ライフサイエンスコーパス: DNA damage

1 on and colony formation caused by UV-induced DNA damage.

2 lexes that help protect chromosome ends from DNA damage.

3 reduces cellular proliferation and increases DNA damage.

4 ir pathway and decreases cell viability upon DNA damage.

5 and led to defects in nuclear integrity and DNA damage.

6 sm; reduced nuclear MSH3 increases EMAST and DNA damage.

7 mportant hub for processing various types of DNA damage.

8 g differentiation, making them vulnerable to DNA damage.

9 uding cell proliferation and the response to DNA damage.

10 o influences the repair of radiation-induced DNA damage.

11 l for both DNA replication and the repair of DNA damage.

12 s consistent with induction of a response to DNA damage.

13 suggesting that sertraline induces oxidative DNA damage.

14 ptional activity and survival in response to DNA damage.

15 otects the genome from transcription-induced DNA damage.

16 t DNA molecules during repair of ICL-induced DNA damage.

17 but allowing for an enhanced p53 response to DNA damage.

18 Bs), or "nicks," are the most common form of DNA damage.

19 els by causing lethal replication stress and DNA damage.

20 cals are important reactive intermediates in DNA damage.

21 we studied links between cAMP signaling and DNA damage.

22 ains genomic stability through the repair of DNA damage.

23 ciency in homologous recombination repair of DNA damage.

24 a and are secreted in macrophage media after DNA damage.

25 sult in dental fluorosis, kidney failure, or DNA damage.

26 e completion of cell division over repair of DNA damage.

27 metabolism or other perturbations that cause DNA damage.

28 reaks (DSB) are the most deleterious type of DNA damage.

29 but at the expense of incurring substantial DNA damage.

30 tion in the next mitosis generates extensive DNA damage.

31 ed ssDNA and repair genomic loci affected by DNA damage.

32 titutively localized in the nucleus prior to DNA damage.

33 ication arrest, allowing replication despite DNA damage.

34 pecies participating in endogenous oxidative DNA damage.

35 esponse protein regulated in development and DNA damage 1 (REDD1) is necessary for the development of

36 h cell-cycle regulation by Growth Arrest and DNA Damage 45 gamma (Gadd45gamma).

37 This results in DNA damage, a loss of genome organization, and broad tra

38 n of G4 DNAs leads to replication stress and DNA damage accumulation and is therefore considered a pr

39 The connection between differentiation and DNA damage accumulation reveals a novel mechanism of gen

40 quired WNT signaling and was associated with DNA damage accumulation.

41 Cell stress and DNA damage activate the tumor suppressor p53, triggering

42 SW48) that were untreated or treated with a DNA-damaging agent.

43 unity, and in anticancer therapies involving DNA damage agents.

44 levels in E. coli cells exposed to exogenous DNA damaging agents, including many commonly used antibi

45 renders cells highly sensitive to a range of DNA damaging agents.

46 t effects of ionizing radiation, among other DNA damaging agents.

47 ted defects and elevates cell sensitivity to DNA-damage agents, such as cisplatin and olaparib.

48 s and cell survival following treatment with DNA-damaging agents and, as such, may play roles in modu

49 ination (HR) DNA repair and are sensitive to DNA-damaging agents such as platinum and PARP inhibitors

50 Upon exposure of human cells to DNA-damaging agents, NUCKS1 controls the resolution of R

51 hibitors also prevent recovery from multiple DNA-damaging agents, suggesting broad applicability for

52 s causes either sensitivity or resistance to DNA-damaging agents.

53 tein response and PKR and markedly increased DNA damage and apoptosis caused by dysregulation of TDP-

54 se) polymerase (PARP) cleavage indicative of DNA damage and apoptosis.

55 e S70pBcl2 prevents oxidative stress-induced DNA damage and cell death by suppressing mitochondrial R

56 be prevented, leading to the accumulation of DNA damage and cell death.

57 which drives extensive membrane deformation, DNA damage and chromosome fragmentation.

58 following irradiation, causing increased HSC DNA damage and depressed HSC recovery over time.

59 nonapoptotic cell death pathways induced by DNA damage and discuss their interplay with cellular sen

60 entify a surprising role for Cds1 in driving DNA damage and disrupted chromosomal segregation under c

61 increase DNA repair after cisplatin-induced DNA damage and exacerbates tubular injury through the up

62 event drug-induced oxidative stress-mediated DNA damage and execution with potential therapeutic impl

63 gical processes, they can also contribute to DNA damage and genome instability.

