ライフサイエンスコーパス: the damaged

1 Rather, the damaged/activated endothelium and possibly other blo

2 This permits them to invade the damaged adjacent normal tissue despite the acid grad

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

4 entiated cells in the retina, the removal of the damaged and dysfunctional mitochondria by a double-m

5 distinguish between the events occurring in the damaged and undamaged DNA strand.

6 e damage recognition process contacting both the damaged and undamaged DNA strand.

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

8 peration between brain regions lying outside the damaged area contributes to spatial deficits in a wa

9 F peptides accelerate cell migration to seal the damaged area from luminal contents, whereas chronic

10 ; however, to date, how revascularization of the damaged area happens remains unknown.

11 tex that normally receives visual input from the damaged area of the retina.

12 in or spinal cord is injured, glial cells in the damaged area undergo complex morphological and physi

13 migration of newly formed neuroblasts toward the damaged area where they mature to striatal neurons.

14 dent with migration of neighbouring cells to the damaged area, sustaining epithelial continuity.

15 followed by directional process extension to the damaged area.

16 oaches to healable materials require heating the damaged area.

17 minimize inflammation and limit expansion of the damaged area.

18 fish displayed minimal revascularization of the damaged area.

19 isphere "take over" their functions, whereas the damaged areas and other ipsilesional regions play mu

20 lesions, photoreceptors completely filled in the damaged areas by 4 months.

21 h stress or induce deposition of minerals on the damaged areas from the increase in mechanical stress

22 empirical connectivity values, especially of the damaged areas, correlated better with simulated valu

23 ets, circulating progenitor cells home in on the damaged areas.

24 ct orderly rescue and recovery operations in the damaged areas.

25 d transdifferentiaton of supporting cells in the damaged auditory organ of birds lead to robust regen

26 phosphatidylserine, which becomes exposed on the damaged axon to function as a "save-me" signal, defi

27 resulting in leakage of serum proteins from the damaged barrier.

28 base-displaced intercalation motif in which the damaged base and its partner are extruded from the h

29 esult in a profound effect on both repair of the damaged base and the SSB.

30 that lesion recognition by Nei occurs before the damaged base flips into the glycosylase active site.

31 higher temperature shifts the preference of the damaged base from the anti to the syn conformation,

32 Nei mutants that interfere with eversion of the damaged base from the helix (QLY69-71AAA, DeltaQLY69

33 ched dNTP structures are less distorted when the damaged base is syn than when it is anti, at the hig

34 ts show that NI adopts a planar structure at the damaged base level.

35 hydroxyl groups at C5 and C6 in a Tg lesion, the damaged base loses its aromatic character and become

36 hOGG1, that interact with the DNA containing the damaged base oxoG and the normal base G while they a

37 We first demonstrated that the damaged base should be excised before SSB repair can

38 ated free energy surfaces during eversion of the damaged base through the major and minor grooves.

39 ), which transfers the O(6)-alkyl group from the damaged base to a cysteine residue within the protei

40 lalanine residue, which intercalates next to the damaged base, changed to either alanine (F110A) or f

41 n of a short patch of nucleotides containing the damaged base, re-synthesis of a new DNA strand and l

42 Rather than repairing the damaged base, replication past it may proceed via on

43 the lesion followed by specific excision of the damaged base.

44 thesis of a new Okazaki fragment upstream of the damaged base.

45 highly mutagenic and genotoxic properties of the damaged base.

46 ippage and realignment extension across from the damaged base.

47 recedented base-flipping mechanism to access the damaged base: it squeezes together the two bases fla

48 s possess multiple glycosylases to recognize the damaged bases and to initiate the Base Excision Repa

49 Because of this increased acidity, the damaged bases would be expected to be more easily cl

50 cytes in the neurovascular niche that repair the damaged BBB.

51 In the damaged blood vessel wall, for example in atheroscle

52 Previously, we showed that the damaged blood-brain barrier (BBB) was involved in su

53 a mitotic protein accumulated aberrantly in the damaged brain areas of Alzheimer's disease and strok

54 t potential therapeutic treatments to repair the damaged brain endothelium.

