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

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

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

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

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

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

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

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

13 followed by directional process extension to the damaged area.

14 minimize inflammation and limit expansion of the damaged area.

15 oaches to healable materials require heating the damaged area.

16 e viability and growth of these cells within the damaged area.

17 fish displayed minimal revascularization of the damaged area.

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

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

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

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

22 s for cellular and functional restoration in the damaged auditory epithelium and other sensory system

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

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

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

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

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

28 formational changes may also take place when the damaged base binds to its cognate repair enzyme.

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

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

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

32 which are presumed to be in the vicinity of the damaged base in the glycosylase-substrate complex.

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

34 damage is base extrusion, a process in which the damaged base lesion or, in some cases, its partner d

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

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

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

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

56 feature of bFGF signaling in the intact and the damaged brain, respectively.

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 ed by p53 upon irradiation and then protects the damaged cell from apoptosis by directly repressing p

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

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

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

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

65 DNA repair or trigger apoptosis to eliminate 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 xpectation that neural precursors can repair the damaged central nervous system of multiple sclerosis

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

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

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

80 An alternative method to repair the damaged CNS is to stimulate endogenous cells within

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

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

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

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

85 ernal tolerance for low survivability (i.e., the "damaged cohort" explanation).

86 equilenin ring system near perpendicular to the damaged cytosine, are located in the B-DNA major or

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

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

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

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

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

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

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

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

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

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

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

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

99 recombinant Rad26 increases accessibility of the damaged DNA in chromatin for interaction with repair

100 ns, the repair machinery must gain access to the damaged DNA in the context of chromatin.

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

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

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

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

107 excision repair, where they act by cleaving the damaged DNA strand on the 5'-side of the lesion.

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

109 ily play an important role in recognition of the damaged DNA substrate.

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 ion influencing the response of the cells to the damaged DNA.

119 checkpoint proteins in chromatin surrounding the damaged DNA.

120 tic flavin adenine dinucleotide cofactor and the damaged DNA.

121 DDB1, a subunit of the damaged-DNA binding protein DDB, has been shown to f

122 DDB2 is an essential subunit of the damaged-DNA recognition factor DDB, which is involve

123 The damaged DNAs diffuse in gel matrix and form observab

124 he activation of resident primitive cells in the damaged dog heart can promote a significant restorat

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

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

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

128 hydrogen bonding and stacking properties of the damaged duplexes.

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

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

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

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

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

134 The damaged epithelial cells were associated with increa

135 The damaged epithelium impairs mucus removal and facilit

136 The damaged epithelium is a source of alarmins that acti

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

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

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

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

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

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

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

144 cruitment and phosphorylation of proteins at the damaged fork.

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

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

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

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

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

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

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

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

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

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

155 g structures by intracytoplasmic contents of the damaged hair cells.

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

157 active and innovative solution for repairing the damaged heart.

158 , with deficient leukocyte infiltration into the damaged heart.

159 ystems biology as therapeutic strategies for the damaged heart.

160 g conserved molecular programs to regenerate the damaged heart.

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

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

163 on that favors enhanced effector function in the damaged, "high-antigen load" environment of the pneu

164 Furthermore, the damaged-induced Rad9 phosphorylation is significantl

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

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

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

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

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

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

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

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

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

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

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

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

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

178 se of the entire articular surface to repair the damaged matrix, which is not restricted to the lesio

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

180 uld appear to represent an attempt to repair the damaged matrix.

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

182 endosomes, donate their membranes to reseal the damaged membrane.

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

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

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

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

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

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

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

190 rate, and eventually differentiate to repair the damaged muscle.

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

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

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

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

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

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

197 g high concentrations of therapeutics within the damaged myocardium.

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

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

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

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

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

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

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

205 The damaged nucleobases are found to be more acidic than

206 t is recognized by the DNA glycosylase MutY, the damaged nucleoside underwent spontaneous and reprodu

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

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

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

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

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

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

213 Incorporation of the damaged nucleotides in nucleic acids is detrimental

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

215 ntegrated structurally and functionally with the damaged organ.

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

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

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

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

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

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

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

223 s a pivotal role in determining the fates of the damaged proteins.

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

225 The damaged Pt electrodes are recessed and contaminated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 mplexes by recruiting proteins like BRCA1 to the damaged site.

250 rom one helix), fullerenes can stably occupy the damaged site.

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

252 The sequences of the damaged sites indicated that the damage arose as a r

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

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

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

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

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

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

259 barrier against ultraviolet irradiation over the damaged skin.

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 The damaged strand probes consisted of dNTP analogs link

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

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

267 hat dATP and dTTP are better incorporated in the damaged system than in their respective mismatched b

268 15 days after the lesion, were increased in the damaged telencephalon, mostly suddenly after the les

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

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

271 cs in the intact brain, and its release from the damaged tissue and surrounding astrocytes mediates a

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

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

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

275 air, inflammatory cells must infiltrate into the damaged tissue to orchestrate wound closure.

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

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

278 extracellular matrix components that replace the damaged tissue.

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

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

281 important in setting up secondary events in the damaged tissue.

282 iverse cell populations capable of repairing the damaged tissue.

283 The damaged tryptophan residues cause large fluctuations

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

285 r abnormalities compromise interactions with the damaged vascular wall.

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

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

288 s and/or synthetic extracellular matrices to the damaged ventricle to restore function.

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

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

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

292 ered diffusivity and decreased anisotropy in the damaged white matter.

293 In the damaged zebrafish retina, Muller glia dedifferentiat

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

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

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

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

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

299 esponse was observed in ORN clusters outside the damaged zone, including mature clusters in the contr

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