ライフサイエンスコーパス: DDR

1 DDR activation and maintenance at telomeres depend on th

2 DDR activation is viewed as a physiological barrier agai

3 DDR activation results in cell-cycle blockade and inhibi

4 DDR also attenuates gene expression by silencing global

5 DDR involves a temporary arrest of the cell cycle to all

6 DDR-PARPs detect DNA strand breaks, leading to a dramati

7 DDRs are frequently inactivated in cells with extra geno

8 (rho, range, -0.07 to 0.10), while 13 of 17 DDR gene sets are strongly correlated with androgen rece

9 ancer patients in parallel sequencing of 796 DDR genes, were studied for disease association.

10 Profiling of 9 DDR pathways using 17 gene sets for GSEA (Gene Set Enric

11 A DDR pathway profile prognostic signature built in the tr

12 A DDR pathway signature showed strong prognostic performan

13 A DDR-resistant MYOD mutant could overcome this barrier by

14 rylation site alone is sufficient to cause a DDR deficiency phenotype in the mouse.

15 c.7253dupT in TEX15, encoding a DDR factor important in meiosis, associated with heredit

16 s study, we demonstrate that HBoV1 induces a DDR that plays significant roles in the replication of t

17 such replication is likewise dependent on a DDR.

18 mplex protein TRF2 from telomeres promotes a DDR that involves DNA-dependent protein kinase (DNA-PK).

19 n maintenance of genomic stability through a DDR-independent pathway.

20 Accordingly, DDR-P cells exhibit reduced sensitivity to MK-1775 upon

21 Decompacted telomeres accumulate DDR signals and become more accessible to telomere-assoc

22 Dysfunctional telomeres activate DDR in ageing, cancer and an increasing number of identi

23 s exhibit evidence for a partially activated DDR during mitosis, which leads to ongoing chromosome se

24 Unrepaired SSB activates DDR and increases the expression of inflammatory cytokin

25 Growth in low serum did not alter DDR signalling but increased the sensitivity of A2058 an

26 g the causative role of SSB accumulation and DDR activation in the pathogenesis of heart failure.

27 PD, CAL, and DDR% were evaluated in two subgroups in both the placebo

28 sters of DDR pathways within the cohort, and DDR pathway enrichment is only weakly correlated with cl

29 DNA damage and DDR activation are observed in the failing heart, howeve

30 cycle progression is remarkably delayed and DDR markers are upregulated in cerebellar ventricular zo

31 nection between p53-regulated metabolism and DDR, both of which play crucial roles in tumor suppressi

32 regulators required for DNA replication and DDR activation, thus disabling SASP expression.

33 protein response, acute-phase response, and DDR in hepatocytes.

34 Elevated [Ca2+]i, ROS, and DDR signals are normalized with dantrolene.

35 linking impaired glutamatergic signaling and DDR to neurodegeneration in preCGG brain.

36 t from DDR pathway profiles was studied, and DDR pathway gene mutation in published cohorts was analy

37 stress and elucidated the role of the apical DDR kinases ATR, ATM and DNA-PKcs in the cellular defens

38 ncoproteins and a global MRN-independent ATM DDR to viral nuclear domains that does not impact viral

39 es to adenovirus genomes: a critical MRN-ATM DDR that must be inactivated by E1B-55K/E4-ORF3 viral on

40 for SSB repair, which is rescued by blocking DDR activation through genetic deletion of ATM, suggesti

41 231 breast cancer cells were not affected by DDR kinase inhibition.

42 , as well as Blm helicase, but not canonical DDR signaling.

43 atin structure in the regulation of cellular DDR regulation.

44 fy USP7 as a novel component of the cellular DDR involved in preserving the genome stability.

45 BF and PTTG expression in well-characterised DDR gene panel RNA-seq data.

46 ged chromatin and activation of the ATR-Chk1 DDR pathway in response to oxidative stress in Xenopus e

47 In published cohorts, DDR pathway genes are rarely mutated.

48 e that immature lymphocytes exploit a common DDR signaling pathway to limit DSBs at multiple genomic

49 addition, transcriptional elongation-coupled DDR signalling involves topoisomerase II because inhibit

50 Critically, DDR genes were extensively repressed in primary thyrocyt

51 DNA repair proficient (DDR-P) or deficient (DDR-D).

52 ugh the initiation of a type I IFN-dependent DDR.

