ライフサイエンスコーパス: damage

1 neages (one to four cells) without radiation damage.

2 first line of defense against pathogens and damage.

3 , can mobilize the genome in response to DNA damage.

4 for preventing and treating IR-induced liver damage.

5 repair system that deals with oxidative DNA damage.

6 d radical-induced oxidative cellular and DNA damage.

7 f [4Fe-4S] clusters of dehydratases, and DNA damage.

8 opment, maturation and repair in response to damage.

9 -ATR-pS435 complex to sites of cisplatin DNA damage.

10 of cognitive decline resulting from housing damage.

11 s for the induction of tau-mediated neuronal damage.

12 y heals after experiencing severe mechanical damage.

13 cted cells and their high sensitivity to DNA damage.

14 MD-dependent manner following persistent DNA damage.

15 nted cell death upon oxidative telomeric DNA damage.

16 and is traditionally related to neurological damage.

17 t is implicated in the repair of nitrosative damage.

18 ATM and histone H2AX without triggering DNA damage.

19 control of infection or mediate inflammatory damage.

20 d how cell fate is affected by severe tissue damage.

21 roper control of toxicity from on-target DNA damage.

22 N in GN development and in inducing podocyte damage.

23 disruption of cell-wall homeostasis, and DNA damage.

24 target gene transcription in response to DNA damage.

25 l risks and mitigate potential environmental damage.

26 alanine transaminase, an indicator of liver damage.

27 ondrocytes attenuates joint inflammation and damage.

28 transcription recovery after UV-induced DNA damage.

29 uminemia, reduced GFR, and marked glomerular damage.

30 (sCD141) and ICAM-1, reflecting endothelial damage.

31 Atlantic, resulting in an immense ecological damage.

32 Chk1-dependent response to replication fork damage.

33 is quantitatively as important as oxidative damage.

34 uction of EndoMT mitigates intestinal tissue damage.

35 y be further optimized for the repair of CNS damage.

36 state, formation of microthrombi, and tissue damage.

37 e irreversible loss of vision or serious eye damage.

38 kidney energy metabolism and prevents kidney damage.

39 ammed cell death that signal tissue and cell damage.

40 ible for bringing the kinase to sites of DNA damage.

41 ve polymerase to resume beyond the offending damage.

42 can result in replication-associated genome damage.

43 est that C3 protects from early glaucomatous damage, a process that may involve EGFR signaling and ot

44 seizures and PDs, suggesting that additional damage after acute brain injury may be reflected by freq

45 s a potential mediator of pathophysiological damage after demyelination.

46 Cellular contact with most damaging agents is reduced by the action of the mucocili

47 inuously exposed to endogenous and exogenous damaging agents, representing a significant challenge to

48 ) are unsaturated imines that are potent DNA damaging agents, thereby confirming an earlier mechanism

49 ow growth and renders cells sensitive to DNA damaging agents.

50 t are targeted by subsequent exposure to DNA damaging agents.

51 e construct to the natural environment could damage an ecosystem irreversibly.

52 mutations, they are both a source of genome damage and a means for creating sequence diversity.

53 exan protozoan parasite that can cause fetal damage and abortion in both animals and humans.

54 red constructs to control the cellular-level damage and cell-cell distance in individual tissues to e

55 accumulation through increases in oxidative damage and cellular energy deficits; these, in turn, imp

56 mine deficiency on cellular responses to DNA damage and chemotherapeutic treatment remains unclear.

57 ayed, neutrophils can cause extensive tissue damage and chronic disease.

58 sulting in increased inflammation and tissue damage and consequent invasiveness.

59 poE (E2, E3, E4) also leads to some neuronal damage and death compared with the absence of ApoE, with

60 cking their progression and preventing bowel damage and disability.

61 Ctn had a lag phase before inducing membrane damage and exhibited more complex cell-killing activity,

62 recurrence presumably by limiting epithelial damage and facilitating microbiome recovery.

63 he repair of CX-5461 and CX-3543-induced DNA damage and failure to do so leads to lethality.

64 A composition have focused especially on DNA damage and genotoxicity.

65 age therapy was accompanied by decreased OLT damage and increased SIRT1/LC3B expression, whereas adju

66 eaks (DSBs) represent highly deleterious DNA damage and need to be accurately repaired.

67 t mTORC1 signaling suppresses endogenous DNA damage and replication stress.

68 ment light chain (NFL), reflective of axonal damage and sCD27, known to best predict the presence of

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

70 c and non-resolving and can lead to arterial damage and thrombosis-induced organ infarction.

