ライフサイエンスコーパス: destruction

1 Dbf4-dependent Cdc7 kinase) is central to SC destruction.

2 s an autoimmune disease leading to beta-cell destruction.

3 ic or adipose contents and of sacral erosion/destruction.

4 fied by Slt2 to stimulate SCF(Grr1)-mediated destruction.

5 endent mechanism by which axons undergo self-destruction.

6 to target them for lysosomal or proteasomal destruction.

7 tudies to identify novel correlates of joint destruction.

8 tivity Score (DAS), is associated with joint destruction.

9 them at the site of inflammation and tissue destruction.

10 h severe hyperinflation and less parenchymal destruction.

11 are particularly vulnerable to alteration or destruction.

12 ase of the pancreas, leading to its fibrotic destruction.

13 ng cells, dampening of cytokines, and tissue destruction.

14 , to a greater extent than overt acinar wall destruction.

15 or release that can lead to wholesale tissue destruction.

16 s through a narrow pore for their controlled destruction.

17 ration of proteasomes en route to autophagic destruction.

18 which hypoxia augments inflammation and bone destruction.

19 propogate chronic inflammation and articular destruction.

20 he erythrocyte and may lead to its premature destruction.

21 d13 most likely primes the phosphodegron for destruction.

22 ctive T cells are key mediators of beta cell destruction.

23 contribute to stress-mediated bacterial self-destruction.

24 e hyperactive autoubiquitination and E3 self destruction.

25 ic target for treatment of inflammatory bone destruction.

26 rately measure red blood cell production and destruction.

27 branes to target intracellular pathogens for destruction.

28 ing to multiple organ pathologies and kidney destruction.

29 NAs to target complementary invasive DNA for destruction.

30 ntial metabolite NAD(+) and induces neuronal destruction.

31 conditions in Tmc mutants or after tip-link destruction.

32 ction caused by beta-cell dysfunction and/or destruction.

33 ft, thereby playing a role in the autoimmune destruction.

34 verse mangrove species suffered much greater destruction.

35 s employed to study the pattern of beta cell destruction.

36 pread, and avoid immunologic and therapeutic destruction.

37 petition, cooperation, and long-term habitat destruction.

38 eptus of an infected mother at high risk for destruction.

39 s of periodontitis with severe alveolar bone destruction.

40 ical specimens of NFPAs with or without bone destruction.

41 and is thus relevant to the prevalent tissue destruction.

42 itin ligase targeting cell-cycle factors for destruction.

43 The controlled and localized cell destruction achieved by activation of both capsule formu

44 o crRNA present in the complex and its ssDNA destruction activity was activated by target RNA.

45 orna disease virus (BDV) results in neuronal destruction and behavioral abnormalities with differenti

46 n chronic arthritis with excessive cartilage destruction and bone loss.

47 nic inflammation that associates with tissue destruction and cancer.

48 (MMPs), which have key roles in local tissue destruction and cavitation.

49 arthritis (OA) is characterized by cartilage destruction and chondrocytes have a central role in this

50 obustness of the signaling network to signal destruction and demonstrating the ability to program sys

51 e their reciprocal relationship, periodontal destruction and diabetes may be independent risk factors

52 indicate additive interaction of periodontal destruction and diabetes regarding all-cause and CVD mor

53 ts-1 deubiquitination blocks its proteasomal destruction and enhances tumorigenicity, which could be

54 velops in the skeleton causing profound bone destruction and fractures.

55 ake in the process of skyrmion nucleation or destruction and identify that the transition facilitated

56 The tissue destruction and inflammation which characterize C. diffi

57 nsil/gut was associated with histopathologic destruction and inflammation.

58 the potential to be used as weapons of mass destruction and instigate population-based fear.

59 ould be reduced significantly with less bone destruction and less hepatotoxicity compared with equimo

60 cted joints of Nfat5+/- mice increased joint destruction and macrophage infiltration, demonstrating t

61 ed by inflammatory cell infiltration, tissue destruction and neovascularization.

62 vity and to prevent subsequent alveolar bone destruction and osteoclastogenesis.