64 multiple factors, including cellular stress, DNA damage and immune surveillance.

65 erative vascular disease are associated with DNA damage and impaired signaling of BMPR2 (bone morphog

66 ays that exploit fluorescence for studies of DNA damage and its consequences.

67 with a displaced single-stranded DNA) create DNA damage and lead to genomic instability.

68 DNA damage and metabolic disorders are intimately linked

69 ted S phase entry causes replication stress, DNA damage and oncogenesis, highlighting the need for st

70 rovascular) endothelial cells in response to DNA damage and oxidant stress regulated in part by a BMP

71 Mitochondria respond to DNA damage and preserve their own genetic material in a

72 amentarium of DNA repair pathways to counter DNA damage and prevent mutation.

73 biquitination on lysine 13/15 (K13/K15) upon DNA damage and promotes the accrual of downstream repair

74 protecting cells from replication-associated DNA damage and promoting cellular recovery.

75 y is a widely used test for the detection of DNA damage and repair activity.

76 mutational signatures are joint products of DNA damage and repair and suggest that multiple factors

77 ome ends from inappropriately activating the DNA damage and repair responses.

78 Because DNA damage and replication stress are major sources of g

79 rated" MC simulation to calculate both early DNA damage and subsequent biological responses with time

80 uced carcinogenesis by causing inflammation, DNA damage, and activation of beta-catenin signaling.

81 induces transcription-replication conflicts, DNA damage, and cell death in oncogenic cells.

82 from IECs increases markers of inflammation, DNA damage, and cell proliferation and increases colorec

83 maintenance of osmotic pressure, response to DNA damage, and control of central metabolism, biofilm f

84 cells that retained short telomeres, accrued DNA damage, and exhibited p53 stabilization, successfull

85 ce and gerbils and attenuated isoLG adducts, DNA damage, and somatic mutation frequency.

86 Shot loss leads to double-strand break (DSB) DNA damage, and the apoptotic response is exacerbated by

87 on cAMP activation and we previously showed DNA damage, aneuploidy, and senescence in somatotroph ad

88 in model organisms, such as the response to DNA damage, apoptosis, and homeostasis.

89 Among the most deleterious types of DNA damage are DNA double-strand breaks (DSBs), which ca

90 The measurement of UV-induced DNA damage as a dosimeter of exposure and predictor of s

91 Moreover, DNA damage as determined by hepatocellular expression of

92 rogen receptor-dependent transactivation and DNA damage at concentrations relevant to exposures in hu

93 bination (HR), which leads to persistence in DNA damage but not an increase.

94 oocytes are unable to respond immediately to DNA damage, but instead mount a G2/M DDR that evolves sl

95 PI3K/mTORi also augmented CHK1i-induced DNA damage by attenuating DNA homologous recombination r

96 sliding clamp, PCNA, activates a pathway of DNA damage bypass that facilitates the replication of da

97 class of compounds that not only targets the DNA damage cancer response machinery but also simultaneo

98 As NEIL2 or Exo1 depletion mitigates the DNA damage caused by A3B expression, we suggest that abe

99 ues the DNA synthesis defects and suppresses DNA damage caused by INO80 depletion.

100 ase chain reaction for markers of autophagy, DNA damage, cell proliferation, and inflammation.

101 Large amounts of DNA damage, cellular debris, and by-products of cellular

102 The DNA damage checkpoint (DDC) is often robustly activated

103 etion of the Trp53 tumor suppressor or Chek2 DNA damage checkpoint kinase rescued Smc5 cKO neurodevel

104 n-induced foci (TIFs), indicating defects in DNA damage checkpoint signaling.

105 letion of the conserved helicase PIF1 and/or DNA damage checkpoint-mediator RAD9.

106 matid cohesion, and inactivated a third, the DNA damage checkpoint.

107 DSBs persist are therefore eliminated by the DNA-damage checkpoint.

108 cumulate on the lagging strand, resulting in DNA damage-checkpoint arrest and cell death.

109 cells in a clonal population to cisplatin, a DNA-damaging chemotherapeutic agent.

110 hibitors to alter the biological response to DNA-damaging chemotherapy and enhance the efficacy of ch

111 ons of proteins at DNA damage sites serve as DNA damage codes to recruit specific DNA repair factors.

