ライフサイエンスコーパス: DNA damage

1 s on transcription recovery after UV-induced DNA damage.

2 forms of hydrolytic, oxidative or alkylative DNA damage.

3 ing in increased cancer cell survival during DNA damage.

4 tion effect against hydroxyl radical-induced DNA damage.

5 ALC1 remodeling upon recruitment to sites of DNA damage.

6 ycling defects, and partially mitigates HSPC DNA damage.

7 tion is critical for cell survival following DNA damage.

8 ify tDNAs as a new source of R-loop-mediated DNA damage.

9 hyper-phosphorylated and ubiquitylated after DNA damage.

10 rotein stability is also decreased following DNA damage.

11 ated a biosensor and induced apoptosis after DNA damage.

12 a challenging environment in which to repair DNA damage.

13 e oxygen species (ROS) and induces oxidative DNA damage.

14 th untreated samples, indicating significant DNA damage.

15 d in homologous recombination in response to DNA damage.

16 ce displayed enhanced liver regeneration and DNA damage.

17 pathways through which stem cells cope with DNA damage.

18 tiple sources of genotoxic stress that cause DNA damage.

19 ing, in a manner that depends on the type of DNA damage.

20 which was previously linked to resistance to DNA damage.

21 the cell cycle preventing S phase associated DNA damage.

22 replication forks to protect from RS-induced DNA damage.

23 nditions that potentially promote endogenous DNA damage.

24 tutively, whereas PRP19 recognizes RPA after DNA damage.

25 ponsible for bringing the kinase to sites of DNA damage.

26 inuous stimulation with activation beads and DNA damage.

27 ough the accumulation of genotoxic levels of DNA damage.

28 mics, can mobilize the genome in response to DNA damage.

29 ->T mutation signature typical of UV-induced DNA damage.

30 biting MCM7 and Rb and subsequently inducing DNA damage.

31 NuRD binding to chromatin and recruitment to DNA damage.

32 TbCPR-activated prodrugs and do not promote DNA damage.

33 e suppression of UV-induced inflammation and DNA damage.

34 ucing antibiotic entry and quinolone-induced DNA damage.

35 DNA repair system that deals with oxidative DNA damage.

36 bited radical-induced oxidative cellular and DNA damage.

37 on of [4Fe-4S] clusters of dehydratases, and DNA damage.

38 XPA-ATR-pS435 complex to sites of cisplatin DNA damage.

39 onnected cells and their high sensitivity to DNA damage.

40 nd NMD-dependent manner following persistent DNA damage.

41 ugmented cell death upon oxidative telomeric DNA damage.

42 or proper control of toxicity from on-target DNA damage.

43 ween ATM and histone H2AX without triggering DNA damage.

44 ex, disruption of cell-wall homeostasis, and DNA damage.

45 ate target gene transcription in response to DNA damage.

46 o-7,8-dihydro-2'-deoxyguanosine, a marker of DNA damage.

47 en is essential to enhance radiation-induced DNA damages.

48 chanisms involved in the generation of early DNA damage, a new calculation chain based on the Geant4-

49 presses de novo dTMP biosynthesis and causes DNA damage, accounting for the pathophysiology of megalo

50 ponse to treatment with the chemotherapeutic DNA-damaging agent temozolomide.

51 A DNA-damaging agent that induces DNA double-stranded brea

52 Exposure of neurons to DNA damaging agents or the excitotoxin NMDA elicited sim

53 THRAP3 and/or BCLAF1 leads to sensitivity to DNA damaging agents, defective DNA repair and genomic in

54 tins) are unsaturated imines that are potent DNA damaging agents, thereby confirming an earlier mecha

55 n slow growth and renders cells sensitive to DNA damaging agents.

56 that are targeted by subsequent exposure to DNA damaging agents.

57 AZD1775 and DNA-damaging agents have displayed favorable activity in

58 phase DSBs, and increased the sensitivity to DNA-damaging agents.

59 s apoptosis to both endogenous and exogenous DNA-damaging agents.

60 tigate their potential as radical-generating DNA-damaging agents.

61 metabarcoding and assessment of post-mortem DNA damage allowed us to authenticate ancient DNA retrie

62 resistance of GAPDH-overexpressing cells to DNA damage and apoptosis, which indicated that Ape1 is i

63 nting alveolar epithelial cell mitochondrial DNA damage and apoptosis.