63 ection may reveal strategies to limit tissue destruction and prevent the onset of disease.

64 pathways that oversee mRNA and nascent chain destruction and recycle ribosomal subunits.

65 MD patients exhibit ongoing cycles of muscle destruction and regeneration that promote inflammation,

66 x virus (HSV) reactivation, peripheral nerve destruction and sensory anesthesia are rare.

67 evidence that ADAMTS-4 contributes to aortic destruction and sporadic AAD development.

68 a pancreatic insulitis with beta-islet cell destruction and systemic glucose intolerance.

69 Antibiotic-mediated microbiota destruction and the consequent loss of colonization resi

70 ntent and related structural changes causing destruction and/or masking of some epitopes.

71 l activation, memory differentiation, tissue destruction, and a loss of TCR diversity.

72 creases in gut permeability, colonic mucosal destruction, and colonic IL-1beta expression.

73 re were calculated for outpatient visits, AK destruction, and medications for AKs, and the total of t

74 min is critical for the subsequent myofibril destruction, and over time, myofibrillar proteins become

75 re progressive disorder leading to bile duct destruction; approximately 75% of patients have comorbid

76 plastic cells that mediate tissue repair and destruction, are prominent within dystrophic skeletal mu

77 can be regulated to mitigate the collateral destruction associated with macrophage activation.

78 grey matter, associated with variable tissue destruction, astrogliosis and secondary myelin loss.

79 -like kinase, and CDK1 promotes efficient SC destruction at the end of prophase I to ensure faithful

80 ween the formation (at mid-ocean ridges) and destruction (at subduction zones) of ocean basins influe

81 the myocardium by ultrasound targeted hs-MB destruction attenuates myocardial ischemia-reperfusion i

82 A CYCLIN1B destruction box was fused to TANGLED1-YFP to generate a

83 ect from or exacerbate crestal alveolar bone destruction but were responsible for promoting different

84 CenpH protects cyclin B1 from destruction by competing with the action of APC/C(Cdh1)

85 lycan puts bacteria at risk of detection and destruction by host peptidoglycan recognition factors an

86 rance mechanisms exist to prevent autoimmune destruction by self-reactive T cells that escape thymic

87 nclusions seem to protect against autophagic destruction by sequestering capsid proteins and coordina

88 that this reduction is mediated by increased destruction by the anaphase promoting complex/cyclosome

89 ronate (L-ALD) can sensitise cancer cells to destruction by Vgamma9Vdelta2 T cells.

90 I effector helicase and nuclease for invader destruction, Cas3.

91 Habitat destruction, characterized by habitat loss and fragmenta

92 In later stages, extensive islet destruction coincides with preferential antigen presenta

93 ad, our findings suggest that TNKS regulates destruction complex activity at the level of both Axin a

94 is maintained at very low levels that limit destruction complex activity, a property that is current

95 blocks Wnt signalling not only by increasing destruction complex activity, but also by impeding signa

96 In the cytoplasm, TIAM1 localizes to the destruction complex and promotes TAZ degradation by enha

97 ose product is an important component of the destruction complex that regulates beta-catenin levels.

98 nsible for the formation of the beta-catenin destruction complex.

99 AZ requires inactivation of the beta-catenin destruction complex.

100 the centrilobular phenotype of emphysematous destruction COPD is driven by a Th1 response activated b

101 elivery of the liposomal constructs and cell destruction correlated well with the EGFR expression pat

102 since most lncRNAs are quickly targeted for destruction during synthesis or shortly thereafter.

103 herent reactive nature renders them prone to destruction especially under stress conditions.

104 the contribution of mast cells to local bone destruction following oral infection with P. gingivalis

105 rts capable of delaying or halting beta-cell destruction has been limited.

106 osis, the underlying mechanism regulating SC destruction has remained elusive.

107 enomenon may play a role in immune cartilage destruction; however, the mechanisms of chondrocyte reco

108 ion of WNT-5A in vivo attenuated lung tissue destruction, improved lung function, and restored expres

109 aepithelial cytotoxic T cells mediate tissue destruction in celiac disease.