53 romatin using an orthogonal method displaces DDR signals from telomeres.

54 f HOTAIR induces NF-kappaB activation during DDR and interleukin-6 and interleukin-6 expression, both

55 ives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemother

56 1 (MRN) complex, at serine 649 (S649) during DDR.

57 kinases have been thoroughly studied during DDR activation, the role of protein dephosphorylation in

58 releasing macrophage-derived HB-EGF, enhance DDR in neighboring cells suffering from DNA damage.

59 L4 could induce drug resistance by enhancing DDR and DNA repair through promoting glycolysis and subs

60 in replicative human senescent fibroblasts, DDR precluded MYOD-mediated activation of the myogenic p

61 ysfunctional telomeres and are necessary for DDR activation and they validate the viability of locus-

62 Prognostic signature development from DDR pathway profiles was studied, and DDR pathway gene m

63 linical parameters and significantly greater DDR compared with the ATV group in treatment of mandibul

64 tegy used by adenovirus to abrogate the host DDR and show how viruses can modify cellular processes t

65 During the past 2 decades, understanding how DDR drives cancer development and contributes to the agi

66 Impaired DDR in SALL4-deficient human cancer cells can be rescued

67 ngthens the emerging notion that an impaired DDR may be a key factor in the pathogenesis of JS and ot

68 se (DDR) pathway and SETD2 mutation impaired DDR, blunting apoptosis induced by cytotoxic chemotherap

69 Because polyploidy and impaired DDRs can promote cancer, our findings provide insight in

70 olyploidy can reveal how cells with impaired DDRs/genome damage continue dividing.

71 sion of various HR-associated genes, impairs DDR and sensitizes MLL leukemia to PARP inhibitors (PARP

72 not address the role of enhancer elements in DDR-mediated transcriptional regulation.

73 lity to identify a PPI inhibitor, 26 PPIs in DDR pathways (BER, MMR, NER, NHEJ, HR, TLS, and ICL repa

74 (DDRNAs), have been shown to play a role in DDR signalling and DNA repair.

75 s suggest that Sam68 plays a crucial role in DDR via regulating DNA damage-initiated PAR production.

76 As part of its role in DDR, Filia interacts with PARP1 and stimulates its enzym

77 binds SET, we investigated a role for SET in DDR inhibition by protein VII.

78 ne deacetylases, regulates multiple steps in DDR and is closely associated with many physiological an

79 e (DDR) through multiple pathways, including DDR signaling, cell-cycle checkpoints and damage repair,

80 While camptothecin and H2O2 both induce DDR activation, nitric oxide suppresses only camptotheci

81 An essential aspect of the MVM-induced DDR is establishment of a potent premitotic block.

82 An essential aspect of the MVM-induced DDR is the establishment of a potent premitotic block, w

83 es in radiosensitization through influencing DDR and support the rationale of blocking TRIP12 to impr

84 beta cells, as nitric oxide fails to inhibit DDR signaling in macrophages, hepatocytes, and fibroblas

85 s, which promotes apoptosis while inhibiting DDR signaling.

86 iation, indicating that protein VII inhibits DDR signaling.

87 icing and export of transcripts encoding key DDR proteins, including the ATM kinase.

88 stern blotting and immunofluorescence of key DDR proteins.

89 otein-protein interactions (PPIs) of the key DDR components.

90 quitin-specific protease 11 (USP11), a known DDR-component, as a functional interactor of RNF4.

91 How cells lacking DDRs cope with broken chromosomes during mitosis is poor

92 Notably, the late DDR protein, 53BP1 shows in live-cell imaging strikingly

93 Likewise, DDR inhibition could also restore MYOD's ability to acti

94 omains from those of PARP-1, the other major DDR-PARP, and highlights the specialization of the multi

95 ng of the inter-dependency between two major DDR mechanisms during the response to a conventional che

96 A significantly greater mean DDR% was found in the MF group than the placebo group at

97 l type-specific actions of the HUS1-mediated DDR in vivo.

98 e intrinsic connections between p53-mediated DDR and metabolic regulation remain incompletely underst

99 nce of HP1alpha-Glut1 axis in SALL4-mediated DDR.