55 n, more than twice as many neurospheres from the damaged brain were tripotential, suggesting an incre

56 n the brain damage produced by ischemia, and the damaged brain, in turn, exerts an immunosuppressive

57 nhance successful neurogenesis for repairing the damaged brain.

58 sed the rate of localized VOC emissions from the damaged branch.

59 heart lacks sufficient ability to replenish the damaged cardiac muscles, extensive research has been

60 ination of the damaged parts of the cells or the damaged cell in its entirety.

61 chemical injury and regenerate a portion of the damaged cell layer.

62 get cell, which triggers a process to repair the damaged cell membrane.

63 y increasing IAA accumulation and recovering the damaged cell structure in root tips.

64 DNA repair or trigger apoptosis to eliminate the damaged cell.

65 to resolve the stress or apoptosis to clear the damaged cell.

66 t of the caspase CED-3, but the clearance of the damaged cells partially depends on the phagocytic re

67 uncontrolled positive feedback loop in which the damaged cells release acetylated H3.3, which causes

68 ituting gastric epithelial cells adjacent to the damaged cells.

69 roved therapy that promotes remyelination in the damaged central nervous system (CNS).

70 ne modulation, neuroprotection, or repair of the damaged central nervous system in multiple sclerosis

71 ionizing radiation in the laboratory and in the damaged Chernobyl nuclear reactor suggest they have

72 dependent cNHEJ reinforces 53BP1 assembly at the damaged chromatin and shifts DSB repair to mutagenic

73 Lys(63)-linked ubiquitin (K63-Ub) adducts at the damaged chromatin but is endowed with K63-Ub deubiqu

74 urface and nucleosome dynamics in processing the damaged chromatin template during DSB repair.

75 iately after DSB production and that prepare the damaged chromatin template for processing by the DSB

76 ckpoint mediator proteins BRCA1 and 53BP1 to the damaged chromatin, on one hand through the phospho-d

77 as the molecular platform to anchor UBC13 at the damaged chromatin, where localized ubiquitylation ev

78 ks (DSBs) by serving as a master scaffold at the damaged chromatin.

79 omere deletion, cells maintain and segregate the damaged chromosome without repairing it.

80 Axotomized neurons within the damaged CNS are thought to be prevented from functio

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

82 recaptured after regeneration of neurons in the damaged CNS remains unclear.

83 elicits a protective role for astrocytes in the damaged CNS.

84 herapeutic agents for neural regeneration in the damaged CNS.

85 and guide efforts to restore connectivity in the damaged cochlea.

86 generated in vitro and in vivo and by which the damaged cofactors are repaired is providing insight

87 sts showed highly elevated concentrations of the damaged cofactors S-NADHX, R-NADHX and cyclic NADHX.

88 airments to specific motor domains linked to the damaged cortical subregion and that damage encroachi

89 by mitochondrial fission and degradation of the damaged daughter mitochondrion.

90 In primary neurons, bexarotene ameliorated the damaged dendrite complexity and loss of neurites cau

91 ulations indicate that at glancing incidence the damaged depth within the solid is smallest.

92 pensatory proliferation and re-patterning of the damaged discs, and our results indicate that cell de

93 before irradiation and rapidly escorts it to the damaged DNA after UV irradiation in a DDB2-independe

94 at the replication fork to bypass and extend the damaged DNA and then switch off of the DNA substrate

95 site of DNA damage, facilitate processing of the damaged DNA and, importantly, are essential to repac

96 the decreased growth allows cells to repair the damaged DNA before mitosis, and failure to repair da

97 Here we report that induced deletion of the damaged DNA binding protein 1 (DDB1) abrogates the s

98 nisms can lead to genomic restoration or, if the damaged DNA cannot be adequately repaired, to the ex

99 rate approximately equal binding affinity to the damaged DNA duplex (K(D) approximately (0.5 +/- 0.1)

100 pportunity for elucidating the properties of the damaged DNA duplexes that favor NER.