110 is found in broccoli, can prevent cartilage destruction in cells, in in vitro and in vivo models of

111 destroyed before the onset of emphysematous destruction in COPD.

112 iate climatic conditions, led to significant destruction in Ecuador.

113 g the cell wall biosynthesis, as well as its destruction in immune cells, to be tracked.

114 B virus causes brainstem destruction in infected humans in the absence of timely

115 the centrilobular phenotype of emphysematous destruction in lungs donated by persons with very severe

116 E-CDK2 activity while also enabling cyclin E destruction in mitosis, when inappropriate cyclin E expr

117 in fibroblasts, which may contribute to bone destruction in NFPA patients.

118 therapeutic modality for prevention of bone destruction in RA.

119 nfection may exacerbate pancreatic beta cell destruction in T1D by influencing proinflammatory M1 mac

120 rough an unknown mechanism, thereby avoiding destruction in the autophagolysosome.

121 how an amelioration of inflammation and bone destruction in the serum-induced arthritis model.

122 lants, and its emissions contribute to ozone destruction in the stratosphere.

123 It is widely expected that habitat destruction in the tropics will cause a mass extinction

124 tude of the torque in causing effective cell destruction in these experiments.

125 ogenic T cells and cause selective beta cell destruction in type 1 diabetes (T1D) has focused on pept

126 therapeutic approach to preventing beta cell destruction in type 1 diabetes.

127 s expressed by islet cells and induced their destruction in vitro; however, passive transfer of the s

128 is study was to evaluate whether periodontal destruction interacts with diabetes on all-cause and car

129 upporting the premise that evasion of immune destruction is of importance for NSCLC progression.

130 We focus on selected fibre tracts whose destruction is recognised to elicit predictable behaviou

131 Here we report that Ets-1 destruction is regulated by the deubiquitinating enzyme,

132 f the mechanisms of aggressive NFPAs in bone destruction is required in order to guide the clinical d

133 r, the mechanism of SARM1-dependent neuronal destruction is still obscure.

134 Because tissue destruction is the prominent characteristic of emphysema

135 Key to this destruction is the virally encoded alkaline exonuclease

136 er their relative contribution to the tissue destruction is unknown.

137 wever, their relative contribution to tissue destruction is unknown.

138 d NK cells with IC, would cause innate tumor destruction, leading to increased presentation of tumor

139 time, their replication implies that ongoing destruction likewise occurs.

140 vided for vaccine registration, procurement, destruction, logistics, and management across countries

141 tivity of O2 toward both these modes of self-destruction maintains its abundance in the ecosphere and

142 at the microbial biofilm, followed by tissue destruction mediated by leucocytes which clinically caus

143 proach using ultrasound-targeted microbubble destruction-mediated delivery of phosphorothioated TRAF3

144 autophagy or more traditional phagolysosomal destruction methods.SIGNIFICANCE STATEMENT Alzheimer's d

145 ime-averaged disease activity fits the joint destruction model better than one-time disease activity.

146 e inflammatory immune response drives tissue destruction, morbidity, and mortality.

147 tion while, later, its binding leads to mRNA destruction, most likely as a consequence of translation

148 tently, when Ventx2 lacked a functional PEST-destruction motif, it was stabilized, displayed symmetri

149 essed between fibroblasts isolated from bone destruction NFPAs (BD-NFPAs) and fibroblasts isolated fr

150 FPAs) and fibroblasts isolated from non-bone destruction NFPAs (NBD-NFPAs).

151 This suggests that beta-cell destruction occurs more precipitously than previously as

152 ed low-spin Fe(II)4L6 cage 3 resulted in the destruction of 1 and the release of its guest.

153 antitative detection, removal as well as the destruction of a variety of bacterial pathogens.

154 chlorination for disinfection because of the destruction of a wide variety of organic compounds.

155 ERAD) pathway, an important UPR function for destruction of aberrant proteins, mediates HA degradatio

156 molecules required for glial recognition and destruction of Abeta are still unclear.