100 ppressorium repolarization involves a novel, DDR-independent S-phase checkpoint, triggered by appress

101 a feedback loop from the PCM to the nuclear DDR in which CHK1 regulates pericentrin-dependent PCM ex

102 on, which was proposed to minimize access of DDR factors.

103 ulation of chromatin may influence access of DDR proteins to the host genome.

104 ntion of mitochondria-mediated activation of DDR.

105 ization of the multi-domain architectures of DDR-PARPs.

106 Deregulation of some aspects of DDR orchestration is potentially pathological and could

107 e histone H2AFX locus to abolish assembly of DDR factors at sites of DNA double-strand breaks.

108 We found that there are distinct clusters of DDR pathways within the cohort, and DDR pathway enrichme

109 tional targeting of the intact components of DDR signaling pathways.

110 These data provide the first evidence of DDR-mediated functional antagonism between senescence an

111 Proper execution of DDR requires careful coordination between these interdep

112 The expression of DDR kinases (pATR, pATM, pChk1, pChk2, and pWee1) and DN

113 Main function of DDR is, however, to prevent the fixation of debilitating

114 lex DNA genome of HBoV1 induces hallmarks of DDR, including phosphorylation of H2AX and RPA32, as wel

115 Inhibition of DDR restored satellite cell differentiation ability.

116 ilitate DSB repair, revealing a new layer of DDR regulation involving specialized RNA molecules.

117 hemotherapy, consistent with a local loss of DDR, and identify a potential therapeutic strategy to ta

118 Consistent with local recruitment of DDR, genomic regions with higher H3K36me3 had a lower mu

119 hus critical to understand the regulation of DDR in cells especially in the light of a strong linkage

120 advances in understanding the regulation of DDR in prostate cancer, and to present potential therape

121 expression caused a reduced up-regulation of DDR messenger RNAs in regenerating hepatocytes.

122 pose that Gene 33 is a proximal regulator of DDR that promotes DNA repair.

123 ls further induced significant repression of DDR genes in Bi-Tg thyrocytes (P=2.4 x 10(-4)) compared

124 Only DDR-P cells showed increased apoptosis as a result of ea

125 nd propene) and the host material (ZSM-58 or DDR) are of practical interest in relation to the develo

126 or RanGTP in promoting cell proliferation or DDR is not clear.

127 Prevention of SSB accumulation or persistent DDR activation may become a new therapeutic strategy aga

128 ormal organ development occurs in polyploid, DDR-impaired Drosophila papillar cells.

129 ion or treatment with POT1a protein prevents DDR, maintained self-renewal activity and rejuvenated ag

130 lines that are either DNA repair proficient (DDR-P) or deficient (DDR-D).

131 cleotide production was essential to promote DDR.

132 mouse and human T cells display a pronounced DDR in vitro and in vivo.

133 80 and promotes RAP80 recruitment and proper DDR.

134 IBDs) and percentage defect depth reduction (DDR%) was done at baseline and 6- and 9-month intervals

135 r mean percentage of defect depth reduction (DDR) was found in the RSV group (30.80% +/- 8.35%, 41.86

136 l nuclear functions of Gene 33 that regulate DDR.

137 port that a deubiquitinase, USP13, regulates DDR by targeting RAP80.

138 itors of the DNA damage response and repair (DDR) pathways by focusing on protein-protein interaction

139 2 pathways are central in DNA damage repair (DDR) and their over-activation may confer aggressive mol

140 inding proteins (RBPs) in DNA damage repair (DDR) pathways.

141 n, such as metabolism and DNA damage repair (DDR), are also essential for p53-dependent tumor suppres

142 RNF168 levels, repressed DNA damage repair (DDR), increased 53BP1 foci and enhanced radioresponsiven

143 s compared to two out of four representative DDR-P (MIA PaCa2 and PANC-1) cell lines.

144 complete disruption of DNA damage response (DDR) adaptor proteins in ETI cells causes severe growth

145 sustained activation of DNA damage response (DDR) after platinum treatment.

146 ched as cells mounted a DNA damage response (DDR) against exposed chromosome ends.

147 de proteins involved in DNA damage response (DDR) and are characterized by rare loss-of-function muta

148 ucture is important for DNA damage response (DDR) and DNA repair.