101 erase can "sense" bulky lesions to partition the damaged DNA into the exonuclease domain.

102 s) that tightly bind alkylated DNA and shunt the damaged DNA into the nucleotide excision repair path

103 can be rationalized either by assuming that the damaged DNA is characterized by a higher barrier for

104 block initiations absolutely, duplication of the damaged DNA is expected to increase the genetic vari

105 ilure to stop or stall the cell cycle before the damaged DNA is passed on to daughter cells.

106 The detailed structure of the damaged DNA macromolecule has remained elusive.

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

108 e which then coordinate the dual incision of the damaged DNA strand.

109 influence the orientation of XPA and RPA on the damaged DNA substrate, remains poorly characterized.

110 s suggested that due to the heterogeneity of the damaged DNA substrates with which Pol lambda as well

111 ating chromatin packing during processing of the damaged DNA template.

112 hydantoin lesion, were detected by tethering the damaged DNA to streptavidin via a biotin linkage and

113 ficiencies lead to a failure to fully repair the damaged DNA upon exposure of glioma cells to IR with

114 3B complex is preferentially cross-linked to the damaged DNA when the photoreactive FAP-dCMP (exo-N-{

115 of recombination proteins to perfectly align the damaged DNA with homologous sequence located elsewhe

116 (TLS), specialized DNA polymerases replicate the damaged DNA, allowing stringent DNA synthesis by a r

117 (XPC) protein in chromatin is stimulated by the damaged DNA-binding protein 2 (DDB2), which is part

118 CC1s were equally efficient at localizing to the damaged DNA.

119 The damaged DNAs diffuse in gel matrix and form observab

120 trated, with the former cells predominant in the damaged ducts.

121 ermodynamic understanding of the features of the damaged duplexes that produce the most robust NER re

122 ynamic roles of the flanking amino groups in the damaged duplexes.

123 We demonstrate that delivery of PEDF to the damaged ear ameliorates hearing loss by restoring in

124 ruitment and the functions of macrophages in the damaged ear are unclear.

125 -coated and EDTA-loaded albumin NPs targeted the damaged elastic lamina while sparing healthy artery.

126 Cytosolic galectins immediately recognized the damaged endosome and targeted it for autophagy.

127 We propose a model in which stiffening of the damaged ends by the repair complex, combined with gl

128 t survive, proliferate, and differentiate in the damaged environment of the reconstituting niche.

129 The damaged epithelial cells were associated with increa

130 The damaged epithelium impairs mucus removal and facilit

131 The damaged epithelium is a source of alarmins that acti

132 The intraclass correlation score for the damaged field indicated excellent correlation betwee

133 ld restitution therapies, in which vision in the damaged field is itself improved.

134 In the damaged field, kappa values were highly significant,

135 se results suggest that albumin loss through the damaged filtration barrier impairs podocyte regenera

136 nt of the damage recognition factor, XPC, to the damaged foci and concomitantly reduced the removal o

137 irs recruitment of the repair protein XPC to the damaged foci and inhibits the repair process.

138 that depends on MUS81-catalyzed cleavage of the damaged fork.

139 cruitment and phosphorylation of proteins at the damaged fork.

140 Consequently, the damaged forks become unstable and resistant to repai

141 a preferred retinal locus (PRL) in place of the damaged fovea to fixate a target.

142 These species will enhance the corrosion of the damaged fuel and, being thermodynamically stable and

143 ons recorded in surface seawater offshore of the damaged Fukushima Dai-ichi nuclear power plant were

144 4)Cs and (137)Cs released in March 2011 from the damaged Fukushima Dai-ichi nuclear power plant.

145 Radioactive isotopes originating from the damaged Fukushima nuclear reactor in Japan following

146 oming integrins permissive of migration into the damaged GI tract, resulting in the lethal feed-forwa

147 il swarming and microglial reconstitution of the damaged glial limitans.