157 (+) T cells orchestrate immune responses and destruction of allogeneic organ transplants, but how thi

158 Far from the usual destruction of antiferromagnetism via spin polarization,

159 thritis (OA) is characterised by progressive destruction of articular cartilage and chondrocyte cell

160 nic autoimmune disease that results from the destruction of beta (beta) cells in the pancreatic islet

161 in that controls a rate-limiting step in the destruction of beta-catenin, the central activator of th

162 introduce a non-invasive method for thermal destruction of biofilm on metallic implants using high-f

163 aplastic anemia results from immune-mediated destruction of bone marrow.

164 a interactions has been shown to promote the destruction of cancer cells by phagocytes, including mac

165 marker, and facilitating the immune-mediated destruction of cancer cells.

166 oteoglycans such as aggrecan, leading to the destruction of cartilage and osteoarthritis.

167 egy provides a promising opportunity for the destruction of CD44-positive populations that include ca

168 Destruction of clonogenic cells in the crypt following i

169 ase that is characterized by immune-mediated destruction of CNS myelin.

170 eucocytes which clinically cause significant destruction of connective tissue and bone.

171 The scope for loss associated with the destruction of coral reef systems is economically, biolo

172 We found that the autoimmune destruction of CXCL10-deficient islet isografts was sign

173 Autophagy coordinates lysosomal destruction of cytosolic constituents and is systemicall

174 biosensor or as a bioreactor for continuous destruction of DNAN.

175 , we have also investigated the quantitative destruction of E.

176 bition of lysosomal fusion and autolysosomal destruction of ehrlichiae.

177 omputational model to simulate a force-based destruction of elastic networks representing emphysema p

178 assemia pathology is the premature apoptotic destruction of erythroblasts causing ineffective erythro

179 nsor for the targeted detection, removal and destruction of Escherichia coli bacteria was developed o

180 , and GBP4 to cause the proteasome-dependent destruction of existing GBP coats.

181 eolytic cascades leading to the pathological destruction of extracellular matrices such as cartilage

182 roles in the formation, remodeling, and the destruction of extracellular matrix.

183 signaling pathway that governs GNA-mediated destruction of EZH2 as a promising anti-cancer strategy.

184 mbedded protein complex that coordinates the destruction of folding-defective proteins in the early s

185 ces Fe-mediated reduction of O2 to O2(-) and destruction of H2O2 to OH to 5.1 +/- 1.5 and (4.3 +/- 1.

186 Destruction of hair cells causes supporting cells to gen

187 ge has led to the killing of health workers, destruction of health facilities, and displacement of hu

188 Immune destruction of hemopoietic stem cells plays an important

189 ol of a targeted eukaryotic cell, leading to destruction of host cell membranes.

190 The programmed self-destruction of infected cells is a powerful antimicrobia

191 T1D results from selective destruction of insulin-producing beta cells leading to h

192 s characterized by Ag-specific targeting and destruction of insulin-producing beta cells.

193 1 diabetes (T1D) results from the autoimmune destruction of insulin-producing beta-cells in the pancr

194 e 1 diabetes results from chronic autoimmune destruction of insulin-producing beta-cells within pancr

195 which results in the impairment and eventual destruction of insulin-producing beta-cells.

196 diabetes (T1D) results from T cell-mediated destruction of insulin-producing beta-cells.

197 ronic autoimmune disorder resulting from the destruction of insulin-producing pancreatic beta-cells.

198 A new NMR experiment (Destruction of Interfering Satellites by Perfect Echo Lo

199 utoimmune liver disease characterized by the destruction of interlobular biliary ductules, which prog

200 ed the influence of CXCL10 on the autoimmune destruction of islet isografts using RIP-LCMV mice expre

201 The destruction of lignocellulosic feed followed by oxygen r

202 oor, and their influence on the creation and destruction of marine benthic habitats, has not been exp

203 ediates ubiquitin ligase SCF(Grr1)-dependent destruction of Med13 following oxidative stress.

204 mune disease of the skin that results in the destruction of melanocytes and the clinical appearance o

205 n depigmenting disorder, is caused by immune destruction of melanocytes by cytotoxic CD8(+) T cells.

