ライフサイエンスコーパス: damaged

1 more efficient when the tissue was partially damaged.

2 the structural network in CAE were seriously damaged.

3 levels as low as 30% after being physically damaged.

4 ng pathways in conditions where the liver is damaged.

5 nerative diseases in which myelin is lost or damaged.

6 sed by Hymenoscyphus fraxineus, has severely damaged a large proportion of ash trees (Fraxinus excels

7 Interestingly, 1 mutation damaged a predicted sumoylation site, and another disrup

8 oduction can be dramatically and permanently damaged after a single relatively low TBI dose, accelera

9 The iPLCs were successfully engrafted into a damaged airway, highlighting this significant advancemen

10 type 1 cells (AT1s) during the repair of the damaged alveolar epithelium.

11 conserved catabolic process that eradicates damaged and aging macromolecules and organelles in eukar

12 In the presence of semen fibrils, damaged and apoptotic sperm were more rapidly phagocytos

13 ated cells in the retina, the removal of the damaged and dysfunctional mitochondria by a double-membr

14 lving inflammation and restoring function of damaged and infected tissues.

15 ntrations of regulatory proteins and removes damaged and misfolded proteins from cells.

16 in signaling that the DNA in a cell has been damaged and needs to be repaired.

17 roliferation, thus limiting the expansion of damaged and potentially oncogenic hepatocytes.

18 and have altered HR protein dynamics in both damaged and untreated cells.

19 th over 90% certainty, whilst also detecting damaged and/or excysted oocysts.

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

21 utophagic response that specifically targets damaged, and hence potentially cytotoxic, mitochondria.

22 On average, a damaged apex cost each ramet 5015 seeds.

23 stinal epithelium are related under healthy, damaged (Ara-C treated) and recovering conditions, and h

24 ptides accelerate cell migration to seal the damaged area from luminal contents, whereas chronic infl

25 wever, to date, how revascularization of the damaged area happens remains unknown.

26 otentially adds to neuroprotection outside a damaged area, while other mechanisms control PEA-mediate

27 mize inflammation and limit expansion of the damaged area.

28 r injury, with fast and complete recovery of damaged area.

29 phatidylserine, which becomes exposed on the damaged axon to function as a "save-me" signal, defines

30 ial scarring, which inhibits the regrowth of damaged axons.

31 a DNA glycosylase scanning the genome for a damaged base in the very first stage of lesion recogniti

32 Whether single nucleotide (SN)-BER of a damaged base requires histone deposition or nucleosome r

33 ge and realignment extension across from the damaged base.

34 cision repair apparatus capable of repairing damaged bases and abasic sites.

35 DNA repair enzymes recognize and remove damaged bases that are embedded in the duplex.

36 The prospect of replacing damaged body parts with artificial implants is being tra

37 -inflammatory drugs frequently do not repair damaged bone.

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

39 e cells die when their antigen receptors are damaged by activation-induced cytidine deaminase.

40 rtain provenances in Scotland were the least damaged by ADB, whereas trees from Wales and Southeast E

41 high granular (HG) pool, which then becomes damaged by apoptosis and glycoprotein Ib alpha chain (CD

42 opment can be arrested if the tooth organ is damaged by either trauma or caries.

43 E Immune tissues within the gut are severely damaged by HIV-1, and this plays an important role in th

44 t restores structure and function of tissues damaged by injury or disease.

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

46 Cooperative behaviours can be damaged by the emergence of 'cheating' cells that benefi

47 a cells (BMSCs) are severely and permanently damaged by the pre-conditioning irradiation required for

48 Current therapy to replace damaged cardiac tissue is limited to cardiac transplanta

49 cytes could provide a solution for replacing damaged cartilage.

50 ore homeostasis or eliminate the irreparably damaged cell.

51 erentiation program that halts the growth of damaged cells and must be circumvented for cancer to ari

52 denosine triphosphate (ATP) is released from damaged cells and promotes proliferation and activation

53 roy, and eliminate pathogens and infected or damaged cells and repair tissues.

54 Damaged cells send various signals to stimulate defense

55 of information concerning tissue damage from damaged cells to neighboring healthy cells.

56 ing epithelial cells within 6 hours, and all damaged cells were extruded from the epithelium.

57 ced lung injury (shown as volume fraction of damaged cells) was significantly greater in the terminal

58 ty, and its activation drives the removal of damaged cells, autoantigens and environmentally derived

59 nflammatory danger signal ATP, released from damaged cells, is degraded by the ectonucleotidases CD39

60 oxidative stress and is capable of rescuing damaged cells.

61 calcium entry from extracellular fluid into damaged cells.