64 al compound for the effects of PM10, causing DNA damage and cell death.

65 lutamine deficiency on cellular responses to DNA damage and chemotherapeutic treatment remains unclea

66 DNA damage and DDR activation are observed in the failin

67 or the repair of CX-5461 and CX-3543-induced DNA damage and failure to do so leads to lethality.

68 , is sufficient to account for the extent of DNA damage and genomic variation observed experimentally

69 n DNA composition have focused especially on DNA damage and genotoxicity.

70 ctive nitrogen species, as well as increased DNA damage and impaired DNA repair.

71 tes dATM, allowing cells to sense and repair DNA damage and increasing replication of loci that are n

72 d in the failing heart, however, the type of DNA damage and its role in the pathogenesis of heart fai

73 genome-destabilizing effect of environmental DNA damage and may be expected to result in a more conse

74 expressing male germ cells exhibit excessive DNA damage and meiotic defects.

75 d breaks (DSBs) represent highly deleterious DNA damage and need to be accurately repaired.

76 es, being an adaptive response to endogenous DNA damage and oncogene-induced replication stress.

77 stimulates the BRCA1-PALB2 interaction after DNA damage and promotes PALB2 localization to DNA damage

78 olved in translation initiation, cell cycle, DNA damage and proteolysis processes that affect multipl

79 LBH-deficient FLS had increased DNA damage and reduced expression of the catalytic subun

80 insight into factors that affect UV-induced DNA damage and repair and ultimately UV carcinogenesis.

81 humans and the recent genome-wide mapping of DNA damage and repair in these organisms at single-nucle

82 ase-deficient cells to tolerate constitutive DNA damage and replication stress.

83 that mTORC1 signaling suppresses endogenous DNA damage and replication stress.

84 ibition of MRE11 nuclease activity increased DNA damage and selectively induced apoptosis in cells ov

85 PDH down-regulation potentiated H2O2-induced DNA damage and SMC apoptosis.

86 monogenic autoinflammation, after exogenous DNA damage and spontaneously in human cancer cells.

87 Since p53 regulates cell death upon DNA damage and various cellular stresses, we hypothesize

88 by diverse mechanisms such as shear stress, DNA damage, and heat shock.

89 promotes survival by suppressing endogenous DNA damage, and may control cell fate through the regula

90 n and the proinflammatory response following DNA damage are cell-cycle dependent.

91 d by dA, the increased dA(*+) pKa results in DNA damage arising from hole transfer.

92 ONSON leads to severe replication-associated DNA damage arising from nucleolytic cleavage of stalled

93 and presence of AP endonuclease (APE1) on AP DNA damage arrays.

94 Here, we present evidence for DNA damage as an unexpected means to shape a protective

95 of ST6Gal-I potentiates gemcitabine-induced DNA damage as measured by comet assays and quantificatio

96 house dust mites (HDM) resulted in enhanced DNA damage, as measured by the CometChip and the stainin

97 repair to mitigate the detrimental impact of DNA damage associated with excessive cell division.

98 ents with DKD showed increased mitochondrial DNA damage associated with glomerular endothelial EDNRA

99 regulated transcription factors protect from DNA damage associated with proliferation at key stages o

100 Extension from DNA damage at primer termini remains poorly understood.

101 DNA damage at tDNAs in the absence of these helicases is

102 ccumulation of replication intermediates and DNA damage at tDNAs is higher in pif1Delta rrm3Delta tha

103 promotion of replication and suppression of DNA damage at tDNAs.

104 in chromatin induced by PARPi, resulting in DNA damage being channelled through repair by non-homolo

105 Upon DNA damage, binding of PARylated PARP1 by the macro doma

106 ed constitutive PARP activation, spontaneous DNA damage by alkaline comet assay, basal micronuclei le

107 Using an inducible system of DNA damage bypass, we further show that H2Bub is require

108 Importantly, HDM-induced DNA damage can be prevented by the antioxidants glutathi

109 sites, which are a common type of endogenous DNA damage, can forge interstrand DNA-DNA cross-links vi

110 lication of this technique is the absence of DNA damage caused by radiation exposure.