71 ) and induce a comparable degree of membrane damage and toxicity to S. oneidensis.

72 ated Zika vaccine prevents infection, testis damage and transmission to the fetus during pregnancy in

73 wed potential to ameliorate the gliovascular damage and working memory impairments after hypoperfusio

74 motes survival by suppressing endogenous DNA damage, and may control cell fate through the regulation

75 le sclerosis that prevent worsening, reverse damage, and restore function are a major unmet need.

76 n these animals are seizures and hippocampal damage, and they have been proposed as a natural animal

77 ls parasite burden and contributes to tissue damage, and what mechanisms underlie neurological and mu

78 th is also required for removal of infected, damaged, and cancerous cells.

79 al deficits, E/I imbalance, and histological damage are all ameliorated by treatment with NitroSynaps

80 Motion-induced neuron deformation and damage are associated with several neurodegenerative con

81 N leads to severe replication-associated DNA damage arising from nucleolytic cleavage of stalled repl

82 , and autoimmunity, and preventing oxidative damage associated with inflammation.

83 Uric acid is a damage-associated molecular pattern (DAMP), released fro

84 to pathogen-associated molecular pattern and damage-associated molecular pattern recognition by the i

85 Although endogenous RNAs acting as damage-associated molecular patterns (DAMPs) for pattern

86 eceptors for sensing microbial molecules and damage-associated molecular patterns released from host

87 ient mice developed profound RPE and retinal damage at doses that caused minimal effects in wild-type

88 DNA damage at tDNAs in the absence of these helicases is sup

89 e incomplete remyelination will irreversibly damage axonal connections, treatments effectively promot

90 onstitutive PARP activation, spontaneous DNA damage by alkaline comet assay, basal micronuclei levels

91 tive induction of DNA replication stress and damage by ATR inhibition and cytarabine, and the ability

92 owever, it's unclear how many cells would be damaged by a particular bursting bubble, or more precise

93 ce between the region of interest and region damaged by stroke, in particular within the parietal ass

94 Importantly, HDM-induced DNA damage can be prevented by the antioxidants glutathione

95 ften attenuated to protect the detector from damage caused by intense Bragg spots.

96 ms, determining aspects that could limit the damage caused by the disease.

97 um could protect immature mouse oocytes from damages caused by oxidative stress.

98 Brain damage causing acquired amusia disrupts the functional m

99 the voltage delivered by the wires does not damage cells.

100 oxidative stress and is capable of rescuing damaged cells.

101 owed by lineage differentiation to replenish damaged cells.

102 teration as a mechanism of resistance to DNA-damaging chemotherapy, consistent with a local loss of D

103 ons in the adult mouse motor cortex restored damaged cortical pathways.

104 nd U-Th-Pb dating is the effect of radiation damage, created by alpha-recoils from alpha-decay events

105 Drought can severely damage crops, resulting in major yield losses.

106 istry and molecular biology of PARP-1 in DNA damage detection and repair, the mechanistic and functio

107 The extent of this damage directly confounds the determination of somatic v

108 Reactive oxygen species (ROS) can damage DNA, proteins, and lipids, so cells have antioxid

109 re irradiation and rapidly escorts it to the damaged DNA after UV irradiation in a DDB2-independent m

110 Genotoxic stress drives damaged DNA out of the nucleus by forming micronuclei.

111 ), specialized DNA polymerases replicate the damaged DNA, allowing stringent DNA synthesis by a repli

112 -pS435 and XPA's associations with cisplatin-damaged DNA.

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

114 with polymicrobial sepsis whereas glomerular damage due to glycerol-induced kidney-injury had stronge

115 s in biological fluids that resist oxidative damage during heme-driven inflammation.

116 bility of alveolar macrophages to limit lung damage during influenza infection.

117 eptionally mild heating, thus preventing the damaging effects of excessive heat.

118 that the five amino acid substitutions have damaging effects on DNA binding of EBF3.

119 Antimony, which has damaging effects on the human body and the ecosystem, ca

120 the cross talk of innate lymphoid cells with damaged epithelia and with the recipient microbiome, the

121 o form Ca2+-permeable pores in the membrane, damaging epithelial cells in small intestine and colon.

122 vy alcohol use can lead to progressive liver damage, especially in individuals with chronic hepatitis

123 s accounted for >90% of the variation in the damage footprints.

124 d Si, are analyzed with a model of radiation damage formation which accounts for the fractal nature o

125 hair cells of the cochlea, vulnerability to damage from noise trauma.

