ライフサイエンスコーパス: damaged

1 its nsDNA-binding activity is significantly damaged.

2 d that muscle deprived of SMN was profoundly damaged.

3 011 to 2013, with a cost of $163 to $227 per damaged acre.

4 cleotide rATP and of its naturally occurring damaged analog 1,N (6)-ethenoadenosine (1,N (6)-erA) on

5 reated with SS1P, proximal tubular cells are damaged and albumin in the urine is increased.

6 The removal of both damaged and healthy mitochondria under disease and physi

7 Whether the stromal ME is damaged and how it recovers after irradiation is unknown

8 essential for the repair and replacement of damaged and old bone.

9 s including unburnt areas, manage repeatedly damaged and potentially collapsed ecosystems, and expand

10 ether facilitate degradation of superfluous, damaged and toxic cellular components.

11 A mix of both damaged and undamaged cells was observed over the cathod

12 We conclude that the damaged and unrepaired ribonucleotide 1,N (6)-erA in DNA

13 Retinal mitochondria remain damaged and vicious cycle of free radicals continues to

14 ic conditions, the endothelial glycocalyx is damaged, and its degradation is accompanied by shedding

15 relations (DVCs) showed no difference for AN-damaged animals in their use of energy and envelope cues

16 tion between brain regions lying outside the damaged area contributes to spatial deficits in a way th

17 ress or induce deposition of minerals on the damaged areas from the increase in mechanical stress to

18 Our data show that proteolytically damaged areas in porcine metacarpophalangeal joints pres

19 nt reburning of recently and previously fire-damaged areas, 3) the magnitude of resource loss for ind

20 rderly rescue and recovery operations in the damaged areas.

21 We characterized undamaged and damaged articular cartilage from 22 participants having

22 When the ventral route is damaged, as in the case of neurodegeneration affecting t

23 en-associated molecular patterns (PAMPs) and damaged-associated molecular patterns (DAMPs), and they

24 Chronic demyelination leads to damaged axons and irreversible destruction of the centra

25 p slows the removal of both active zones and damaged axons.

26 1, that interact with the DNA containing the damaged base oxoG and the normal base G while they are n

27 orporating two pyrene deoxynucleotides and a damaged base, enable the direct, real-time detection of

28 ears have enabled high-resolution mapping of damaged bases.

29 have to navigate through ribonucleotides and damaged bases.

30 rt gaps in dsDNA that result from removal of damaged bases.

31 an abnormal context, for example, glycans on damaged BCVs [2-4].

32 subacute infarcts, reactive astrocytes, and damaged blood vessels in multi-infarct dementia when com

33 ger signals released into the circulation by damaged brain cells lead to activation of systemic immun

34 tential therapeutic treatments to repair the damaged brain endothelium.

35 old in stored agricultural produce and water-damaged buildings.

36 air, replace, or restore function to tissues damaged by aging, disease, or injury.

37 turbidity current in 2006 and its rock berm damaged by another 10 years later.

38 s in long tracts of single-stranded (ss) DNA damaged by apolipoprotein B mRNA editing enzyme, catalyt

39 ssland, woodland and two peatland sites, one damaged by drainage and one undergoing restoration by dr

40 Mice epidermal barrier was damaged by epicutaneous application of proteases and cho

41 features replaces esophageal squamous mucosa damaged by gastroesophageal reflux disease.

42 us nucleic acids, for example when cells are damaged by genotoxic agents and in certain autoinflammat

43 Apoptotic death of cells damaged by genotoxic stress requires regulatory input fr

44 ation, the retinal pigment epithelium can be damaged by light acting on photosensitizers like N-retin

45 Pancreatic beta-cells become irreversibly damaged by long-term exposure to excessive glucose conce

46 esised that, similar to other systems, cells damaged by radiation might be effecting this donor cell

47 Cellular DNA can be damaged by spontaneous hydrolysis, reactive oxygen speci

48 ds producing Cry3Bb alone that were severely damaged by this pest in 25 crop-reporting districts of I

49 d when a cell membrane or its components are damaged by various factors.

50 d effect on motor function and some severely damaged capillaries were noted.