148 und nonesterified fatty acids (NEFAs) across the damaged glomerular filtration barrier and subsequent

149 cells (podocytes) and mesangial cells within the damaged glomerulus, leading to a partial restoration

150 promising therapeutic strategies to restore the damaged glycocalyx and to attenuate its deleterious

151 Translocation of microbial products from the damaged gut causes increased immune activation in hu

152 nic identity have been studied for repair of the damaged heart, but the relative utility of the vario

153 ystems biology as therapeutic strategies for the damaged heart.

154 g conserved molecular programs to regenerate the damaged heart.

155 active and innovative solution for repairing the damaged heart.

156 , with deficient leukocyte infiltration into the damaged heart.

157 ispheric inhibition (IHI) from the intact to the damaged hemisphere before movement execution (premov

158 pathological state of inhibition exerted on the damaged hemisphere by the hyperexcited intact hemisp

159 atients with neglect alpha oscillations over the damaged hemisphere were pathologically enhanced both

160 mode/frontoparietal regions, particularly in the damaged hemisphere.

161 ctions, they were primarily localized around the damaged interlobular bile ducts in PBC.

162 t elimination of luminal antigens that cross the damaged intestinal barrier.

163 ta-driven FGF2 and IL-17 cooperate to repair the damaged intestinal epithelium through Act1-mediated

164 , verbal and visual memory function utilized the damaged, ipsilateral hippocampus and also the contra

165 us epilepticus in mice, comparing changes in the damaged, ipsilateral hippocampus to the spared, cont

166 blood urea nitrogen and creatinine levels in the damaged kidneys.

167 ndrocyte Implantation (ACI) in order to heal the damaged knee cartilage.

168 ring process, and the acid treatment removes the damaged layer of carbon.

169 which then participate in the restoration of the damaged liver tissue.

170 dherent to the vessel walls and infiltrating the damaged livers of wild-type mice after liver I/R inj

171 eal and, in many instances, permanently seal the damaged location.

172 n fibrosis following loss of myeloid VEGF in the damaged lungs was also marked by increased levels of

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

174 Bone cracks can be detected by utilizing the damaged matrix itself as both the trigger and the fu

175 rtilage can up-regulate mechanisms to repair the damaged matrix.

176 -2 and ALG-2-interacting protein X (ALIX) to the damaged membrane.

177 d endosomes donate their membranes to reseal the damaged membrane.

178 for repairing injured spinal cord is to seal the damaged membranes at an early stage.

179 ome activated based on specific signals from the damaged microenvironment.

180 d proliferation of cardiomyocytes to replace the damaged/missing tissue; at present, however, little

181 l activation of autophagy selectively clears the damaged mitochondria and thus repairs mitochondrial

182 l, which in turn promotes the degradation of the damaged mitochondria by autophagy (mitophagy).

183 ly triggers quarantine and/or degradation of the damaged mitochondria by the proteasome and autophagy

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

185 y output and aggravate ROS overproduction by the damaged MRC.

186 loma and rheumatoid arthritis and to restore the damaged mucosa in experimental colitis, respectively

187 re to bacterial products translocated across the damaged mucosa.

188 in slow- or fast-type muscle, we found that the damaged-muscle phenotype had a very limited impact o

189 Gomez-Sanchez et al. find that clearance of the damaged myelin within Schwann cells occurs not by ph

190 em facilitates scar formation, which repairs the damaged myocardium but compromises cardiac function.

191 lacks the capacity to repair and regenerate the damaged myocardium from ischemic injury.

192 apy, is a promising strategy for recovery of the damaged myocardium.

193 lls offer a provocative method to regenerate the damaged myocardium.

194 g high concentrations of therapeutics within the damaged myocardium.