126 onal dystrophin protein results in excessive damage from normal muscle use due to the compromised str

127 Defects in this BM lead to muscle fiber damage from the force of contraction.

128 thousand tons of precursor emissions (health damage functions) varied significantly across source-sta

129 nonesterified fatty acids (NEFAs) across the damaged glomerular filtration barrier and subsequent rea

130 that cattle classified as having liver fluke damage had on average 10 days greater slaughter age than

131 DNA damage has long been established as a cause of cancer de

132 ntion to a region of space opposite to where damage has occurred in the brain, usually the left side

133 rug concentration at the target site without damaging healthy tissues.

134 disease courses, supporting the dynamic CNS damage hypothesis to explain MS heterogeneity.

135 luding their ability to induce target tissue damage in a unique in vitro human graft-versus-host dise

136 meres and stabilizes TRF1 at telomeres after damage in an ATM activation-dependent manner.

137 ruzi infection have been used to study heart damage in Chagas disease.

138 their association with progressive glomeruli damage in disease states.

139 duction in the spinal cord and oxidative DNA damage in dorsal horn neurons.

140 ed T-helper 1 cytokine-mediated inflammatory damage in heart.

141 njury in a model of severe antibody-mediated damage in highly sensitized recipients.

142 The buildup of radiation damage in ion-irradiated crystals often depends on the s

143 ABC294640, an inhibitor of SK2, reduces DNA damage in neurons and increases survival in two neuron m

144 defects in intron removal in SMA promote DNA damage in part through the formation of RNA:DNA hybrid s

145 expect that clarifying the nature of myelin damage in preclinical AD may be informative on the disea

146 2-deficient cancer cell line exacerbated DNA damage in response to chemotherapeutics.

147 in cell death signaling secondary to axonal damage in retinal ganglion cells (RGCs) and other neuron

148 nin/E-cadherin in vitro and ameliorated skin damage in rodent models.

149 wth of embryos after the accumulation of DNA damage in seeds.

150 This review focuses on the etiology of DNA damage in the nervous system and the genome stability pa

151 rize the SOS transcriptional response to DNA damage in the Patescibacteria superphylum.

152 er for identifying and tracking inflammatory damage in the spinal cord after TAR in a mouse model.

153 ltures, we show that naturally occurring DNA damage incurred over S-phase causes p53-dependent accumu

154 preferential protease motifs during podocyte damage indicated activation of caspase proteases and inh

155 on, cancer therapy can also cause myocardial damage, induce endothelial dysfunction, and alter cardia

156 We also observed that DNA damage induced acetylation of HIPK2 along with an increa

157 which may contribute to ameliorating retinal damage induced by HFD.

158 DNA damage induced by reactive carbonyls (mainly methylglyox

159 Biaxial stretch damage induced shrunken neurites and cell death.

160 AP-mediated APA of PTEN is essential for DNA damage-induced increase of PTEN protein levels.

161 t appear to be driven by distinctions in DNA damage induction or repair capacity.

162 ost-directed therapeutic target to limit the damaging inflammation associated with overt production o

163 Accumulation of endogenous DNA damage is concomitant with defective ATM-mediated DNA re

164 generation, the clinical outcome after nerve damage is frequently poor.

165 r capillaries and were stained for oxidative damage markers using nitrotyrosine immunohistochemistry.

166 fies gaps in our knowledge of what molecular damage may be incurred by oxidative stress that is impar

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

168 ings implicate TOP2A cleavage as a broad DNA damage mechanism in oncogenic translocations as well as

169 ssociated increased O2(*-) and resulting DNA damage mediate the increased susceptibility of old fibro

170 ory improvement, neuropathic pain and tissue damage mitigation, and myelin preservation.

171 NK1 overexpression promotes the clearance of damaged mitochondria by augmenting autophagy signalling

172 pecifically regulate autophagic clearance of damaged mitochondria.

173 rial reactive oxygen species (ROS), membrane damage, mitochondrial DNA (mtDNA) integrity, morphology,

174 dentinogenesis using an in vivo mouse tooth damage model.

175 ically aggravates the ischemia-induced brain damage, motor deficits and mortality.

176 Additionally, it degrades abnormal/damaged/mutant/misfolded proteins, which serves a qualit

177 To determine whether rare, damaging mutations shared identity-by-descent in familie

178 neuronal connections, after injury to clear damaged neurons, or pathologically during disease.