51 to chondrocytes has potential for repairing damaged cartilage or to generate disease models via gene

52 ostatic and hypertrophic chondrocytes, while damaged cartilage was enriched for prefibro- and fibro-,

53 ignaling involves the sensing of collapse of damaged cells and a local auxin signaling activation to

54 response that eliminates foreign organisms, damaged cells and physical irritants; however, inappropr

55 ropagation of oncogenic cells and eliminates damaged cells during ageing.

56 ifferentiation, which may serve to eliminate damaged cells from the proliferative pool.

57 ntributes to anemia and splenic retention of damaged cells in infected animals.

58 ed a crucial contribution of the collapse of damaged cells in wound perception and detected an auxin

59 ic acid (cfDNA) released from either dead or damaged cells serves as a key autoantigen in rheumatoid

60 -induced transformation was reversible, with damaged cells slowly reacquiring normal gene expression

61 hogens, chemical and physical irritants, and damaged cells subsequently initiating a well-orchestrate

62 stmitotic tissues are incapable of replacing damaged cells through proliferation, but need to rely on

63 mechanisms that minimize the contribution of damaged cells to developing embryos remain poorly unders

64 senescence and failed apoptosis of severely damaged cells) contribute to uncontrolled cell division

65 repair via NHEJ and suppressing apoptosis of damaged cells, our results suggest that BRN2 contributes

66 Since poloxamers have been shown to rescue damaged cells, the cells were treated with the FDA-appro

67 m cells to generate new cells that replenish damaged cells.

68 xylem and phloem and included the cytosol of damaged cells.

69 in response to injury and regenerate lost or damaged cells.

70 of normal cells and in a model of normal and damaged cells.

71 by wound healing, a complex process by which damaged cellular material is removed and tissue repaired

72 the regulation of RNA-editing efficiency in damaged chloroplasts and suggests that MORF2 is involved

73 ndent cNHEJ reinforces 53BP1 assembly at the damaged chromatin and shifts DSB repair to mutagenic NHE

74 Inhibiting 53BP1 recruitment to damaged chromatin completely abolished the survival adva

75 w NHEJ factors are sequentially recruited to damaged chromatin remains unclear.

76 the accrual of downstream repair factors at damaged chromatin.

77 ronment and recruits DNA-repair complexes to damaged chromatin.

78 he DDR by hampering the activity of 53BP1 at damaged chromosomes.

79 ich is the concept of neuronal allocation to damaged circuits.

80 The failure of axonal regeneration in the damaged CNS limits functional recovery.

81 ters to discriminate structural changes in a damaged cornea.

82 keratocyte phenotype and the regeneration of damaged corneal stroma.

83 ups: control (non-treated) and NaOH-treated (damaged) corneas (n = 8).

84 ents to specific motor domains linked to the damaged cortical subregion and that damage encroaching o

85 n to melting-point depression in deformed or damaged crystals relative to their pristine counterparts

86 Degradation of damaged D1 and its replacement by nascent D1 are at the

87 the cell cycle exit or death of genomically damaged differentiated pericentral hepatocytes, and this

88 lecular strategy for the direct detection of damaged DNA base excision activity by a ratiometric fluo

89 A repair pathway that recognises and excises damaged DNA bases to help maintain genome stability.

90 ocess causes death of cells with methylation-damaged DNA bases, so we measured proportions of cells t

91 and protein cofactors that hasten repair of damaged DNA bases.

92 y, we report that the XPE gene product DDB2 (damaged DNA binding protein 2), a nucleotide excision re

93 CNA ubiquitination allows for replication of damaged DNA by recruiting lesion-bypass DNA polymerases.

94 Damaged DNA ends are dangerous in cells and if left unre

95 osphoglycolate is generated during repair of damaged DNA ends, 2-phospho-L-lactate is a product of py

96 Chemically damaged DNA has been linked to cancer and aging, therefo

97 tion revealed reduced recruitment of PNKP to damaged DNA in cells expressing either XRCC1 variant com

98 From bacteria to mammalian cells, damaged DNA is sensed and targeted by DNA repair pathway

99 cell biology approaches have indicated that damaged DNA mobility exhibits random and directed moveme

100 During HR, damaged DNA must be aligned with an undamaged template t

101 guish between random and directed motions of damaged DNA or other biological molecules.