206 olved in the opsonization, phagocytosis, and destruction of microorganisms infecting mammals, their i

207 s (AMPs), which facilitate the extracellular destruction of microorganisms that become entrapped with

208 In principle, selective destruction of mutant proinsulin offers a rational appro

209 hanical or enzymatic, leads to near complete destruction of mycelial microcolonies of a Streptomyces

210 alance of two opposing processes: persistent destruction of myelin and myelin repair by differentiati

211 of the CNS characterised by immune-mediated destruction of myelin and progressive neuroaxonal loss.

212 mulation of ubiquitinated proteins and rapid destruction of myofibrils.

213 o incomplete 3' end processing and increased destruction of nascent TERC RNA transcripts, resulting i

214 ironmental disturbance, namely anthropogenic destruction of natural habitats and wildfire frequency e

215 Production and destruction of O3 are also influenced by these changes,

216 led to both T-cell infiltration and specific destruction of orexin(+) neurons.

217 d under oxidized conditions conducive to the destruction of organics.

218 repulsion and loss of positive charge due to destruction of oxonium and pyridine, possibly caused the

219 et inflammation and contribute to autoimmune destruction of pancreatic beta cells.

220 and environmental factors, resulting in the destruction of pancreatic beta cells.

221 tes (T1D) is characterized by the autoimmune destruction of pancreatic beta cells.

222 an autoimmune disease that results from the destruction of pancreatic beta-cells by the immune syste

223 iabetes (T1D) results from a T cell-mediated destruction of pancreatic beta-cells following the infil

224 ancreas facilitate progression to autoimmune destruction of pancreatic beta-cells.

225 regarded as a mere degradative mechanism in destruction of proteins or turnover in maintaining physi

226 for metastasis and access to the lungs, and destruction of remote tissues.

227 uced/abolished Dbf4 phosphorylation hampered destruction of SC proteins.

228 0-APC/C), thereby preventing the proteolytic destruction of securin and cyclin and delaying anaphase

229 AVMs typically progress, causing destruction of surrounding tissue and, sometimes, cardia

230 Here we report that the destruction of SVs in boutons lacking Piccolo and Bassoo

231 -crRNA complex but are due to the more rapid destruction of targets with fully matching protospacers.

232 nt infrastructure networks and the effective destruction of terrorist communication networks.

233 The disease is characterized by destruction of the alveolar bone due to an aberrant host

234 ological analysis showed that remodeling and destruction of the bronchiolar and alveolar tissue is as

235 MSC-Ex recovered the destruction of the epithelial barrier in the differentia

236 that hepsin, like matriptase, induces potent destruction of the extracellular matrix whilst displayin

237 monstrate in roots that it is the programmed destruction of the mitotically compromised stem cell nic

238 s, are specific to situations that involve a destruction of the objects-to-representations correspond

239 e permeabilization facilitate the autophagic destruction of the organelle.

240 r pathogen Toxoplasma gondii by inducing the destruction of the parasitophorous vacuole (PV).

241 and the release of mediators involved in the destruction of the periodontium.

242 f mucosal explants was greatly enhanced upon destruction of the respiratory epithelium integrity with

243 s in the testis, resulting in cell death and destruction of the seminiferous tubules.

244 higher aluminum contents will result in the destruction of the Si-O bonds, leading to the formation

245 decreased thymic output and parasite-induced destruction of the thymic epithelium, as well as disrupt

246 2 or more adjacent vertebral bodies, severe destruction of the vertebral body, focal/heterogeneous c

247 Lateral chest radiograph demonstrated lytic destruction of the xiphisternum.

248 Targeted destruction of these proteins may have therapeutic impac

249 Destruction of UH(+) ions in the stripper tube of the SS

250 t enhancement of vertebral bodies, low-grade destruction of vertebral bodies, hyperintense/homogeneou

251 d mild heating profile to cause hyperthermic destruction of vessel-encasing tumors while safeguarding

252 hanical catalysts" to promote the mechanical destructions of the associated complexes, which, in conc