149 ive role of the mitotic DNA damage response (DDR) and evidence suggesting that its untimely activatio

150 ides with activation of DNA damage response (DDR) and impaired ability to differentiate into myotubes

151 t1a knockdown increases DNA damage response (DDR) and inhibits self-renewal.

152 in kinase regulates the DNA damage response (DDR) and is associated with cancer suppression.

153 vates the ATR-dependent DNA damage response (DDR) and is required for DSB repair by homologous recomb

154 d a uniquely attenuated DNA damage response (DDR) and muted DNA repair.

155 ubsequent activation of DNA damage response (DDR) and permanent cell cycle arrest of cardiomyocytes.

156 t include a compromised DNA damage response (DDR) and prominent nervous system phenotypes.

157 any factors involved in DNA damage response (DDR) and the cell cycle depends on their Ran GTPase-regu

158 genes involving in the DNA-damage response (DDR) are often tumor prone owing to genome instability c

159 plex that represses the DNA damage response (DDR) at chromosome ends.

160 ces a caspase-dependent DNA damage response (DDR) at telomeres in non-apoptotic cells.

161 s a central role in the DNA damage response (DDR) by controlling the levels of various DNA repair and

162 Plk1 contributes to the DNA damage response (DDR) by targeting multiple factors downstream of the cor

163 re shielded against the DNA damage response (DDR) by the shelterin complex.

164 plication blockade, the DNA damage response (DDR) cell signalling network is activated, with checkpoi

165 significantly modulate DNA damage response (DDR) genes, including p53 target genes, required to main

166 multiple cell cycle and DNA damage response (DDR) genes.

167 hinery and the elicited DNA damage response (DDR) have not yet been studied.

168 DNA damage response (DDR) includes the activation of numerous cellular activi

169 y linked Gene 33 to the DNA damage response (DDR) induced by hexavalent chromium (Cr(VI)), but the mo

170 hromatin.IMPORTANCE The DNA damage response (DDR) is a cellular network that is crucial for maintaini

171 The DNA damage response (DDR) is a set of cellular events that follows the genera

172 us genome, the cellular DNA damage response (DDR) is considered a barrier to successful infection.

173 have determined that a DNA damage response (DDR) is directed to viral genomes but is distinct from t

174 IFICANCE STATEMENT: The DNA damage response (DDR) is essential for prevention of a broad spectrum of

175 these pathways for the DNA damage response (DDR) is underscored by the growing appreciation that def

176 ese agents activate the DNA damage response (DDR) kinases ATM and DNA-PKcs through the generation of

177 rely on a multifaceted DNA damage response (DDR) network to maintain genomic integrity.

178 The DNA damage response (DDR) orchestrates a network of cellular processes that i

179 lizes components of the DNA damage response (DDR) pathway and SETD2 mutation impaired DDR, blunting a

180 on of the p53-dependent DNA damage response (DDR) pathway is well established.

181 (IR), cells activate a DNA damage response (DDR) pathway to re-program gene expression.

182 ivation of the ATR-Chk1 DNA damage response (DDR) pathway via ill-defined mechanisms.

183 ulation of the cellular DNA damage response (DDR) pathway, a key pathway involved in the maintenance

184 with activation of the DNA damage response (DDR) pathway, as evidenced by elevated DNA damage, prima

185 t that acts through the DNA damage response (DDR) pathway, involving the Cds1 kinase.

186 n the regulation of the DNA damage response (DDR) pathway, we challenged Plk1-overexpressing mice wit

187 al apical kinase of the DNA damage response (DDR) pathway.

188 pathways, including the DNA damage response (DDR) pathway.

189 to date, pertain to the DNA damage response (DDR) pathway.

190 oads of three different DNA damage response (DDR) pathways involved in protecting stressed replicatio

191 ly Checkpoint (SAC) and DNA Damage Response (DDR) pathways.

192 The DNA damage response (DDR) plays a pivotal role in maintaining genome integrit

193 essed activation of the DNA damage response (DDR) protein gammaH2AX induced by selective genotoxins t

194 r inclusions containing DNA damage response (DDR) proteins are causally linked to abnormal synaptic f

195 targeting genes for the DNA-damage response (DDR) proteins MDC1, 53BP1, RIF1 and P53, plus the nuclea

196 Execution of the DNA damage response (DDR) relies upon a dynamic array of protein modification

197 l component of multiple DNA damage response (DDR) signaling networks.