102 l eta) and other Y-family TLS polymerases to damaged DNA relies on proliferating cell nuclear antigen

103 destabilization of RAD51 nucleofilaments at damaged DNA replication forks.

104 luence the orientation of XPA and RPA on the damaged DNA substrate, remains poorly characterized.

105 thase (cGAS) recognizes cytosolic foreign or damaged DNA to activate the innate immune response to in

106 tail the interaction of Pol eta with PCNA at damaged DNA to prevent harmful mutagenesis.

107 tion of p53 and PPARgamma-p53 genes repaired damaged DNA utilizing genes from the nucleotide excision

108 The increased mobility of damaged DNA within the nucleus can promote genome stabil

109 he mechanisms behind the increased motion of damaged DNA within the nucleus will reveal more of the s

110 ases in the random and directional motion of damaged DNA, can promote genome repair.

111 We demonstrate that damaged DNA-binding protein 1 (DDB1) and Cullin4, two co

112 entified Cullin 1 (CUL1), Cullin 4A (CUL4A), damaged DNA-binding protein 1 (DDB1), and S-phase kinase

113 Molecular dynamics simulations of damaged DNA-Pol IV complexes reveal the van der Waals in

114 esistance is enhanced by efficient repair of damaged DNA.

115 ylori increases survival of human cells with damaged DNA.

116 were equally efficient at localizing to the damaged DNA.

117 ear antigen (PCNA) sliding clamps encircling damaged DNA.

118 spin-dependent transport through oxidatively damaged DNA.

119 y of these XRCC1 variants to recruit PNKP to damaged DNA.

120 e bypass that facilitates the replication of damaged DNA.

121 ty for DNA lesions and shows less pausing on damaged DNA.

122 uanosin-8-yl)-2-acetylaminofluorene over non-damaged dsDNA.

123 t dissociation constants to well-matched and damaged duplex substrates are 100 +/- 20 nM and 80 +/- 3

124 lecular patterns (DAMPs) released from cells damaged during ischemia-reperfusion injury (IRI), in hea

125 Post-ovulation oocytes were frequently damaged during spermathecal contraction.

126 to the auditory synapse, more so in already damaged ears, and severely impact auditory sensitivity i

127 nversely, in the absence of LRRK2 and Rab8A, damaged endolysosomes are targeted to lysophagy.

128 LRRK2 recruits the Rab GTPase Rab8A to damaged endolysosomes as well as the ESCRT-III component

129 by either repairing the damage or targeting damaged endolysosomes for degradation via lysophagy.

130 rvive, proliferate, and differentiate in the damaged environment of the reconstituting niche.

131 explore how specific features of the tissue-damaged environment such as hypoxia, oxidative stress, a

132 olysis, macrophages in the liver phagocytose damaged erythrocytes to prevent the toxic effects of cel

133 uced fibrosis in normal tissue correlates to damaged fat reservoirs in the pelvic region.

134 mising therapeutic strategies to restore the damaged glycocalyx and to attenuate its deleterious cons

135 Damaged grains exhibited values varying from 3.6% to 25.

136 trials using adult stem cells to regenerate damaged heart tissue continue to this day(1,2), despite

137 trategies to replace coronary vasculature in damaged hearts.

138 F480 macrophages and increased clearance of damaged hepatocytes.

139 s and an attenuated inflammatory capacity of damaged hepatocytes.

140 ognize foreign RNA comes with a cost as also damaged host cells can release nucleic acids that might

141 Whether these connections are equally damaged in multiple sclerosis is unknown, as is their re

142 al for specific language functions and often damaged in primary progressive aphasia (PPA).

143 cell death is a major mechanism to eliminate damaged, infected, or superfluous cells.

144 parasitic' dependencies between collaterally damaged ischaemic areas.

145 Fusarium-damaged kernels and deoxynivalenol analyses supported th

146 cyte Implantation (ACI) in order to heal the damaged knee cartilage.

147 Many of these tablets are damaged, leading to missing information.

148 Beetle larvae were more likely to move from damaged leaves and leaves that had been exposed to volat

149 at had been exposed to volatiles from nearby damaged leaves compared to undamaged control leaves.