195 Engraftment of hMDSPCs into the area of the damaged nerve promoted axonal regeneration, which le

196 d be used to harness astrocytic responses in the damaged nervous system to promote an environment mor

197 aph theory properties of intact nodes within the damaged network show evidence of dysfunction compare

198 , graph theoretical measures are computed on the "damaged" network.

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

200 Instead of directly interacting with the damaged nucleobase, AlkD recognizes aberrant base pa

201 site of damage and catalyzes the excision of the damaged nucleobase.

202 The damaged nucleobases are found to be more acidic than

203 n nucleosomes is repaired upon incubation of the damaged nucleosomes with PIMT and AdoMet.

204 quantitate Pol X-catalyzed incorporation of the damaged nucleotide 8-oxo-dGTP opposite to undamaged

205 s on the 5' face of the pyrimidine moiety at the damaged nucleotide between base pairs T(4).A(17) and

206 to catalyze base excision without extruding the damaged nucleotide from the DNA helix.

207 s on the 5' side of the pyrimidine moiety at the damaged nucleotide, we conclude that favorable 5'-st

208 ss-links to 5I-dUMP located exactly opposite the damaged nucleotide.

209 Incorporation of the damaged nucleotides in nucleic acids is detrimental

210 ay be essential for long-term restoration of the damaged ocular surface.

211 ntegrated structurally and functionally with the damaged organ.

212 in turn results in cleavage and shedding of the damaged part of the cell membrane.

213 rization of cortical F-actin and excision of the damaged part of the plasma membrane.

214 pair of such damage and/or by elimination of the damaged parts of the cells or the damaged cell in it

215 pecific component of the material, e.g. only the damaged parts.

216 PcpC is susceptible to oxidative damage, and the damaged PcpC produces glutathionyl (GS) conjugates,

217 the periphery of the cell and then fuse with the damaged PM.

218 CRT III complex, which helps excise and shed the damaged portion of the plasma membrane during wound

219 epair involving the selective degradation of the damaged protein by FtsH protease(3).

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

221 ptosis-resistant PTCs proliferated to repair the damaged proximal tubule segment.

222 The damaged Pt electrodes are recessed and contaminated

223 hyl group protrudes axially from the ring of the damaged pyrimidine and hinders stacking of the adjac

224 Transplanted stellate cells repopulated the damaged rat liver by contributing to the oval cell r

225 es that are recruited into the glomeruli and the damaged rat mesangial cells leads to diabetic nephro

226 oactive lanthanides were likely to remain in the damaged reactor cores.

227 Pu, Nb, and Sr were likely contained within the damaged reactors during venting.

228 heir distance from the source indicated that the damaged reactors were the major contributor of pluto

229 the bulk removal of residual materials from the damaged reactors.

230 a few of newly generated cells migrated into the damaged region in aged brain after focal ischemia.

231 t revealed that the photoreceptors occupying the damaged region lost all light-driven signaling durin

232 ransplantation improves communication across the damaged region of the injured spinal cord, even in c

233 In larger lesions, the damaged region was surrounded by an area in which th

234 ic connections to adopt the function lost in the damaged region.

235 c-kit(+) cells, and increased vasculature in the damaged region.

236 s around the wound migrate collectively into the damaged region.

237 sms involved in PPC and RPC migration within the damaged retinal microenvironment.

238 g guiding migration of transplanted cells in the damaged retinal microenvironment.

239 ndings of the CSB's investigation related to the damaged school buildings and the lack of regulation

240 Using stem cells to recover the damaged sensory circuitry is a potential therapeutic

241 Duplication of proton signals near the damaged site differentiates two enantiomeric duplexe

242 e recognition mode, thus enabling it to find the damaged site efficiently.

243 cate that both polymerases stop precisely at the damaged site without nucleotide incorporation opposi

244 amma-HMHP-dA but was unable to extend beyond the damaged site, and a complete replication block was o

245 teractions, both distant and in proximity to the damaged site, for accurate and efficient uracil exci

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

247 nd not of decreased binding of the enzyme to the damaged site.

248 caffolds and cells separately or together to the damaged site.