111 ce complex components (MCMs) and mediator of DNA damage checkpoint 1 (MDC1) expression.

112 4 was required for rapid inactivation of the DNA damage checkpoint after DSB repair.

113 Here, we find that within minutes of DNA damage checkpoint proteins are assembled at the kine

114 The metabolic conversion of ANI-7 induces DNA damage, checkpoint activation, S-phase cell cycle ar

115 uces systemic resistance to a broad range of DNA-damaging chemotherapeutics.

116 ating lymphocytes and overall survival after DNA damaging chemotherapy, whereas single blockade does

117 2 alteration as a mechanism of resistance to DNA-damaging chemotherapy, consistent with a local loss

118 al women undergoing commonly used genotoxic (DNA-damaging) chemotherapy experience an accelerated los

119 th deoxycholate, a component of bile, caused DNA damage consistent with the exposure to reactive oxyg

120 her, our findings demonstrate that recurrent DNA damage contributes to the chromatin landscape to ens

121 chemistry and molecular biology of PARP-1 in DNA damage detection and repair, the mechanistic and fun

122 ir enzymes is considered to be important for DNA damage detection.

123 liseconds to minute and found that following DNA damage, DNA exhibits distinct sub-diffusive regimes.

124 MJD2B silencing led to an enhancement of the DNA-damage driven induction of p21 and PIG3.

125 creases S-phase cell population, accumulates DNA damage during DNA replication and decreases apoptosi

126 These DNA damage foci tended to colocalize with telomeres, whi

127 he authors uncover functions, in response to DNA damage, for the bromodomain of the ISWI subunit BAZ1

128 , preventing BAP1(+/-) cells that accumulate DNA damage from executing apoptosis.

129 ation fork dynamics, massive accumulation of DNA damage, genome-wide double-strand breaks enriched at

130 DNA damage has long been established as a cause of cance

131 to DNA duplexes containing a single site of DNA damage (here a base mismatch) which inhibits DNA cha

132 Upon DNA damage, histone modifications are dynamically reshap

133 By generating localized telomere-specific DNA damage in a real-time fashion and a dose-dependent m

134 Mechanistically, doxorubicin-induced DNA damage in c-kit(+) cells resulted in expression of p

135 of a p53/PINCR/Matrin 3 axis in response to DNA damage in CRC cells.

136 production in the spinal cord and oxidative DNA damage in dorsal horn neurons.

137 int activation does not occur in response to DNA damage in fully mature eggs during meiosis II, despi

138 Track structures and resulting DNA damage in human cells have been simulated for hydrog

139 cells expressing IGF-1R, externally induced DNA damage in IGF-1R-negative cells caused G1 cell cycle

140 ABC294640, an inhibitor of SK2, reduces DNA damage in neurons and increases survival in two neur

141 hat defects in intron removal in SMA promote DNA damage in part through the formation of RNA:DNA hybr

142 BRCA2-deficient cancer cell line exacerbated DNA damage in response to chemotherapeutics.

143 rotected telomeres and localized to sites of DNA damage in S phase.

144 growth of embryos after the accumulation of DNA damage in seeds.

145 This review focuses on the etiology of DNA damage in the nervous system and the genome stabilit

146 acterize the SOS transcriptional response to DNA damage in the Patescibacteria superphylum.

147 d unexpected FDA-approved drugs that induced DNA damage, including clinically relevant microtubule de

148 n multiple cellular responses to UVB-induced DNA damage, including through a failure to properly supp

149 g cultures, we show that naturally occurring DNA damage incurred over S-phase causes p53-dependent ac

150 S2-013 cells increases gemcitabine-mediated DNA damage, indicating that suppressing ST6Gal-I activit

151 We also observed that DNA damage induced acetylation of HIPK2 along with an in

152 DNA damage induced by reactive carbonyls (mainly methylg

153 The mechanism of DNA damage-induced blockade of HIV-1 infection involved

154 onstrate a role for micronuclei formation in DNA damage-induced immune activation.

155 ar-PAP-mediated APA of PTEN is essential for DNA damage-induced increase of PTEN protein levels.

156 , initiated by progesterone and amplified by DNA damage-induced NF-kappaB signaling, that likely acco

157 gation plays an important role in regulating DNA damage-induced transcriptional silencing, distinct f

158 l rate-limiting steps that are essential for DNA-damage-induced inflammation.