150 ikely to choose undamaged leaves compared to damaged leaves or those exposed to volatile cues of dama

151 nes misincorporated opposite the oxidatively damaged lesion, 8-oxo-7,8-dihydroguanine (OG), to initia

152 nd pro-oxidants, and accumulated oxidatively damaged lipids because of the reactivity of unchaperoned

153 liferative pressure, observed in chronically damaged liver tissues, on polyploid cells.

154 ary damage, the other pattern shows severely damaged lungs, low ISGs (ISG(low)), low viral loads and

155 irradiations, neutrons produce more heavily-damaged lymphocytes with multiple micronuclei/binucleate

156 iquitination of TAK1 thus activating AMPK on damaged lysosomes.

157 Larvae damaged many leaves on a plant but removed relatively li

158 the metabolic recovery of their irradiated, damaged ME via mitochondria transfer.

159 nd ALG-2-interacting protein X (ALIX) to the damaged membrane.

160 ite repair disorder in which accumulation of damaged metabolites likely triggers devastating effects

161 o the more complex environment of intact and damaged metaphase chromosomes, unravelling their structu

162 nd extent of reparative dentine formation in damaged mice molars by triggering the natural process of

163 removes dangerous constituents, particularly damaged mitochondria and peroxisomes, which are major so

164 tosolic protein, but is rapidly recruited to damaged mitochondria and target them for mitophagy.

165 ng mitophagy and accelerating the removal of damaged mitochondria are of interest for developing a di

166 ria and can rescue the membrane potential of damaged mitochondria by ER-associated fusion.

167 ase well-known for facilitating clearance of damaged mitochondria by ubiquitinating proteins on the o

168 Persistent accumulation of damaged mitochondria has been implicated in many neurode

169 1 (Ulk1) and the small GTPase Rab9 to clear damaged mitochondria independently of conventional autop

170 Mdm2 translocates to damaged mitochondria independently of parkin, enhances p

171 One highly conserved mechanism to clear damaged mitochondria involves the E3 ubiquitin ligase Pa

172 Accumulation of damaged mitochondria is a hallmark of aging and age-rela

173 led mitophagy that identifies and eliminates damaged mitochondria through the autophagosome and lysos

174 HFD suppressed mitophagy activity and caused damaged mitochondria to accumulate in the heart, which w

175 in ligase Parkin promotes the degradation of damaged mitochondria via mitophagy and mutations in Park

176 se function together to regulate turnover of damaged mitochondria via mitophagy, but our mechanistic

177 is by signalling the targeted destruction of damaged mitochondria, however, how disrupting this proce

178 been demonstrated to restore the function of damaged mitochondria, increase the production of cytopro

179 Mitophagy, the selective removal of damaged mitochondria, is thought to be critical to maint

180 le in reducing ROS levels via the removal of damaged mitochondria, which is required for cell surviva

181 rane potential, promoting the elimination of damaged mitochondria.

182 stability of Mitofilin (IMMT, MIC60) in the damaged mitochondria.

183 equestosome 1 (SQSTM1, p62) translocation to damaged mitochondria.

184 Parkin, is an essential coordinator to sort damaged mitochondrial-derived cargo to the lysosomes.

185 our data highlight the burden of chemically damaged mRNA on cellular homeostasis and suggest that or

186 o bacterial products translocated across the damaged mucosa.

187 is regulated by the fate of cholesterol from damaged myelin and oligodendroglial sterol synthesis.

188 The brain's endogenous capacity to restore damaged myelin deteriorates during the course of demyeli

189 ted molecular patterns (DAMPs) released from damaged/necrotic host cells are crucial factors in induc

190 , whether and how grafts functionally repair damaged neural circuitry in the adult brain is not known

191 to unravel the role of sleep in clearance of damaged neural processes.

192 n peripheral tissues, which serve to isolate damaged neural tissue and restore barrier functions.

193 clude that non-neuronal optogenetics targets damaged neurons and signaling subcircuits, providing a n

194 ase (PD) aim to delay progression or replace damaged neurons by restoring the original neuronal struc

195 marked contrast, axotomy rapidly transformed damaged neurons into just two new and closely-related cl

196 sleep may be influenced by the clearance of damaged neurons.

197 stoma cells, which correlates with repairing damaged neurons.