62 lt in autophagy and cell death, to eliminate damaged cells.

63 owed by lineage differentiation to replenish damaged cells.

64 lication forks and prevents origin firing in damaged cells.

65 when released into extracellular space from damaged cells.

66 onses as it is highly induced in stressed or damaged cells.

67 e latter by recruiting immune cells to clear damaged cells.

68 Damaged central nervous system (CNS) neurons have a poor

69 odulation, neuroprotection, or repair of the damaged central nervous system in multiple sclerosis.

70 efficient APE2-dependent RPA recruitment to damaged chromatin and activation of the ATR-Chk1 DDR pat

71 A and BAZ1B each recruit SMARCA5 to sites of damaged chromatin and promote survival.

72 nding protein replication protein A (RPA) on damaged chromatin and severely abrogated ATR signaling i

73 A, and we find that its accumulation on UVB-damaged chromatin is partially attenuated in cells with

74 show that ZMYM3 links the HR factor BRCA1 to damaged chromatin through specific interactions with com

75 H3K4 to allow ZMYND8-NuRD to operate within damaged chromatin to repair DSBs.

76 e sensor, is involved in localizing Fun30 to damaged chromatin, and thus is required for efficient lo

77 the assembly of Lys11-linkage conjugates on damaged chromatin, including histone H2A/H2AX.

78 By regulating ABRA1 recruitment to damaged chromatin, ZMYM3 facilitates the fine-tuning of

79 route for the degradation of superfluous and damaged constituents of the cytoplasm.

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

81 e for immunoproteasomes in elimination of FA-damaged cytoplasmic proteins through ubiquitin-independe

82 ding products of oxidatively and nitratively damaged DNA (8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-

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

84 the DNA damage response, detects and repairs damaged DNA and prevents cell division until the repair

85 If left unrepaired, these damaged DNA bases can disrupt cellular processes such as

86 gulates the ability of tumor cells to repair damaged DNA by regulating BRCA2 stability.

87 eotide selectivity on normal and oxidatively damaged DNA by three single-subunit RNAPs provides the b

88 Damaged DNA can be repaired by removal and re-synthesis

89 cial nucleoside that inhibits replication of damaged DNA can safely enhance therapeutic responses.

90 s can lead to genomic restoration or, if the damaged DNA cannot be adequately repaired, to the execut

91 Accumulation of damaged DNA in hematopoietic stem cells (HSC) is associa

92 This mutation impairs PNKP recruitment to damaged DNA in human cells and provides a possible disea

93 hesis (TLS) Pols in the replication of 3-MeA-damaged DNA in human cells.

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

95 rosyl-DNA phosphodiesterases that can repair damaged DNA resulting from topoisomerase inhibitors and

96 on repair, coupled incisions are made in the damaged DNA strand on both sides of the adduct.

97 re to properly suppress DNA synthesis on UVB-damaged DNA templates.

98 nction DNA kinase/phosphatase that processes damaged DNA termini and that, if mutated, results in ata

99 ects DNA damage response factors to sites of damaged DNA to promote the signaling and repair of DNA l

100 genome integrity is important for cells and damaged DNA triggers autoimmunity.

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

102 of ATR and XPA's associations with cisplatin-damaged DNA, indicating that ATR phosphorylation at S435

103 S688 inhibited loading of the MRN complex to damaged DNA, leading to both premature DNA damage checkp

104 ase, prevents immune activation by depleting damaged DNA, thus preventing the development of certain

105 Damaged DNA-binding protein 2 (DDB2), a nuclear protein,

106 is facilitated in the genomic context by UV-damaged DNA-binding protein 2 (DDB2), which is part of a

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

108 otein (CTIP), a DNA-end resection factor, to damaged DNA.

109 incorporate nucleotides opposite and beyond damaged DNA.

110 ral human DNA polymerases that can replicate damaged DNA.

111 mage response (DDR) to mediate the repair of damaged DNA.

112 omatin in a manner coupled to replication of damaged DNA.

113 ed malignancies by attenuating the repair of damaged DNA.IMPORTANCE This study expands the understand

114 at caErbB2 markedly enhances regeneration of damaged dorsal roots, while evoking little change in int

115 hat during EIS the gold surface is seriously damaged due to the presence of CN(-) ions, which are rel

116 These results suggest that if complex III is damaged during ischemia, PTP opening may result in succi

117 Eyes of patients with glaucoma may be damaged during sleep.

118 w impairment in the selective degradation of damaged/dysfunctional mitochondria through mitophagy may

119 both mitochondrial biogenesis and removal of damaged/dysfunctional mitochondria via mitophagy.

