugs targeting the DNA damage response (DDR) exploit genetic or functional

121 ion-resistant prostate cancer is enriched in DNA damage response (DDR) gene aberrations.

122 Alterations in DNA damage response (DDR) genes are common in advanced p

123 uppressing the expression of BRCA1 and other DNA damage response (DDR) genes.

124 cumulating evidence supports the role of the DNA damage response (DDR) in the negative regulation of

125 To better understand the DNA damage response (DDR) in these cells, we exposed pre

126 We describe how recent research on DNA damage response (DDR) inhibitors in combination with

127 DNA damage response (DDR) involves dramatic transcriptio

128 The DNA damage response (DDR) is a DNA damage surveillance a

129 The DNA damage response (DDR) is an evolutionarily conserved

130 A proper DNA damage response (DDR) is essential to maintain genom

131 particularly dangerous lesions that activate DNA damage response (DDR) kinases, leading to initiation

132 wild-type human cells due to a p53-mediated DNA damage response (DDR) limiting the efficiency of gen

133 and any alteration in telomeres may activate DNA damage response (DDR) machinery resulting in telomer

134 g that the canonical immediate-response G2/M DNA damage response (DDR) may be deficient.

135 NA genomes can be recognized by the cellular DNA damage response (DDR) network as DNA damage whose re

136 and cell cycle checkpoint kinase 2 (CHK2), a DNA damage response (DDR) pathway activated during metab

137 MSCI is directed by a DNA damage response (DDR) pathway centered on the phosph

138 The DNA damage response (DDR) pathway coordinates the identi

139 We hypothesized that blocking the DNA damage response (DDR) pathway should further sensiti

140 biquitination plays an important role in the DNA damage response (DDR) pathway.

141 e over-activated or inhibited the endogenous DNA damage response (DDR) pathways by combinations of ac

142 l roles in base excision repair and ATR-Chk1 DNA damage response (DDR) pathways, it remains unknown h

143 report, we show that nitric oxide suppresses DNA damage response (DDR) signaling in the pancreatic be

144 Defective DNA damage response (DDR) signaling is a common mechanis

145 PARP1 also has a major role in DNA damage response (DDR) signaling, and our results sho

146 ted through Rv activates ATM-Chk2 pathway of DNA damage response (DDR) signaling, resulting in altere

147 hagy substrate and a regulator of IR-induced DNA damage response (DDR) signaling.

148 Further analysis reveals two DNA damage response (DDR) signatures could emerge early

149 llmark of PyV infection is activation of the DNA damage response (DDR) to prevent severe host and vir

150 for its function as a chief mobilizer of the DNA damage response (DDR) upon DNA double-strand breaks.

151 Elucidating the interplay among the DNA damage response (DDR), cyclic GMP-AMP synthase-stimu

152 ated (ATM) kinase, an upstream kinase of the DNA damage response (DDR), is rapidly activated followin

153 m was to investigate the association between DNA damage response (DDR), replication stress, and novel

154 other RNA/DNA binding proteins, like FUS in DNA damage response (DDR), the role of TDP-43 in DDR has

155 -strand breaks (DSBs) requires a coordinated DNA Damage Response (DDR), which includes phosphorylatio

156 Telomeric macroH2A1.2 is re-deposited in a DNA damage response (DDR)-dependent manner to promote ho

157 us end joining (NHEJ) repair pathway and the DNA damage response (DDR).

158 the unfolded protein response (UPR) and the DNA damage response (DDR).

159 tumor suppressor p53, which coordinates the DNA damage response (DDR).

160 osphorylated during resection as part of the DNA damage response (DDR).

161 ily conserved cellular response pathway, the DNA damage response (DDR).

162 can cause genome instability and activate a DNA damage response (DDR).

163 sensor, a critical factor in initiating the DNA damage response (DDR).

164 endent manner has been shown to regulate the DNA damage response (DDR).

165 trinsically disordered domains (IDPs) in the DNA damage response (DDR).