112 ly, H. pylori-induced replication stress and DNA damage depend on the presence of co-transcriptional

113 Therefore, having rapid assays to quantify DNA damage, DNA repair, mutations, and cytotoxicity is b

114 report that L1 activity triggers FOA through DNA damage-driven apoptosis and the complement system of

115 nhibition with androgen ablation or with the DNA damaging drug, temozolomide, significantly reduces c

116 DNA damage engages IRE1alpha signaling in the absence of

117 5-AzadC-induced DNA damage enhanced P-TEFb occupancy via a mechanism tha

118 3BP1 from its modest status of (yet another) DNA damage factor to master regulator of double-strand b

119 ecruitment of MCPH1 promotes localization of DNA damage factors and homology directed repair of dysfu

120 ng, therefore it is of great interest to map DNA damage formation and repair to elucidate the distrib

121 characterize the factors mitigating cellular DNA damage formation by platinum compounds.

122 that removes RNA polymerase (RNAP)-stalling DNA damage from the transcribed strand (TS) of active ge

123 activation of caspase 3/7, and formation of DNA damage (gamma-H2AX) than the sum of the activities o

124 hile the presence of endogenous or exogenous DNA damage has the potential to impact PGCs, there is li

125 inflammation in skin and reduce UVB-induced DNA damage in both melanocytes and keratinocytes.

126 els of estrogen have been shown to stimulate DNA damage in breast epithelial cells through mechanisms

127 ving mutagenesis, DNA replication stress and DNA damage in cancer cells.

128 on of estrogen receptor alpha, and increased DNA damage in cells.

129 e physiological processes but can also cause DNA damage in certain contexts.

130 Cells confront DNA damage in every cell cycle.

131 or the addition of ADP-ribose moieties after DNA damage in human cells.

132 Such knowledge might help in detecting local DNA damage in live cells, as well as in aiding our bioph

133 reveal that excessive placental DNA damage in murine models for Cornelia de Lange syndro

134 during the sensing, repair and resolution of DNA damage in order to avoid excessive spreading of ubiq

135 taining ploidy and the repair of spontaneous DNA damage in placental cells, suggesting that genotoxic

136 arious forms of replication perturbation and DNA damage in S phase, suggesting it acts as a post-repl

137 dative stress and the induction of oxidative DNA damage in spermatozoa.

138 yguanosine (8-OHdg, a byproduct of oxidative DNA damage) in podocytes and tubular epithelial cells.

139 and recovery of 53BP1-mCherry, a marker for DNA damage, in live MDA-MB-231 cells.

140 that STRIDE can detect low-level spontaneous DNA damage, including age-related DNA lesions, DNA break

141 tegrity by responding to a large spectrum of DNA damage, including double strand breaks (DSBs) that i

142 replication errors due to different forms of DNA damage, including low-abundance DNA adducts induced

143 DNA damage increases in cells harbouring mutations that

144 The presence of DNA damage increases the frequency of pausing.

145 However, the nature of the DNA damage induced by acetaldehyde and how this is repai

146 DNA damage induced by chemotherapy drugs, such as topois

147 ry extracts inhibited the oxidative-mediated DNA damage induced by tert-butylhydroperoxide and scaven

148 spontaneous DSB levels and the estimation of DNA damage induced rather uniformly in the genome (e.g.,

149 pecific deubiquitinase, is essential for the DNA damage-induced beta-catenin activation.

150 y brain and that polyploidy protects against DNA damage-induced cell death.

151 o examine the molecular mechanism underlying DNA damage-induced histone removal, we screened histone

152 ation requires the Gadd45 (Growth arrest and DNA-damage-inducible) gene family, very little is known

153 nation treatment of BAY 1895344 with certain DNA damage inducing chemotherapy resulted in synergistic

154 DINO depletion decreases sensitivity to the DNA damage-inducing chemotherapy agent doxorubicin.

155 sted using a specially developed CRISPR/Cas9 DNA damage induction system, capable of inducing small c

156 romegaly, inhibited cAMP and GH and reversed DNA damage induction.

157 ow that, when apoptosis is inhibited, severe DNA damage is corrected via homologous recombination rep

158 The response to DNA damage is critical for cellular homeostasis, tumor s

159 indicate that modulation of mitophagy after DNA damage is independent of the type of DNA damage stim

160 Knowing the amount and type of DNA damage is of great significance for a broad range of

161 hromosome ends, where they re-integrate when DNA damage is present.