179 aptic strength exceeds acceptable levels and damages neurons, explaining pathology of human syndromes

180 s aeruginosa infections coupled with robust, damaging neutrophilic inflammation characterize the chro

181 RAIL) selectively kills tumor cells, without damaging normal cells.

182 wer risk of the composite end point of brain damage, nursing home admission, or death (hazard ratio,

183 2016, we scored trees by their level of ADB damage observed in field at the two worst affected (base

184 with poor cyclic stability due to structural damage occurring during the redox process.

185 data indicate that the reduction in mucosal damage occurs through decline in stem/clonogenic epithel

186 sclerosis (MS) is caused by immune-mediated damage of myelin sheath.

187 ificantly improved the alveolar bone and PDL damage of the knockdown phenotype, which are thus shown

188 ustained, can result in chronic histological damage of which interstitial fibrosis and tubular atroph

189 c brain injury (TBI) causes extensive neural damage, often resulting in long-term cognitive impairmen

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

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

192 sters from single cells and/or cause cluster damage or dissociation during processing.

193 kin sensitization did not require prior skin damage or enzymatic activity within HDM extract, yet was

194 unction after stroke can arise from cortical damage or from white matter disconnection.

195 nder CPR was associated with a risk of brain damage or nursing home admission that was significantly

196 Cell emergence onto damaged or organized fibrous extracellular matrix (ECM)

197 control component to specifically recognize damaged or stressed compartments within the mitochondria

198 fter loss of ATM in order to counter protein damage originating from oxidative stress.

199 Upon DNA damage, p53 mRNA is released from stress granules and as

200 We developed new genomic measures of damaging passenger load that can accurately predict the

201 Frost is an important episodic event that damages plant tissues through the formation of ice cryst

202 e of complement activation, endothelial cell damage, platelet activation, and thrombosis.

203 Microbial pathogens are exposed to damaging reactive oxygen species (ROS) produced from a v

204 cin and it was associated with increased DNA damage, reduced DNA repair responses, and elevated cellu

205 ne silencing, while H2AX is important in DNA damage repair.

206 Expression of the DNA damage/repair marker, gamma-H2AX and DNA damage response

207 ause of their correlation with renitence and damage-resistant nature, we termed these structures "ren

208 ulation, including DNA synthesis (NPAT), DNA damage response (ATM), mitosis (PMF1, CENPN and MAD1L1)

209 egeneration coincides with activation of DNA damage response (DDR) and impaired ability to differenti

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

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

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

213 ether intranuclear inclusions containing DNA damage response (DDR) proteins are causally linked to ab

214 mice (MVM) induces a sustained cellular DNA damage response (DDR) which the virus exploits to prepar

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

216 nding induces a lesion that triggers the DNA damage response (DDR).

217 optosis or senescence as outcomes of the DNA damage response (DDR).

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

219 identifies a critical chromatin-binding DNA damage response factor, ZMYM3, which modulates BRCA1 fun

220 FANCM is a DNA-damage response gene whose heterozygous mutations predis

221 DNA damage/repair marker, gamma-H2AX and DNA damage response marker, phosphorylated ataxia telangiect

222 erved sites disrupt its deacetylation of DNA-damage response proteins by impairing SIRT2 catalytic ac

223 fication coincides with the ATM-mediated DNA damage response that occurs on functional telomeres foll

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

225 Two distinctive phases in the damage response were identified: an early destructive ph

226 esses including nutrient sensing and the DNA damage response, and implicated Vts1 in de novo gene "bi

227 ing transcription with mRNA splicing and DNA damage response.

228 cer subclass through a hormone dependent DNA damage response.

229 h a pathway of autophagy specific to the DNA damage response.

230 3-dependent enhancer activity during the DNA damage response.

231 axias, indicating an association between DNA damage-response and repair pathways and the age at onset

232 hways are crucial in these organelles to fix damage resulting from endogenous and exogenous factors.

233 The extent of Striga-induced host damage results from the interaction between parasite vir

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

235 s reveals a significant upregulation in both damage-sensing and effector components of the inflammaso

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

237 because of increased hydraulic drag through damage site during filtration.

238 x with the nuclear receptor protein, SF1, at damage sites requires phosphorylation by inositol polyph

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

240 or of neutrophil recruitment to inflamed and damaged sites and plays prominent roles in inflammatory

241 Whereas damaged skeletal muscle has a profound capacity to regen

242 cleotides are ligated to adaptors, and after damage-specific immunoprecipitation, the adaptor-ligated

243 correlated positively (R=0.995, p<0.05) with damage starch content.