198 The repair of damaged Ni-based superalloy single-crystal turbine blade

199 ere only able to assess the abundance of DNA-damaged nuclei using gammaH2AX immunohistochemistry.

200 l beta insertion products with mismatched or damaged nucleotides, with the exception of a Watson-Cric

201 Tissue immunostaining revealed changes in damaged OA-only cartilage that was also found in undamag

202 s (MS), neural stem cells (NSCs) can replace damaged oligodendrocytes if the local microenvironment s

203 ctional mitochondria requires degradation of damaged ones within the cell.

204 ired protein homeostasis and accumulation of damaged or abnormally modified protein are common diseas

205 es of the stem cell response to increases in damaged or aggregated proteins remain unclear.

206 evidenced that the painting layers were not damaged or altered because of contact/sampling without l

207 of reparative or regenerative means to treat damaged or degenerated discs is hindered by a lack of ba

208 Ecological restoration - the rebuilding of damaged or destroyed ecosystems - is a critical componen

209 ls grown in culture or can be implanted into damaged or dysfunctional tissue to restore normal functi

210 Neuronal circuits damaged or lost after injury can be regenerated in some

211 e presence of microbial pathogens as well as damaged or malignant cells.

212 Damaged or mismatched DNA bases result in the formation

213 gical targets that modulate the clearance of damaged or old mitochondria (mitophagy), here we develop

214 otein products resulting from translation of damaged or problematic mRNAs.

215 dging their possible, detrimental effects in damaged or stressed tissues.

216 s to the specific removal and degradation of damaged or surplus mitochondria via targeting to the lys

217 Temporally harmonized elimination of damaged or unnecessary organelles and cells is a prerequ

218 ClpP peptidase to degrade proteins that are damaged or unneeded.

219 p a second embryo when the initial embryo is damaged, or when response to the signaling molecule auxi

220 Within neurons, it helps to remove damaged organelles and misfolded or aggregated proteins

221 clearance of aggregation-prone proteins and damaged organelles are vital for post-mitotic neurons.

222 intaining effective turnover of proteins and damaged organelles in cells.

223 maintaining cellular homeostasis by clearing damaged organelles, pathogens, and unwanted protein aggr

224 r process first described for elimination of damaged organelles, regulates DC maturation and other im

225 nt membrane repair and autophagic removal of damaged organelles.

226 dation of differentiated cell components and damaged organelles.

227 nction via clearance of excess nutrients and damaged organelles.

228 sed by accumulation of misfolded proteins or damaged organelles.

229 In right-brain-damaged patients, neglect severity in the line bisection

230 This, together with glutamate released from damaged phloem, activates GLRs, resulting in depolarizat

231 tle as 5-10 min and eliminates primarily the damaged protein rather than the SV en masse.

232 utophagy, a cellular recycling mechanism for damaged proteins and organelles.

233 otect stressed cancer cell by degradation of damaged proteins and organelles.

234 Asymmetric partitioning of damaged proteins is thought to play a key role in preser

235 and chaperone functions and often directing damaged proteins towards proteasome recycling.

236 ity from insufficient clearance of misfolded/damaged proteins underlies many diseases.

237 lational homeostatic mechanisms that replace damaged proteins with new copies.

238 gestion of intracellular materials including damaged proteins, organelles, and foreign bodies, in a b

239 n processing, and mediate the degradation of damaged proteins.

240 m facilitates the degradation of unstable or damaged proteins.

241 significant decrease (p < 0.01) in Fusarium-damaged rachis rate, Fusarium-diseased kernel rate and D

242 Simulations and MALDI spectra of a stroke-damaged rat brain show MS signals from pathological tiss

243 hat are recruited into the glomeruli and the damaged rat mesangial cells leads to diabetic nephropath

244 rom whole cross sections of both control and damaged rat ONs and manually annotated for axon count an

245 bulk removal of residual materials from the damaged reactors.

246 and reconstruct ridges in single or multiple damaged regions of incomplete fingerprint images, and he

247 arker of intrinsic kidney injury produced by damaged renal cells and by neutrophils.