162 Nevertheless, DNA damage is sufficient to induce activation of canonic

163 cumulation of co-transcriptional R-loops and DNA damage leading to genomic instability and neurodegen

164 tes of subsignatures resulting from distinct DNA damage lesions.

165 loss of FANCJ and RAP80 not only accentuates DNA damage levels in human cells but also adversely affe

166 defective in DNA synthesis and had increased DNA damage levels, suggesting a role for zinc in maintai

167 entional slide scanner for quantification of DNA damage levels.

168 p (17% of newly diagnosed patients) with low DNA damage (low genomic scar score with chromosome 9 gai

169 e mechanisms including the oxidative stress, DNA damage, lysosomal dysfunction, inflammatory cascade,

170 alysis has shown that SHOC2 can modulate the DNA-damage mediated by p53.

171 DNA damage occurring in response to different natural an

172 Here, we show that H. pylori-induced DNA damage occurs co-transcriptionally in S-phase cells

173 age, unlike nuclear-envelope-rupture-induced DNA damage, occurs primarily in S/G2 phase of the cell c

174 DNA damage onset most likely arises from formaldehyde, a

175 heir ability to distinguish between types of DNA damage or limited in their sensitivity and reproduci

176 however, are not expected to cooperate with DNA-damaging or antimitotic chemotherapies as the former

177 e-dependent growth defects in the absence of DNA damage, pointing out unknown physiological functions

178 Phosphorylation of H2AX after DNA damage propagated more than 100 kilobases per minute

179 se mitochondrial function trigger release of DNA damaging reactive oxygen species.

180 terminal region of NEIL3 is involved in both DNA damage recruitment and enzymatic regulation.

181 s in diverse biological processes, including DNA damage repair (Fanconi anemia), telomere maintenance

182 b, nltp), reproduction (cyb5, cyp17A, ovos), DNA damage repair (wdhd1, rad51, hus1), and epigenetic m

183 compounds that interfere with transcription, DNA damage repair and the cell cycle.

184 WS) and Bloom Syndrome (BS) are disorders of DNA damage repair caused by biallelic disruption of the

185 These patient cell lines displayed DNA damage repair defects that were comparable to previo

186 n cancer xenograft models that carry certain DNA damage repair deficiencies.

187 uring neurodevelopment, but it also mediates DNA damage repair essential to proliferating neural prog

188 ibition of an analog-sensitive CDK12 reduces DNA damage repair gene expression, but selective inhibit

189 and restored Pol II CTD phosphorylation and DNA damage repair gene expression.

190 Radiation induced DNA damage repair is an attractive therapeutic target to

191 radiotherapy and chemotherapy by inhibiting DNA damage repair is proposed as a therapeutic strategy

192 ti-gammaH2AX-TAT allows visualization of the DNA damage repair marker gammaH2AX in PanIN-3s in an eng

193 act, these activities are crucial for proper DNA damage repair pathway choice.

194 Alterations of genes involved in the DNA damage repair pathway have been associated with sarc

195 tance (drug extrusion, drug degradation, and DNA damage repair) and using rate constants of these rea

196 PBRM1, BAP1 and SETD2), DNA methylation and DNA damage repair, all of which have been associated wit

197 n X-chromosome inactivation, imprinting, and DNA damage repair, and mutations in SMCHD1 can cause fac

198 g the cancer stem cell population, enhancing DNA damage repair, facilitating transcriptional plastici

199 ultured IECs with 11G5 induced autophagy and DNA damage repair, whereas infection with 11G5DeltaclbQ

200 olase (PARG), which plays important roles in DNA damage repair.

201 ordinated roles in DNA binding during HR and DNA damage repair.

202 t autophagy is required for bacteria-induced DNA damage repair.

203 eutic efficacy of the emerging inhibitors of DNA damage repair.

204 protect 3D genome structure integrity during DNA damage repair.

205 imply that NTMT1 regulates cell mitosis and DNA damage repair.

206 ct with AR-FL to drive gene transcription or DNA-damage repair in prostate cancer cells that co-expre

207 lular processes, including transcription and DNA-damage repair(1,2).