120 rought recovery time, leading to permanently damaged ecosystems and widespread degradation of the lan

121 that the danger receptor galectin-8 detects damaged endomembranes and activates autophagy through re

122 tion, indicating that autophagy triggered by damaged endomembranes during the entry of assembled tau

123 hrin-independent endocytosis and escape from damaged endomembranes into the cytosol, where they seed

124 l, venous thrombi, thrombotic depositions on damaged endothelial surface, and small cerebral emboli w

125 e propose a model in which stiffening of the damaged ends by the repair complex, combined with global

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

127 les in axonal pathfinding, in the healing of damaged epithelia in Drosophila.

128 The damaged epithelial cells were associated with increased

129 The damaged epithelium is a source of alarmins that activate

130 Consequently, the damaged forks become unstable and resistant to repair.

131 replication and protect, repair and restart damaged forks.

132 sm by which the fittest, strongest, or least damaged germ cells are selected for transmission to the

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

134 evealed de novo expression of connexin 43 in damaged glomeruli in patients with glomerular diseases a

135 nism of DNA synthesis opposite undamaged and damaged guanine.

136 Translocation of microbial products from the damaged gut causes increased immune activation in human

137 When the V1-damaged hemisphere was challenged by incoming visual sti

138 Damaged hepatocytes from ASH mice are a key EV source wi

139 rt planning, intact planning in animals with damaged hippocampi has been repeatedly observed.

140 The 10% CP dietary treatment damaged ileal mucosal morphology, and decreased the expr

141 materials that when punctured, cut, shot or damaged in a variety of ways, are capable of autonomousl

142 No single brain region was damaged in all cases.

143 es and Southeast England were the most badly damaged in both trial sites.

144 ouse model in which the mitochondrial DNA is damaged in dopaminergic neurons.

145 ites to include areas that were consistently damaged in the patients with phonological impairments.

146 t of proteins, specifically those containing damaged iron-sulphur clusters.

147 circulating and FSGS can recur even after a damaged kidney is replaced with a healthy donor organ.

148 In damaged kidneys and cytokine-stimulated renal cells, JQ1

149 In sepsis, this emergency myelopoiesis is damaged, leading to failure of bacterial clearance, and

150 fferent changes in phytohormones to those in damaged leaves, including a lower but more potent burst

151 s-lesion synthesis to allow replication past damaged lesions in S phase.

152 tial, stem cells might be used to regenerate damaged liver tissue.

153 iferate from the portal areas of chronically damaged livers, but their significance to regeneration h

154 y, and immunohistochemistry demonstrate that damaged lobes underwent multilineage regeneration, refor

155 and, in many instances, permanently seal the damaged location.

156 CCL17 and had impaired expansion of ILC2 in damaged lung tissue compared with wild-type controls.

157 ion body myopathy and neurodegeneration, and damaged lysosomes accumulate in affected patient tissue

158 irected AAA-ATPase, p97, in the clearance of damaged lysosomes by autophagy.

159 ubiquitin conjugates from a subpopulation of damaged lysosomes to promote autophagosome formation.

160 deep ocean floor following release from the damaged Macondo Well.

161 al hypoxia produces graded damage, including damaged macromolecules and inflammation.

162 he progressive accumulation and retention of damaged material, including protein aggregates.

163 e IL-23R(+), demonstrated that DNA repair of damaged melanocytes requires IL-23.

164 activated based on specific signals from the damaged microenvironment.

165 ses the expression of chaperones that refold damaged misfolded proteins or facilitate their degradati

166 the autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in

167 Propofol damaged mitochondria and decreased cytosolic ATP.

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

169 The removal of unwanted or damaged mitochondria by autophagy, a process called mito

170 gulate the mitophagy pathway, which recycles damaged mitochondria following oxidative stress.

171 e of IL-10 signaling, macrophages accumulate damaged mitochondria in a mouse model of colitis and inf

172 ndrial density and increased the presence of damaged mitochondria in BAT.

173 ophagy receptors, efficient sequestration of damaged mitochondria in response to mitochondrial stress

174 Vms1 translocates to damaged mitochondria in response to stress, whereupon it

175 Damaged mitochondria pose a lethal threat to cells that

176 Damaged mitochondria release danger molecules, such as r

177 pate in mitochondrial turnover, by targeting damaged mitochondria with low membrane potential to mito

178 es and transports specific cargos, including damaged mitochondria, other broken organelles, or pathog

179 pecifically regulate autophagic clearance of damaged mitochondria.

180 uitment of the ubiquitin E3 ligase Parkin to damaged mitochondria.