159 Persistent DNA damage induces profound alterations in gene expressi

160 ciated with decreased overall survival after DNA damage-inducing platinum chemotherapy.

161 s not appear to be driven by distinctions in DNA damage induction or repair capacity.

162 dentify novel factors required for repair of DNA damage inflicted by IR.

163 When combined with DNA damage, inhibition of mTORC1/2 blocked transcription

164 , negative regulation of mTORC1 signaling by DNA damage is abrogated in many cancer cells, thus mTORC

165 Endogenous DNA damage is causally associated with the functional de

166 Accumulation of endogenous DNA damage is concomitant with defective ATM-mediated DN

167 tivation and HR, but how it is stimulated by DNA damage is still unclear.

168 pathway utilized for the repair of oxidative DNA damage, is compromised in Foxo3(-/-) primitive hemat

169 s from doxorubicin induction of gammaH2ax, a DNA damage marker.

170 During S-phase, minor DNA damage may be overcome by DNA damage tolerance (DDT)

171 findings implicate TOP2A cleavage as a broad DNA damage mechanism in oncogenic translocations as well

172 ge-associated increased O2(*-) and resulting DNA damage mediate the increased susceptibility of old f

173 Moreover, endogenous LMP1 blocks DNA damage-mediated apoptosis.

174 in lysogens until an induction event such as DNA damage occurs, triggering viral-mediated lysis.

175 eins are able to search for, detect, and fix DNA damage on a biologically relevant time scale.

176 In the absence of DNA damage, on the other hand, chromatin association of

177 cell death accompanied by S phase arrest and DNA damage only in ADK-expressing cells.

178 nvolved in tissue-specific stresses, such as DNA damage or inefficient autophagy.

179 Autophagy activated after DNA damage or other stresses mitigates cellular damage b

180 chronic HFD on beta-cells, wherein continued DNA damage owing to persistent oxidative stress results

181 ion in response to multiple stimuli, such as DNA damage, oxidative stress, and heat shock.

182 Upon DNA damage, p53 mRNA is released from stress granules an

183 EK1 and its interaction partners trigger the DNA damage pathways responsible for correcting DNA cross

184 and thus it is applicable to essentially all DNA damages processed by nucleotide excision repair.

185 1B, even when non-standard, are critical for DNA damage recovery in part by regulating ISWI factors l

186 eomycin and it was associated with increased DNA damage, reduced DNA repair responses, and elevated c

187 onse to telomere dysfunction and genome-wide DNA damage, reduced end resection at sites of DNA damage

188 pression reprogramming induced by persistent DNA damage remains poorly understood.

189 TR-Chk1 and ATM-Chk2 pathways are central in DNA damage repair (DDR) and their over-activation may co

190 mTORC1 and mTORC2 are both required to enact DNA damage repair and cell survival, resulting in increa

191 his underscores a previously unknown role of DNA damage repair in the pathophysiology of DFUs coloniz

192 on of genes that are crucial in coordinating DNA damage repair mechanisms.

193 ys63-linkage ubiquitin in the recruitment of DNA damage repair proteins 53BP1 and BRCA1.

194 putative targets of miR-424 that function in DNA damage repair, CHK1 and Wee1, are suppressed in HPV-

195 ts repressive chromatin proteins to sites of DNA damage repair, including DNA methyltransferases wher

196 f gene silencing, while H2AX is important in DNA damage repair.

197 NA accessibility and have been implicated in DNA damage repair.

198 with Dtx3L, a histone E3 ligase involved in DNA damage repair.

199 ying DNA for transcription, replication, and DNA damage repair.