244 The damaged starch content of barley cultivars ranged betwee

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

246 days after the lesion, were increased in the damaged telencephalon, mostly suddenly after the lesion.

247 esses usually occur simultaneously and cause damages that exceed single stresses.

248 -induced ulcerative cystitis (KIC) initially damaged the bladder mucosa and induced contracted bladde

249 nd trabecular spacing, but it simultaneously damaged the bone.

250 These DNA cross-links can be mutagenic by damaging the integrity of the DNA structure.

251 eases the sensitivity of the germline to DNA damage, thereby protecting the integrity of gamete genom

252 jor damage to plant communities, but species damage thresholds and postdrought recovery of forest pro

253 Experimentally determined damage thresholds were compared to a theoretical heat tr

254 determination of laser-induced nanoparticle damage thresholds.

255 monocytes and dendritic cells to the site of damage through a breached blood-brain barrier or via bra

256 nd to the release of IL-33 upon liver tissue damage through expression of type 2 cytokines thereby pa

257 Their recruitment to damaged tissues upon acute sterile injuries is necessary

258 ltiple signals, such as those from microbes, damaged tissues, and the normal tissue environment.

259 e doses are in excess of the doses needed to damage TMD-based electronics due to defects generated in

260 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by rest

261 This research shows UV-induced damage to adenoviral proteins across the germicidal UV s

262 bstacles, postponing repair of the offending damage to complete the cell cycle and maintain cell surv

263 adiation therapy and chemotherapy induce DNA damage to drive cells into apoptosis or senescence as ou

264 US, aHUS, and secondary HUS are simultaneous damage to endothelial cells, intravascular hemolysis, an

265 n the HRGS system in promoting the oxidative damage to food proteins.

266 urce footprints are highly representative of damage to human health and biodiversity.

267 ynamic phosphorylation of DNA-PKcs after DNA damage to mediate NHEJ.

268 pression of polyglutamine-expanded AR causes damage to motor neurons and skeletal muscle cells.

269 Drought can cause major damage to plant communities, but species damage threshol

270 and form EETs at sites of airway epithelial damage to protect the host from infections in patients w

271 rome (MetS) has been associated with chronic damage to the cardiovascular system.

272 when abnormal experience could cause lasting damage to the developing brain.

273 MENT Zika virus (ZIKV) can cause substantial damage to the developing human brain.

274 s include loss of neuronal progenitor cells, damage to the developing vascular system of the brain, a

275 We propose a model for NSAID-induced damage to the gastrointestinal tract that includes these

276 ensory neuron-macrophage communication after damage to the peripheral nerve.

277 reat microvessels without causing collateral damage to the surrounding tissue.

278 aused by increased precipitation followed by damages to buildings associated with near-surface permaf

279 re often needed during RT, leading to severe damages to normal tissues adjacent to tumors.

280 vent and to mitigate the direct and indirect damages to public health and resources.

281 ictyota) cervicornis were significantly more damaging to the coral Acropora intermedia growing in the

282 ase, minor DNA damage may be overcome by DNA damage tolerance (DDT) pathways that bypass such obstacl

283 riginally used to detect discrete neurotoxic damages, TSPO has generally turned into a biomarker of '

284 rmal repair and innate immune response after damaging UVB exposure.

285 inocytes from UV-B-induced apoptosis and DNA damage via ATR.

286 WRN responds to site-specific telomeric damage via its RQC domain, interacting at Lysine 1016 an

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

288 Cardiac damage was assessed after mechanical conditioning or pha

289 AMP-enhanced repair of cisplatin-induced DNA damage was dependent on PKA-mediated phosphorylation of

290 Oxidative damage was observed in livers from Ppargc1a(f/+)Alb-cre(

291 ), on cell proliferation, cell death and DNA damage was studied in two ovarian cancer cell lines (OVC

292 The largest source of damages was road flooding caused by increased precipitat

293 m photo-stimulation without causing cellular damage, we formulated new photo-inert media called MEMO

294 n, matricellular protein release, and tissue damage were measured at admission.

295 force/endurance as well as increased muscle damage when compared to regular mdx mice.

296 5B to protect cells from consequences of DNA damage, which can be triggered by viral infection.

297 tes G quadruplex (G4) DNA in response to DNA damage, which suppresses repair by nonhomologous end-joi

298 dentify patients with severe disease-related damage who should avoid pregnancy, counsel patients to c

299 is protected from stretch-induced eccentric damage with age.

300 lso observed a congruent pattern of cellular damage with tissue-specific expression of APOL1.