253 Moreover, lysosomal destruction or damage abolishes these TFEB-dependent eff

254 as photo-scattering, photo-excitation, photo-destruction, photo-physical modification, photochemical

255 he toxic consequences of nonspecific protein destruction, principles found in one system likely gener

256 Since joint destruction reflects the history of disease activities,

257 SC destruction relieved meiotic inhibition of the ubiquitou

258 lated lung pathology characterized by tissue destruction/remodeling, accumulation of foamy macrophage

259 hree-dimensional molecularly targeted US and destruction-replenishment 3D DCE US provide complementar

260 CE US with nontargeted microbubbles, and (c) destruction-replenishment DCE US with nontargeted microb

261 Repair that cannot keep pace with destruction results in progressive loss of myelin.

262 uding those of creating concurrent formation-destruction systems, continuously maintaining chemical s

263 e activity would better correlate with joint destruction than one-time disease activity.

264 ptosis and less efficient at promoting joint destruction than were NFAT5-sufficient macrophages.

265 potent protease that contributes to the lung destruction that accompanies cigarette smoking; it simul

266 ibute to the chronic inflammation and tissue destruction that characterize periodontal diseases.

267 Upon cell destruction, the dual-partner defense system is activate

268 man placental trophoblasts without host cell destruction, thereby serving as a likely permissive rese

269 o-apoptotic signaling proteins leads to cell destruction through activation of the cysteine-aspartic

270 presents a key first step in achieving tumor destruction through immunotherapy.

271 y infects the skin, causing lesions and cell destruction through its primary virulence factor, alpha

272 One mechanism of interference is signal destruction through the production of an enzyme that cle

273 the severity and distribution of parenchymal destruction throughout the lungs.

274 i associated with differential emphysematous destruction throughout the lungs.

275 pective, potentially capable of causing mass destruction to a civilian or military population by inha

276 Ultrasound targeted hs-MB destruction triggered H2S release and increased the conc

277 ion by Pseudomonas leads to progressive lung destruction ultimately requiring lung transplantation (L

278 Consequently, species' responses to habitat destruction vary as other species become extinct.

279 damts-4-/- mice showed reduced elastic fibre destruction, versican degradation, macrophage infiltrati

280 a complex balance of prion sequestration and destruction via local tissue macrophages, prion traffick

281 TTP-bound mRNAs are targeted for destruction via recruitment of the eight-subunit deadeny

282 ptase acts as a novel initiator of cartilage destruction via the induction and activation of matrix m

283 The autoimmune destruction was also diminished in mice administered wit

284 Periodontal destruction was assessed via clinical attachment level (

285 he dynamics of red blood cell production and destruction was designed to characterise primaquine-indu

286 otective effect of ultrasound targeted hs-MB destruction was investigated in a rodent model of myocar

287 The persistent protection from autoimmune destruction was paralleled by an increase in FoxP3(+) re

288 y other structures or with a small degree of destruction was seen.

289 vel-a measure of lifetime periodontal tissue destruction-was conducted in a large, community-based sa

290 matory environment resulting in local tissue destruction, we hypothesized that the controlled release

291 rincipal target for HIV-mediated CD4+ T-cell destruction, we investigated M. tuberculosis-specific re

292 udy the order of events leading to myofibril destruction, we investigated the slower atrophy induced

293 their cognate proteases to promote substrate destruction, whereas others primarily activate the targe

294 cerevisiae, oxidative stress triggers Med13 destruction, which thereafter releases cyclin C into the

295 Unlike SzV-1287, LJP-1207 induced cartilage destruction, which was confirmed in vitro.

296 d phosphorylation of Dbf4 and accelerated SC destruction, while reduced/abolished Dbf4 phosphorylatio

297 finally, in its most severe form, capillary destruction with hemorrhage.

298 orocarbon gas bubbles before and after their destruction with high intensity ultrasound.

299 The lignin structure tended to undergo more destruction with the elevated NaOH concentration.

300 ospacer, CRISPR interference-that is, target destruction without acquisition of additional spacers-is