181 ergistic processes required for clearance of damaged mitochondria: (i) general autophagy initiation a

182 f mitochondria, including complementation of damaged mitochondrial DNAs and the maintenance of membra

183 hat cancer cells with advantageous levels of damaged mitochondrial genomes will selectively prolifera

184 ic lesion, macrophages ingest high levels of damaged modified low-density lipoproteins (LDLs), genera

185 mportant roles in human health, by detecting damaged molecules in the nucleotide pool and deactivatin

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

187 sal tissues, but it also inhibited repair of damaged mucosa induced by mesenteric ischemia/reperfusio

188 movement, and reduced percentage of severely damaged muscle cells.

189 markedly enhanced and accelerated repair of damaged muscles following intramuscular delivery of PGE2

190 s that are essential for the regeneration of damaged muscles in vertebrates, have not been reported i

191 Imaging of bioconstructs implanted in damaged muscles indicates MuSCs survival and growth, and

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

193 vation of Trem2, both necessary for clearing damaged myelin, were markedly reduced in GALC +/- animal

194 Zebrafish regenerate damaged myocardial tissue very effectively.

195 ks the capacity to repair and regenerate the damaged myocardium from ischemic injury.

196 fying improved approaches to revascularizing damaged myocardium in patients with ischemic heart disea

197 in the real RDN group than in sham controls; damaged nerves were found only in the real RDN group.

198 tially increase the regenerative capacity of damaged nerves without deleterious off-target effects.

199 d restore the morphology of their previously damaged neuromuscular junctions (NMJs), suggesting that

200 M) dendrimers target activated microglia and damaged neurons in the injured brain, and deliver therap

201 indings show that intrinsic signaling within damaged neurons regulates synaptic remodeling and involv

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

203 glial migration and phagocytic clearance of damaged neurons.

204 o the critical enhancement of K(+) efflux in damaged neurons.

205 induce a sharp kink in the DNA, exposing the damaged nucleobase to active site residues that project

206 nthesis (TLS), the postreplicative bypass of damaged nucleotides.

207 a cellular process that selectively removes damaged, old or dysfunctional mitochondria.

208 hought to be the major mechanism eliminating damaged oocytes.

209 Damaged or diseased HCEnCs may cause blindness.

210 cell can heal membrane ruptures and rebuild damaged or missing cellular structures remain poorly und

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

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

213 Autophagic responses specific for damaged or superfluous mitochondria are crucial for the

214 nt is extremely rapid upon binding to either damaged or undamaged DNA, much faster than the lesion-re

215 scales providing a strategy to replace old, damaged, or dysfunctional proteins.

216 serves as a protective mechanism to degrade damaged organelles and proteins.

217 disposal of mitochondria is autophagy, where damaged organelles are marked for disposal via ubiquityl

218 Removal of damaged organelles clears the cell of potentially toxic

219 ophagosomes to remove protein aggregates and damaged organelles from the cytoplasm for recycling.

220 is involved in the clearance of proteins and damaged organelles to maintain intracellular homeostasis

221 in the reduced clearance and accumulation of damaged organelles within the cell.

222 a upward arrow) and enhanced regeneration of damaged pancreas (Reg4 upward arrow, PTF1 upward arrow,

223 on and motor deficits in 44 right hemisphere-damaged patients with a first-time stroke at 1-2 weeks p

224 s, as persistent MPs, prevent fusion between damaged phagosomes and intact lysosomes and thereby pres

225 mediate the clearance of activated, aged or damaged platelets.

226 Hypertrophy is a prominent feature of damaged podocytes in diabetic kidney disease (DKD).

227 diabetic kidney and in high glucose-induced damaged podocytes.

228 ion, and mitophagy, are induced to eliminate damaged portions or entire dysfunctional mitochondria.

229 rm of rapid cell death that serves to remove damaged progenitors and promote qNSC activation.

230 to maintain cellular homeostasis by removing damaged proteins and organelles through lysosomal degrad

231 al population also requires the clearance of damaged proteins and organelles.

232 ing cytokinesis in Saccharomyces cerevisiae, damaged proteins are distributed unequally between the d

233 rnover are maintained despite advancing age, damaged proteins are more quickly degraded and replaced,

234 ing protein disaggregase that rescues stress-damaged proteins from an aggregated state.

235 resses mitigates cellular damage by removing damaged proteins, lipids, and organelles.

236 ases critical for the removal of oxidatively damaged proteins.

237 ir of abnormal l-isoaspartyl linkages in age-damaged proteins.

238 with the proteasome to degrade misfolded or damaged proteins.