200 ultraviolet radiation, oxidative stress and DNA damage repair; activation of immune response; regula

201 Expression of the DNA damage/repair marker, gamma-H2AX and DNA damage resp

202 Like other types of DNA damage, replicative stress activates the DNA damage

203 NMD suppression by persistent DNA damage required the activity of the p38alpha MAPK.

204 regulation, including DNA synthesis (NPAT), DNA damage response (ATM), mitosis (PMF1, CENPN and MAD1

205 eptibility genes encode proteins involved in DNA damage response (DDR) and are characterized by rare

206 ed regeneration coincides with activation of DNA damage response (DDR) and impaired ability to differ

207 In mouse HSCs, Pot1a knockdown increases DNA damage response (DDR) and inhibits self-renewal.

208 hrough resection activates the ATR-dependent DNA damage response (DDR) and is required for DSB repair

209 complex syndromes that include a compromised DNA damage response (DDR) and prominent nervous system p

210 The mitotic kinase Plk1 contributes to the DNA damage response (DDR) by targeting multiple factors

211 We recently linked Gene 33 to the DNA damage response (DDR) induced by hexavalent chromium

212 ature of the adenovirus genome, the cellular DNA damage response (DDR) is considered a barrier to suc

213 SIGNIFICANCE STATEMENT: The DNA damage response (DDR) is essential for prevention of

214 Here we show that these agents activate the DNA damage response (DDR) kinases ATM and DNA-PKcs throu

215 and BCLAF1 in the regulation of the cellular DNA damage response (DDR) pathway, a key pathway involve

216 its known functions, to date, pertain to the DNA damage response (DDR) pathway.

217 Whether intranuclear inclusions containing DNA damage response (DDR) proteins are causally linked t

218 FA signaling is crucial in the DNA damage response (DDR) to mediate the repair of damag

219 s of mice (MVM) induces a sustained cellular DNA damage response (DDR) which the virus exploits to pr

220 E-ALI) cultures, HBoV1 infection initiates a DNA damage response (DDR), activating all three phosphat

221 o apoptosis or senescence as outcomes of the DNA damage response (DDR).

222 old protein CCDC98 (Abraxas) and facilitates DNA damage response (DDR).

223 O binding induces a lesion that triggers the DNA damage response (DDR).

224 ontain hepatocytes with a notable persistent DNA damage response (gammaH2AX, 53BP1) due to chronic in

225 of NMD is tolerated, loss of hUPF1 induces a DNA damage response and cell cycle arrest.

226 Ura7 both resulted in the activation of the DNA damage response and imbalanced dNTP pools.

227 t contributes to transcriptional regulation, DNA damage response and limits heterochromatin spreading

228 nerating novel mechanistic inhibitors of the DNA damage response and repair (DDR) pathways by focusin

229 a-telangiectasia mutated (ATM) regulates the DNA damage response as well as DNA double-strand break r

230 work identifies a critical chromatin-binding DNA damage response factor, ZMYM3, which modulates BRCA1

231 takes advantage of signaling pathways in the DNA damage response for efficient genome amplification i

232 he regulatory pathways implicated in the HSC DNA damage response have not been fully elucidated.

233 the DNA damage/repair marker, gamma-H2AX and DNA damage response marker, phosphorylated ataxia telang

234 ranslation of DNA replication, survival, and DNA damage response mRNAs.

235 -specific small non-coding RNAs, also termed DNA damage response RNAs (DDRNAs), have been shown to pl

236 tant roles in transcriptional regulation and DNA damage response signaling.

237 re to ultraviolet light leads to a cell-wide DNA damage response that includes a global reduction in

238 modification coincides with the ATM-mediated DNA damage response that occurs on functional telomeres

239 ese results suggest that CTCF participate in DNA damage response via poly(ADP-ribosylation).

240 DNA damage, replicative stress activates the DNA damage response, a signaling cascade allowing cell c

241 lleviated RSV-induced replication stress and DNA damage response, and consequently attenuating cellul

242 d CDK4/6 blockade on cell-cycle progression, DNA damage response, and immune-modulation and may provi

243 processes including nutrient sensing and the DNA damage response, and implicated Vts1 in de novo gene

244 dified chemotherapy approaches targeting the DNA damage response, angiogenesis inhibitors, immune che

245 y p53-dependent enhancer activity during the DNA damage response.

246 c replication are known to induce a cellular DNA damage response.

247 al event that mediates the first wave of the DNA damage response.

248 yeast, dNTP pools expand drastically during DNA damage response.

249 ng and histone deacetylation) complex in the DNA damage response.

250 to form the triple T complex that regulates DNA damage response.

251 ssion during B lymphocyte activation and the DNA damage response.

252 oupling transcription with mRNA splicing and DNA damage response.

253 cancer subclass through a hormone dependent DNA damage response.

254 blish a pathway of autophagy specific to the DNA damage response.