166 ein is both a functional partner in multiple DNA damage responses (DDR) and a pathway coordinator and

167 DSBs) by RNA polymerase II are necessary for DNA-damage-response (DDR) focus formation.

168 re and pancytopenia among diseases caused by DNA damage response defects.

169 n delivered as a bolus, H(2)O(2) induced the DNA damage response, depleted cellular energy stores, an

170 Accumulating evidence indicates that DNA damage responses differ between plant cell types.

171 cted a siRNA screen to identify genes of the DNA damage response/DNA repair regime that when acutely

172 stic underpinnings for two key facets of the DNA damage response: DSB end-resection and G(2)-checkpoi

173 53BP1 is an enigmatic DNA damage response factor that gained prominence becaus

174 genomic DNA strand breaks, activation of the DNA damage response factors phospho-ataxia-telangiectasi

175 d to the budding yeast Rtt107 and human PTIP DNA damage response factors, but functional similarities

176 DNA damage response gene mutations were associated with

177 tors preferentially selects for mutations in DNA damage response genes (TP53, PPM1D, CHEK2).

178 e that AR-Vs drive expression of a cohort of DNA damage response genes and depletion of AR-Vs sensiti

179 Notably, the constitutive activation of DNA damage response genes is largely SOG1-independent in

180 es in transcription beyond the expression of DNA damage response genes remain unclear.

181 ed expression in methyltransferase genes and DNA damage response genes, and decreased immune cell inf

182 Among direct Notch target genes are multiple DNA damage response genes, including IER5, which we show

183 cell cycle genes while high dox upregulated DNA damage response genes.

184 on, we discover that dosage-sensitive genes, DNA-damage-response genes, and cell-cycle-regulated gene

185 trols the stability of mRNAs involved in the DNA damage response, impacting DNA repair, cell cycle ar

186 FEN1 inhibition induced a DNA damage response in both sensitive and resistant cell

187 e to permeate into cell nuclei and trigger a DNA damage response in cancer cells.

188 ndent slow-growth phenotype and an activated DNA damage response in cells lacking Rep helicase, which

189 fine the mechanisms that control this unique DNA damage response in ES cells, we performed a CRISPR-C

190 ingly, CHD4 suppression results in defective DNA damage response in GBM cells.

191 o provide an unbiased and global view of the DNA damage response in human cells, we undertook 31 CRIS

192 ch for studying XPB and its roles in the UVB DNA damage response in human skin ex vivo and indicate t

193 ivity in normal keratinocytes, and modulated DNA damage response in MCF-7 cells.

194 Here, we show that the virus activates the DNA damage response in order to keep the infected cells

195 F2 at shortened telomeres contributes to the DNA damage response in senescence, the contribution of T

196 The importance of the DNA damage response in the inhibition of cell proliferat

197 s of polyploidy, associated with an elevated DNA damage response in this brain region.

198 ell as linking augmented R-loop formation to DNA damage response induced by driver mutations of key s

199 heat shock and endoplasmic reticulum stress, DNA damage responses, induction of xenobiotic metabolizi

200 Understanding how DNA damage response inhibitors cause cytotoxicity in can

201 ication stress, exposing a susceptibility to DNA damage response inhibitors.

202 nisms were assigned to four broad categories-DNA damage response, intracellular signaling, immune eng

203 Inhibition of the DNA damage response is an emerging strategy to treat can

204 Optimal DNA damage response is associated with ADP-ribosylation

205 The DNA damage response is essential to maintain genomic sta

206 The DNA damage response is known to be hyper-activated in la

207 The DNA damage response is known to be hyperactivated in lat

208 Induction of the DNA-damage response is essential for Mtb to survive part

209 rent study, we report that inhibitors of the DNA damage response kinase ATR can significantly potenti

210 r, our results highlight a role for FBL17 in DNA damage response, likely by ubiquitylating proteins i

211 USP7 in cell death pathways, chromatin, and DNA damage responses limit the use of catalytic inhibito

212 trimental activities of nucleases and of the DNA damage response machinery and participates in the re