208 next-generation sequencing interrogating 37 DNA damage-repair-associated genes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Understanding how DNA damage response inhibitors cause cytotoxicity in can

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 induces replication stress and activates the DNA damage response.

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

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

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

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

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

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

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

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

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

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

258 sensor kinases responsible for orchestrating DNA damage responses.

259 ls, DNA-binding deficiency of UAF1 increased DNA damage sensitivity and impaired HR efficiency, sugge

260 e maintenance of genomic stability relies on DNA damage sensor kinases that detect DNA lesions and ph

261 plays a previously uncharacterized role as a DNA damage sensor, a critical factor in initiating the D

262 g events, expanding our understanding of the DNA damage signaling network.

263 In eya2 mutant axolotls, we found that DNA damage signaling through the H2AX histone variant wa

264 this model, competition between mitogen and DNA damage signalling over the course of the mother cell

265 ly, we found that PARP1 exchanges rapidly at DNA damage sites even in the presence of clinical PARPi,

266 Here we show that RBM14 is recruited to DNA damage sites in a PARP- and RNA polymerase II (RNAPI

267 Recruitment of DNA repair proteins to DNA damage sites is a critical step for DNA repair.

268 t-translational modifications of proteins at DNA damage sites serve as DNA damage codes to recruit sp

269 STUbL-mediated displacement of Pol eta from DNA damage sites.

270 I-dependent generation of RNA:DNA hybrids at DNA damage sites.

271 e, despite increasing RIF1 "end-blocking" at DNA damage sites.

272 ter DNA damage is independent of the type of DNA damage stimuli used and that the protein Spata18 is

273 daughter G1 phase, but remains sensitive to DNA damage, such as single strand breaks, the most frequ

274 ybrids constitute a source of recombinogenic DNA damage taking advantage of Rad51-independent single-

275 tiate a slow-cycling state following stress (DNA damage, targeted therapy, and aging).

276 (ATM) deficiency in CD4 T cells accelerates DNA damage, telomere erosion, and cell apoptosis in HIV-

277 nd DNA crosslinks (ICLs) are a toxic form of DNA damage that block DNA replication and transcription

278 ate fragmentation and presence of sites with DNA damage that can lead to biases such as allelic imbal

279 ggesting the modulation of transcription and DNA damage that may be mediated by the action of HDAC an

280 trand breaks, leading to replication-induced DNA damage that requires BRCA1/2-dependent homologous re

281 interstrand cross-links (ICLs) are a form of DNA damage that requires the interplay of a number of re

282 thio-dG treatment causes telomere-associated DNA damages that are sensed by dendritic cells (DCs) and

283 e and tolerable when combined with localized DNA-damaging therapies and thus has promising clinical p

284 ecruited to DNA lesions within seconds after DNA damage through a mechanism dependent on its DNA bind

285 cumulation of co-transcriptional R-loops and DNA damage to avert genomic instability and neurodegener

286 Chemotherapy and irradiation cause DNA damage to hematopoietic stem cells (HSCs), leading t

287 of cancer and can occur as a consequence of DNA damage to the epithelium by UVR or chemical carcinog

288 and define a role for PrimPol in HR-mediated DNA damage tolerance.

289 PrimPol has been recently identified as a DNA damage tolerant polymerase that plays an important r

290 enhances DNA end-labeling, and protects from DNA damage, ultimately blocking the proneoplastic effect

291 This deformation-induced DNA damage, unlike nuclear-envelope-rupture-induced DNA

292 on is dependent upon EGFR-mediated repair of DNA damage via activation of DNA-PKcs.

293 primary hepatocytes in vitro confirmed that DNA damage was indeed exacerbated by extracellular ATP,

294 atorial approach and proxies for oxaliplatin-DNA damage, we observed no significant differences in re

295 Genes involved in protein synthesis and DNA damage were implicated in etoposide susceptibility.

296 MDM2 autoubiquitination and degradation upon DNA damage, whereas S429A substitution protects MDM2 fro

297 2 is phosphorylated by ATM at Ser-1003 after DNA damage, which enhances the catalytic activity of USP

298 ty, macrophages reduce epithelial cells with DNA damage, which may limit the progression of preneopla

299 ed another mechanism wherein 5-AzadC induced DNA damage, which then resulted in enhanced occupancy of

300 nvestigate how mitochondria respond to acute DNA damage with respect to mitophagy, which is an import