198 including constitutive DNA damage response (DDR) signaling, senescence-associated beta-galactosidase

199 emia-related pathway of DNA damage response (DDR) signaling.

200 DSBs trigger the DNA damage response (DDR) that directs a cell to repair the break, undergo ap

201 s have evolved a common DNA damage response (DDR) that sustains cellular function, maintains genomic

202 grity and regulates the DNA damage response (DDR) through multiple pathways, including DDR signaling,

203 aling is crucial in the DNA damage response (DDR) to mediate the repair of damaged DNA.

204 grates signals from the DNA damage response (DDR) towards PGC-1beta-dependent mitochondrial biogenesi

205 es a sustained cellular DNA damage response (DDR) which the virus exploits to prepare the nuclear env

206 es a sustained cellular DNA damage response (DDR) which the virus then exploits to prepare the nuclea

207 1 infection initiates a DNA damage response (DDR), activating all three phosphatidylinositol 3-kinase

208 423 participates in the DNA-damage response (DDR), raising questions regarding its role as a regulato

209 fects by activating the DNA damage response (DDR), which in turn induces inflammation.

210 ence as outcomes of the DNA damage response (DDR).

211 regulating the cellular DNA damage response (DDR).

212 ding RNA to mediate the DNA damage response (DDR).

213 braxas) and facilitates DNA damage response (DDR).

214 gnalling network called DNA damage response (DDR).

215 se, metabolism, and the DNA damage response (DDR).

216 /nucleus as part of the DNA damage response (DDR).

217 sites (DSBs) during the DNA damage response (DDR).

218 esion that triggers the DNA damage response (DDR).

219 lar activation of early DNA damage response (DDR).

220 le-cell analysis of the DNA damage response (DDR).

221 ted during the cellular DNA damage response (DDR).

222 osis by attenuating the DNA damage response (DDR).

223 n important role in the DNA damage response (DDR).

224 sirtuins (SIRTs) in the DNA damage response (DDR).

225 gnaling molecule in the DNA damage response (DDR).

226 ays collectively termed DNA damage response (DDR).

227 argeted manipulation of DNA damage-response (DDR) signaling pathways would allow for selective therap

228 unleashes a torrent of DNA damage responses (DDRs) at the telomeres, culminating in karyotypic altera

229 Conserved DNA-damage responses (DDRs) sense genome damage and prevent mitosis of broken

230 ated in the control of DNA damage responses (DDRs) through its interactions with checkpoint kinase 1

231 signaling molecule in DNA damage responses (DDRs).

232 y decreased their radiosensitivity, restored DDR function, and increased survival, signifying its rol

233 levation decreases the expression of several DDR genes.

234 ting small changes in telomere volume showed DDR at nearly all telomeres.

235 aims of this review are to discuss specific DDR defects in prostate cancer that occur during disease

236 hey validate the viability of locus-specific DDR inhibition by targeting DDRNAs.

237 s allows the unprecedented telomere-specific DDR inactivation in cultured cells and in vivo in mouse

238 t intracellular signaling of the B. subtilis DDR is achieved via production of L-malic acid, which af

239 t promotes beta-cell survival by suppressing DDR signaling and attenuating DNA damage-induced apoptos

240 s have revealed cell-autonomous and systemic DDR mechanisms that orchestrate adaptive responses that

241 Our findings propose that DDR signalling is required for effective Pol II pause re

242 The DDR induced by the HBoV1 NS1 protein does not cause obvi

243 st protection of chromosome ends against the DDR machinery.

244 s is resolved by telomerase activity and the DDR in two parallel pathways and that deletion of Sml1 p

245 ng revealed patient-level variations and the DDR pathways are rarely affected by mutation.

246 fect the amounts and types of damage and the DDR.

247 ion that promotes cell proliferation and the DDR.

248 in the light of a strong linkage between the DDR impairment and the occurrence of common human diseas

249 icating that recognition of viral DNA by the DDR does not necessarily result in activation of downstr

250 In contrast, ATR coordinated the DDR during neurogenesis to direct apoptosis in cycling n

251 iruses is facilitated by the cell cycle, the DDR triggered by HBoV1 DNA replication or NS1 is not.