213 viral gene expression and by inhibiting the DNA damage response, makes the genome vulnerable to a no

214 (PARylating) PARPs primarily function in the DNA damage response, many noncanonical mono(ADP-ribosyla

215 s than controls had ( P < 0.001) and reduced DNA damage-response markers [( DNA-PKcs, Mre11 ( P < 0.0

216 Mutations in other genes involved in the DNA damage response may simply enhance cell survival.

217 In this study, we show the DNA damage response mechanism in hESCs is composed of kn

218 Here we found an innate DNA damage response mechanism that is evident during bla

219 ependent oxidative damage, requires specific DNA-damage response mechanisms to maintain genomic and t

220 phosphorylated by CK2 and recognized by the DNA-damage response mediator protein TOPBP1.

221 NA for cyclin D2 and suppression of mRNA for DNA damage response mediators ATM, 53BP1, and MDC1.

222 Furthermore, protein levels of these DNA damage response molecules are reduced by IL-15, as i

223 significant correlation for tumor subtypes, DNA damage response mutations, and other biomarkers was

224 DNA double strand breakage triggers the DNA damage response network and two Fanconi anaemia DNA

225 ics provided high-throughput analysis of the DNA damage response network in callus cells.

226 in orchestrating the timing of events in the DNA damage response network.

227 We examined the role of ERbeta in the DNA damage response of GBM cells, and tested whether ERb

228 brid resolution likely rescues the defective DNA damage response of HNRNPD-depleted cells.

229 s that trigger aneuploidy, mitosis-dependent DNA damage responses, p53 stabilization and premature di

230 analysis, we evaluate the effects of Wnt and DNA damage response pathway alterations on metastatic co

231 t cellular antiviral defenses, including the DNA damage response pathway and activation of antiviral

232 and homologous recombination deficiency for DNA damage response pathway inhibitors or resistance (cy

233 highly-regenerative animals employ a robust DNA damage response pathway which involves regulation of

234 plex, activation of the ATR/CHK1 axis of the DNA damage response pathway, and mediated by degradation

235 Within the FA DNA damage response pathway, DNA-dependent monoubiquitin

236 a result, Akt3-expressing cells activate the DNA damage response pathway, express high levels of p53

237 atility of RNA as a mediator molecule in the DNA damage response pathway, which affects the accumulat

238 y, only 6-4PP lesions activated the ATR-Chk1 DNA damage response pathway.

239 s by reducing expression of the genes in the DNA damage response pathway.

240 Defects in the Fanconi anemia (FA) DNA damage-response pathway result in genomic instabilit

241 atasets elucidate that stromal phenotype and DNA damage response pathways are activated in RPV-strati

242 ness through promotion of expression of both DNA damage response pathways as well as cell cycle regul

243 denovirus has evolved, primarily, to inhibit DNA damage response pathways by engaging with the ubiqui

244 Moreover, DNA damage response pathways mediated by the ataxia-tela

245 NCE Viruses have evolved to inhibit cellular DNA damage response pathways that possess antiviral acti

246 hat possess antiviral activities and utilize DNA damage response pathways that possess proviral activ

247 k (ICL) repair requires a complex network of DNA damage response pathways.

248 ion fidelity and gene expression patterns in DNA damage response pathways.

249 ired cell cycle progression and induction of DNA damage-response pathways.

250 Thus, Notch and DNA-damage response pathways converge in squamous cells

251 y-induced quiescence occurs independently of DNA-damage response pathways, and is distinct from mitog

252 ecular mechanism of how mutant HTT activates DNA damage-response pro-degenerative pathways and impair

253 The DNA damage response protein ATM has long been known to i

254 causes transcriptional downregulation of the DNA damage response protein TopBP1, resulting in failure

255 n cofactors, BRN2 is instead associated with DNA damage response proteins and directly binds PARP1 an

256 eceptor axis, immune checkpoint receptors or DNA damage response proteins are being explored in patie

257 -rich repeat immune receptors, oxidative and DNA damage response proteins, and protein quality contro

258 avage that suppresses the expression of core DNA damage response proteins.