248 y, under inflammatory conditions, the eGC is damaged, resulting in enhanced vascular permeability, ti

249 s a reverse transcriptase in the presence of damaged ribonucleotide 1,N (6)-erA but has poor RNA prim

250 Highly damaged rock is present across many areas of the entire

251 that facilitate stabilization and repair of damaged sarcolemmal membranes following myocardial injur

252 Thus, Simu is a general detector of damaged self and represents a novel molecular player reg

253 t the 5'-phosphate group with respect to the damaged site.

254 eveal a novel molecular link between OGG1 at damaged sites and transcription dynamics that may contri

255 Angiogenesis induction into damaged sites has long been an unresolved issue.

256 er domain and facilitates its recruitment to damaged sites.

257 hniques to quantify mutational burden in sun-damaged skin and its reduction by various therapies.

258 In addition, DNA from damaged SMCs was engulfed by macrophages in which it act

259 r how co-morbidities related to an aging and damaged soma can hinder achievement of ACM benefit.

260 r and thus preserves more anatomy in worn or damaged specimens, particularly in mammals with relative

261 ves from p44/p62's high affinity (20 nM) for damaged ssDNA.

262 SEM images revealed damaged starch granules after size reduction.

263 dough stability and lower setback viscosity, damaged starch, arabinoxylans and water absorption than

264 g situations, or when the auditory system is damaged, strains cortical resources, and this may change

265 lpXP, which selectively removes and degrades damaged subunits.

266 of their microglia in removing amyloid-beta-damaged synapses and the distribution of plaques, relati

267 while GLUT1 was decreased 1.7-fold in nerve damaged TA.

268 BRCA1-deficient cells and altered repair of damaged telomeres, can be explained from this viewpoint.

269 omoting the localization of CSB and RAD52 to damaged telomeres.

270 ated LexA cleavage during replication of the damaged template, but not normal replication.

271 replication fork DNA helicase, and 2) on the damaged template, nascent leading-strand gaps were gener

272 g DNA replication of both undamaged and base-damaged templates.

273 Moreover, the radial thread damaged tends to have a greater effect on structural fre

274 Early models simply damaged the rodent brain through toxins or lesions.

275 Mitochondrial DNA (mtDNA) is damaged, the transcription of mtDNA-encoded genes is imp

276 In the liver, targeted inhibition of damaged tissue may be a rational and promising approach

277 icity, initiate organoids and regenerate the damaged tissue remain largely unknown.

278 ic program, proliferate and migrate into the damaged tissue to differentiate into fibroblasts, endoth

279 , the brain stimulates neovascularization of damaged tissue via sprouting angiogenesis, a process reg

280 e process by which organisms replace lost or damaged tissue, and regenerative capacity can vary great

281 Within the damaged tissue, neutrophil migration behavior often swit

282 nction, requiring protein turnover to repair damaged tissue.

283 ls into the inflamed and cytotoxic region of damaged tissue.

284 phila is an excellent model for studying how damaged tissues and organs can regenerate.

285 process in normal development and repair of damaged tissues and organs.

286 models of hindlimb ischemia rescues severely damaged tissues by the ingrowth of neighboring host vess

287 ccordingly, eliminating senescent cells from damaged tissues in mice ameliorates the symptoms of thes

288 lammatory response in the heart that removes damaged tissues to facilitate tissue repair/regeneration

289 nitiates clearance and repair in infected or damaged tissues.

290 flammatory responses to pathogens and repair damaged tissues.

291 equence data generated for 75 healthy and 75 damaged trees from a single seed source.

292 Vancomycin cast could be identified in a damaged tubule.

293 loroplast thylakoids (Thys) are specifically damaged upon (1)O(2) generation and associate with plast

294 The airway epithelium is seriously damaged upon pulmonary Pseudomonas aeruginosa infection,

295 ilable, if the retinal pigment epithelium is damaged, we have to cope with the impossibility of resto

296 mbled by DEP within the crevices of severely damaged wires to create stretchable interconnects that h

297 vers of mice given injections of IL11 became damaged, with increased markers of fibrosis, hepatocyte

298 Our data suggest that the glycocalyx is damaged within human liver grafts during preservation an

299 chanism whereby iron diffuses into radiation-damaged zircon along the cores of dislocations and is pr

300 w-temperature recrystallization of radiation-damaged zircon in the presence of an aqueous fluid.