252 causes endogenous DNA damage and delays the DDR by impaired recruitment of repair factors MDC1 and 5

253 ring infection can globally downregulate the DDR.

254 R have unique and essential roles during the DDR, collectively ensuring comprehensive genome maintena

255 nstrate independent biological roles for the DDR kinases DNA-PKcs, ATM, and ATR during neurogenesis.

256 cell cycle progression is necessary for the DDR-resistant MYOD mutant to reverse senescence-mediated

257 th the bacterial DNA and is required for the DDR.

258 We highlight the DDR pathways that are activated after treatment with rad

259 ir and checkpoint proteins; however, how the DDR communicates with the autophagy pathway remains unkn

260 V and provides a deeper insight into how the DDR is manipulated during viral infection.

261 nisms and execute different functions in the DDR.

262 kinase-like kinases (PI3KKs) involved in the DDR: ataxia telangiectasia mutated (ATM) kinase and ATM

263 two proteins play complementary roles in the DDR; ATM is engaged in the repair of double-strand break

264 t overcome cellular responses, including the DDR.

265 ural protein NS1 is sufficient to induce the DDR and the activation of the three PI3KKs.

266 n SET was recently suggested to modulate the DDR by affecting access of repair proteins to chromatin.

267 radiation and chemotherapy by modulating the DDR with a goal of enhancing the effectiveness of cancer

268 late to other viruses that must navigate the DDR.

269 Nitric oxide suppresses activation of the DDR (as measured by gammaH2AX formation and the phosphor

270 tributing to aROS-mediated activation of the DDR and cell cycle arrest.

271 proteins as key chromatin modulators of the DDR and provide novel insights into how DNA damage withi

272 the aging phenotype, with each stage of the DDR associated with specific aging pathologies.

273 However, a detailed understanding of the DDR at a physiological level is lacking.

274 ly, we place Dicer within the context of the DDR by demonstrating a DNA damage-inducible phosphoswitc

275 ould be, including the ambiguous role of the DDR pathway in human cancers, therapy-induced malignanci

276 Our study provides the first evidence of the DDR-dependent parvovirus DNA replication that occurs in

277 rotein kinases and central regulators of the DDR.

278 ), which generate DNA damage and turn on the DDR-SAC pathway.

279 gnaling also regulates functions outside the DDR, with implications for many other frontiers of resea

280 cular mechanism by which diRNAs regulate the DDR remains unclear.

281 The ability of nitric oxide to suppress the DDR appears to be selective for pancreatic beta cells, a

282 chromosomal instability and suppressing the DDR pathway.

283 It turns out that the DDR factor p53 takes center stage during tumor developme

284 These results suggest that the DDR induced by shelterin removal does not require substa

285 Central to the DDR are the ATM and ATR kinases, which respond primarily

286 tudy establishes a clinical relevance to the DDR induced SAC in oocytes.

287 ethyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate the role of MLL1 in SASP

288 Whereas the DDR that leads to the replication of the DNA of other pa

289 ) are known to interact extensively with the DDR during the course of their replicative cycles.

290 tors upstream of ATM/ATR and regulates their DDR-related functions.

291 are nuclear-localized in keeping with their DDR functions, yet both are also found in cytoplasm, inc

292 the Rag1/Rag2 (RAG) endonuclease engage this DDR to modulate transcription of genes that regulate lym

293 rast to other cell types, initiation of this DDR depends on signaling from the type I interferon rece

294 ly mitotic entry and catastrophe compared to DDR-D cells.

295 e protein VII-SET interaction contributes to DDR evasion by adenovirus.

296 that ectopic expression of Gene 33 triggers DDR in an ATM serine/threonine kinase (ATM)-dependent fa

297 main finger 11) encodes a previously unknown DDR factor involved in 5' end resection, ATR signaling,

298 hese DNA-binding agents may be combined with DDR inhibitors or ionising radiation to achieve more eff

299 domain, a region sharing high homology with DDR proteins Topoisomerase 3alpha (TOP3alpha) and NEIL3

300 treatment of hematological malignancies with DDR defects, where ATM/p53-dependent apoptosis is compro