239 ld provide a path to using more ischemically damaged renal allografts.

240 nking gammaH2A, Rhp18, and Smc5/6 complex at damaged replication forks.

241 Inhibition of mTor in damaged retinas prevented the accumulation of pS6 in Mul

242 Together these studies indicate that damaged salivary gland tissue can grow and differentiate

243 echanism by which an organism can respond to damaged self.

244 oplastic environment and detect non-self and damaged-self patterns as signs of potential danger.

245 ure, particularly during the regeneration of damaged shell.

246 opening can be sustained when complex III is damaged (simulated by antimycin).

247 mutated serine/threonine kinase (ATM) to the damaged site, where it plays a key role in advancing the

248 NPCs) proliferation and migration toward the damaged site.

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

250 DNA repair proteins must locate rare damaged sites within the genome.

251 DNA, increasing the probability of locating damaged sites.

252 l RNAs and DNA repair recognition factors at damaged sites.

253 Whereas damaged skeletal muscle has a profound capacity to regen

254 condition that typically affects actinically damaged skin of the scalp.

255 trol of melanomas arising in chronically sun-damaged skin on the head and neck has favorable recurren

256 and consistently downregulated in radiation-damaged skin.

257 Surprisingly, the ischemically damaged small intestinal and ascending colonic tissue sh

258 of survivin was detected in the ischemically damaged small intestine and ascending colon.

259 The damaged starch content of barley cultivars ranged betwee

260 Jet milling increased the amount of damaged starch in both rye and barley flours.

261 Water absorption and damaged starch were found to be important parameters for

262 ream of the damage, and XPF binds to the non-damaged strand within a repair bubble.

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

264 at the recruitment of BRCA1 and BLM to these damaged telomeres is interdependent and is regulated by

265 novel role of TNKS1 in facilitating SSBR at damaged telomeres through PARylation of TRF1, thereby pr

266 TNKS1 is recruited to damaged telomeres via its interaction with TRF1, which s

267 repair proteins XRCC1 and polymerase beta at damaged telomeres, while the PARP1/2 inhibitor only has

268 incorrect) opposite the G (normal) or 8-oxoG(damaged) template base.

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

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

271 monas syringae pv. actinidiae (Psa) severely damaged the New Zealand kiwifruit industry, which in 201

272 uration, impaired mitochondria function, and damaged the spindle and DNA.

273 nderfunded, poorly managed, and ecologically damaged; the conundrum is how to increase their coverage

274 In contrast, process outgrowth to damaged tissue requires P2Y12 receptor activation but is

275 isms control PEA-mediated neuroprotection in damaged tissue resulting from traumatic brain injury or

276 proinflammatory and restorative functions in damaged tissue through complex dynamic phenotypic change

277 shold of 1400 ms, the volume of irreversibly damaged tissue was in good agreement with the 6-month la

278 rculating pentameric CRP (pCRP) localizes to damaged tissue where it leads to complement activation a

279 al process necessary to restore structurally damaged tissue.

280 lly, are multipotent stem cells that home to damaged tissues and can modulate the immune system.

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

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

283 or M2) macrophages play a role in repair of damaged tissues, including the infarcted hearts.

284 phages regulate the physiology of normal and damaged tissues.

285 amounts of regurgitant or bacteria on H. zea-damaged tomato leaves.

286 break levels and subsequent feeding severely damaged tree fruit as well as other crops.

287 control mechanism that degrades structurally damaged tRNA.

288 necrosis demonstrated high levels of CtsD in damaged tubular cells.

289 cient TRIP13 increased the susceptibility of damaged tubular epithelial cells to progress towards apo

290 in vitro that nitrogenase can be oxidatively damaged under anoxic conditions and that the aforementio

291 rogen (N2) to ammonia (NH3), is irreversibly damaged upon exposure to molecular oxygen (O2).

292 When DNA was damaged using ultraviolet (UV) radiation (lambda=254nm)

293 noncanonical autophagic process that targets damaged vacuoles.

294 heir well-preserved but highly disrupted and damaged vertebrate and botanical remains are reinterpret

295 actor (VWF), which binds exposed collagen at damaged vessels and captures platelets.

296 , suggesting that it may allow for bypass of damaged viral DNA during its replication.

297 t hippocampus at 1 week and reduced neuronal damaged was found in the penumbral at day 14 apoptosis.

298 anterior temporal cortex is most prominently damaged, which may indicate the putative origin of neuro

299 Surprisingly, damaged white matter tracts in Olig1-null mice lacked Ol

300 );Pdgfra-CreER) of Lrp1 attenuates repair of damaged white matter.