249 lamellae under the scab to re-epithelialize the damaged site.

250 ck at the 5'-phosphate group with respect to the damaged site.

251 ls (NPCs) proliferation and migration toward the damaged site.

252 damaged DNA, while catalyzing repair only at the damaged sites.

253 , why BRCA1 and 53BP1 cannot be recruited to the damaged sites.

254 ragment sizes produced by strand breakage at the damaged sites.

255 ired for efficient repair at essentially all the damaged sites.

256 at UBR5 and BMI1 repress SPT16 enrichment at the damaged sites.

257 stem cells with innate capacities to replace the damaged skeleton in cell-based therapy, and permit f

258 barrier against ultraviolet irradiation over the damaged skin.

259 cosa cells (hOMCs) have been transplanted to the damaged spinal cord both pre-clinically and clinical

260 , semi-wet and wet) of milled rice grains on the damaged starch and particle size distribution of flo

261 The damaged starch content of barley cultivars ranged be

262 rmation of hairpins on both the template and the damaged strand of a continuous run of (CAG)(20) or (

263 The endonuclease ERCC1-XPF incises the damaged strand of DNA 5' to a lesion during nucleoti

264 DNA ligase required for filling and sealing the damaged strand.

265 ins at various locations on the template and the damaged strands that were bypassed by DNA polymerase

266 15 days after the lesion, were increased in the damaged telencephalon, mostly suddenly after the les

267 modulates its intrinsic bypass efficiency on the damaged template, but does not affect the choice of

268 imulated LexA cleavage during replication of the damaged template, but not normal replication.

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

270 ls in vivo that exit over time to repopulate the damaged tissue and participate in regeneration of a

271 Vascularization of the damaged tissue and prevention of cardiac fibrosis re

272 hat is important for homing to and resolving the damaged tissue at sites of injury.

273 lasticity, initiate organoids and regenerate the damaged tissue remain largely unknown.

274 ombination thereof are directly implanted at the damaged tissue site or within ectopic sites capable

275 substitutes that are equal to or better than the damaged tissue to be replaced.

276 ryonic program, proliferate and migrate into the damaged tissue to differentiate into fibroblasts, en

277 estoration is regeneration or replacement of the damaged tissue with a scar.

278 its limited intrinsic capacity to regenerate the damaged tissue, making it one of the leading causes

279 Within the damaged tissue, neutrophil migration behavior often

280 extracellular matrix components that replace the damaged tissue.

281 atory cells drawn by danger cues released by the damaged tissue.

282 e of the type I collagen that accumulates in the damaged tissue.

283 iverse cell populations capable of repairing the damaged tissue.

284 ential to restore appearance and function of the damaged tissues.

285 The damaged tryptophan residues cause large fluctuations

286 its additional amino and carbonyl groups on the damaged tryptophan sidechain, thus breaching the int

287 r abnormalities compromise interactions with the damaged vascular wall.

288 ina, they localized to the site of injury in the damaged vasculature and appeared to participate in r

289 ded more numerous water flow pathways around the damaged vein.

290 ented from the outer to the inner surface of the damaged vessel wall, with a greater extent of platel

291 ree main groups: optical therapies, in which the damaged visual field is brought into view by the use

292 ices; eye movement-based therapies, in which the damaged visual field is more effectively sampled wit

293 estimate the velocity of fluids issuing from the damaged well both before and after the collapsed ris

294 In the damaged zebrafish retina, Muller glia dedifferentiat

295 r glia to proliferate during regeneration of the damaged zebrafish retina.

296 ble negative zone on fluorescence images and the damaged zone (transition zone plus coagulation zone)

297 ustained recruitment of circulating cells to the damaged zone and the cardiac persistence of hematopo

298 Photoreceptors located outside of the damaged zone migrated to make new functional connect

299 High uniformity between the damaged zone on NADH-stained images and the DiI bubb

300 of the usual ordered distribution of Cxs in the damaged zones and that the reductions in Cx43 levels