259 This map of the DNA damage response provides a rich resource to study th

260 S-acylated Rif1 mounts a localized DNA-damage response proximal to the inner nuclear membra

261 The DNA damage response relies on protein modifications to e

262 which nuclear lncRNAs directly contribute to DNA damage responses remain largely unknown.

263 overexpression of PACS-1 and suppression of DNA damage response, resulting in the development of che

264 novel class of small non-coding RNAs called DNA damage response RNAs (DDRNAs) generated at DNA doubl

265 SiHa cervical cancer cell lines resulted in DNA damage response, S-phase cell cycle arrest, and redu

266 DNA damage response Ser/Thr kinases, including ataxia te

267 Adenovirus differentially regulates ATR DNA damage response signaling pathways during infection.

268 gnaling, and protein ubiquitination, besides DNA damage response signaling, as being impacted by RAD6

269 tuin 6) is a nuclear deacetylase involved in DNA damage response signaling, inflammation, and metabol

270 luding CHK1, a checkpoint kinase involved in DNA damage response signaling.

271 before implantation, with evidence of strong DNA damage response signalling and apoptosis specificall

272 he PATS show an enrichment of TP53, TGFbeta, DNA-damage-response signalling and cellular senescence.

273 ivation of caspases, which through nonlethal DNA damage response signals then leads to activity-assoc

274 analysis, we show that upon the onset of the DNA-damage response, SMURF2 becomes phosphorylated at Se

275 lia share molecular components implicated in DNA damage response, splicing, gene expression, and sub-

276 gene expression patterns, proliferation and DNA damage response that have been linked to poor clinic

277 e deletion of TRF2, ES cells exhibit a muted DNA damage response that is characterized by the recruit

278 RF2 instead activate an attenuated telomeric DNA damage response that lacks accompanying telomere fus

279 int kinase 1 (CHK1) is a key mediator of the DNA damage response that regulates cell-cycle progressio

280 elomere shortening in human cells leads to a DNA damage response that signals replicative senescence.

281 rtic challenge in wild-type mice induced the DNA damage response, the inflammatory response, dediffer

282 ilization of p53 serves as a "trademark" for DNA damage responses, the requirement for such dramatic

283 In the DNA damage responses, this post-translational modificati

284 Salmonella Typhi activates the host DNA damage response through the typhoid toxin, facilitat

285 , in cancer cells with impaired compensatory DNA damage responses through ATM loss) as monotherapy an

286 Ti) increase PARP trapping and reprogram the DNA damage response to generate HRD, sensitizing BRCA-pr

287 Here, we report that Banf1 controls the DNA damage response to oxidative stress via regulation o

288 ctivation of E2F (E2F transcription factor), DNA damage response, TP53 (tumor protein 53), NFkappaB (

289 The findings denote the E2F/DNA damage response/TP53 axis as a responsible mechanism

290 directions to characterize NSD2 function in DNA damage response, transcriptional regulation, and oth

291 d in chromatin modification and p53-mediated DNA-damage responses, two pathways that play key roles i

292 is an apical kinase in the radiation-induced DNA damage response, we investigated the effects of ATM

293 ng a model of antagonistic pleiotropy in the DNA damage response where histone degradation, and limit

294 s an oxidative stress-induced TP53-dependent DNA damage response, which impairs early cNCC specificat

295 Here we reveal a non-canonical DNA damage response, which we call RING (response induce

296 Bs in Brme1(-/-) reactivate the somatic-like DNA-damage response, which repairs DSBs but cannot compl

297 mechanism for SSB end resection that couples DNA damage response with SSB repair in a eukaryotic syst

298 Targeted chemotherapy induces the DNA damage response without causing DNA breaks or allowi

299 During DNA damage response, WRN is translocated to the nucleopl

300 e) glycohydrolase (PARG) critically regulate DNA damage responses; yet, conflicting reports obscure P