255 Mice lacking genes involving in the DNA-damage response (DDR) are often tumor prone owing to

256 FANCM is a DNA-damage response gene whose heterozygous mutations pr

257 conserved sites disrupt its deacetylation of DNA-damage response proteins by impairing SIRT2 catalyti

258 carboplatin, does not kill cells through the DNA-damage response.

259 r ataxias, indicating an association between DNA damage-response and repair pathways and the age at o

260 the breast epithelium unleashes a torrent of DNA damage responses (DDRs) at the telomeres, culminatin

261 g DSB repair, which led to DSB accumulation, DNA damage responses, and early replication arrest in HG

262 d cyclin-dependent kinase 1 (CDK1) activity, DNA damage responses, or unscheduled DNA synthesis but t

263 omeric overhang of telomeres, elicits potent DNA-damage responses in melanoma cells; however, its mec

264 In late S/G2 phase, the DNA damage-responsive E3 ligase RNF8 conjugates K63-link

265 NA damage, reduced end resection at sites of DNA damage, resulted in compromised HR and misrejoining

266 s and NOX inhibitors can prevent HDM-induced DNA damage, revealing a novel role for antioxidants and

267 Cells with extensive DNA damage should die and not grow into malignancies.

268 ions are dynamically reshaped to accommodate DNA damage signaling and repair within chromatin.

269 Here, we investigated if activation of DNA damage signaling in vitro could be an endpoint for d

270 contexts, dE2F/dDP-dependent suppression of DNA damage signaling is key for cell-cycle control and n

271 eas macroH2A1.2 loss in these cells triggers DNA damage signaling-dependent senescence, a hallmark of

272 NA damage and promotes PALB2 localization to DNA damage sites.

273 riched in the nucleus and are accumulated at DNA damage sites.

274 nd alter the dynamics of ALC1 recruitment at DNA damage sites.

275 tion of RecN, the first protein recruited to DNA damage sites.

276 proximately 100 MPa elicits a RecA-dependent DNA damage (SOS) response in Escherichia coli K-12, desp

277 DNA damage stimulates LMP1 expression, and p53 is requir

278 M2, when it was induced by p53 subjecting to DNA-damaging stimuli such as treatment with doxorubicin,

279 increased oxidant stress, and mitochondrial DNA damage that, in turn, was linked to altered barrier

280 increases the sensitivity of the germline to DNA damage, thereby protecting the integrity of gamete g

281 DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by

282 possible relevance of the different types of DNA damage to AD-in particular, those caused by HSV1-and

283 y, radiation therapy and chemotherapy induce DNA damage to drive cells into apoptosis or senescence a

284 he dynamic phosphorylation of DNA-PKcs after DNA damage to mediate NHEJ.

285 kinase activity could be activated following DNA damage to phosphorylate specific DNA repair proteins

286 n fork machinery and a main regulator of the DNA damage tolerance (DDT) pathway.

287 S-phase, minor DNA damage may be overcome by DNA damage tolerance (DDT) pathways that bypass such obs

288 DNA damage tolerance during eukaryotic replication is or

289 Finally, DNA damage triggers dKDM4A-dependent changes in the leve

290 Replication stress or DNA damage triggers fork stalling and checkpoint signali

291 eratinocytes from UV-B-induced apoptosis and DNA damage via ATR.

292 factors, such as Pol eta, to sites of viral DNA damage via BPLF1, thereby allowing for efficient vir

293 key factor mediating androgen protection of DNA damage via Ku70/Ku80 in prostate cancer cells.

294 cAMP-enhanced repair of cisplatin-induced DNA damage was dependent on PKA-mediated phosphorylation

295 ed transcriptional-translational response to DNA damage was not impaired by rapalog inhibition of mTO

296 T1AM), on cell proliferation, cell death and DNA damage was studied in two ovarian cancer cell lines

297 quired relatively less 1,3-butadiene-induced DNA damage, we observed increased transcription and a mo

298 ADD45B to protect cells from consequences of DNA damage, which can be triggered by viral infection.

299 gulates G quadruplex (G4) DNA in response to DNA damage, which suppresses repair by nonhomologous end

300 0 and HP1a induced ectopic DNA synthesis and DNA damage without much of ectopic apoptosis.