ライフサイエンスコーパス: destruction

1 ecting the insulin-producing beta-cells from destruction.

2 P E3-ubiquitin ligase for ubiquitination and destruction.

3 t unfolds and degrades proteins targeted for destruction.

4 a critical role in vascular inflammation and destruction.

5 ccurate protein targeting to ensure pathogen destruction.

6 x inflammatory immune response mediates bone destruction.

7 in citrullination, ACPA production, and bone destruction.

8 e (P = .06) before and after US-triggered MB destruction.

9 , including enthesitis, dactylitis, and bone destruction.

10 tochondria via targeting to the lysosome for destruction.

11 SENSITIVE DWARF1 (GID1)-promoted proteasomal destruction.

12 een developed for targeting specific protein destruction.

13 eripheral tolerance, contribute to beta-cell destruction.

14 nd young adult behaviors of despair and self-destruction.

15 conditions, which can even accelerate tissue destruction.

16 ing clinical phenotype of periodontal tissue destruction.

17 find foreign nucleic acids and trigger their destruction.

18 ment was protected from inflammation-induced destruction.

19 rotein complex that targets beta-catenin for destruction.

20 standing and prevention of inflammatory bone destruction.

21 ells displayed morphologic deterioration and destruction.

22 c processes that enhance inflammatory tissue destruction.

23 ce 1900 based on an equivalent area of total destruction.

24 to reduced bone formation and enhanced bone destruction.

25 he enzyme transglutaminase 2 (TG2) in tissue destruction.

26 fector functions, ultimately mediating tumor destruction.

27 s subset mediates immunopathology and tissue destruction.

28 ynoviocytes, stimulating articular cartilage destruction.

29 ic because we observed no off-target protein destruction.

30 or complement and Fcgamma-receptor-dependent destruction.

31 positivity or reflect progressive beta-cell destruction.

32 to reduce efficiently paw swelling and joint destruction.

33 characterized by antibody-mediated platelet destruction.

34 kpoint that can limit immune-mediated tumour destruction.

35 esent without radiographic evidence of joint destruction.

36 1 diabetes (T1D) but do not cause beta cell destruction.

37 ies often continue to cause alarming habitat destruction.

38 despite their potential to cause significant destruction.

39 eptide Abs, along with terminal phalanx bone destruction.

40 immunity via a dual mechanism of RNA and DNA destruction.

41 rgo either TARE or TARE with US-triggered MB destruction 1-4 hours and approximately 1 and 2 weeks af

42 Cas nucleases to specify a viral target for destruction(6-9).

43 ute model of P. gingivalis-induced calvarial destruction, administration of Kava-205Me significantly

44 However, how Golgi destruction affects other cellular activities is so far

45 aluating the risk of accelerated OA or joint destruction after IACS injections are needed.

46 oxygen is the essential motor for their self-destruction, after a singlet oxygen-mediated triggering

47 Among other bioeffects, US-triggered MB destruction, also known as UTMD, has been shown to sensi

48 On the contrary, complete tissue destruction and abscesses were seen in placebo recipient

49 roduce long-term benefits in preventing bone destruction and alleviating bone cancer pain by suppress

50 ion of leukocytes in the synovium, cartilage destruction and bone erosion.

51 in uncontrolled immune responses and tissue destruction and can lead to inflammatory disorders such

52 inding that switch RecBCD from bacteriophage destruction and CRISPR spacer acquisition to constructiv

53 As protect fetal germ cells by targeted mRNA destruction and deposition of repressive epigenetic mark

54 e levels in streptozotocin-induced beta-cell destruction and high-fat diet-induced glucose intoleranc

55 ly minor changes at Pu'u 'O'o to cause major destruction and historic changes across the volcano.

56 phils are mutually shared to create collagen destruction and Hyp release into both saliva and plasma.

57 s Sjogren's syndrome can result in glandular destruction and hyposalivation.

58 uberculosis (Mtb) escape from phagolysosomal destruction and limited drug delivery into infected cell

59 irulence factor activity in vitro and tissue destruction and mortality in vivo In summary, we show th

60 is often limited by low volatile solids (VS) destruction and poor pathogen removal efficiency.

61 ons are in decline from overfishing, habitat destruction and poor water quality.

62 d CD8(+) effector T cells can trigger tissue destruction and produce tumor necrosis factor (TNF)-alph

63 ere pain, pus discharge, irreversible tissue destruction and scar development.

64 inflammatory disease characterized by joint destruction and severe morbidity.

65 d promising approach to avoid further tissue destruction and simultaneously preserve beneficial effec

66 interstitial space that leads to cystic lung destruction and spontaneous pneumothoraces.

67 ticipants who underwent both US-triggered MB destruction and TARE (P = .02).

68 m of biliatresone that lead to cholangiocyte destruction and to determine their relationship to GSH.

69 minary efficacy of combining US-triggered MB destruction and transarterial radioembolization (TARE) i

70 The combination of US-triggered microbubble destruction and transarterial radioembolization is feasi

71 in periodontal inflammation, gingival tissue destruction, and alveolar bone loss through sustained ex

72 tem cells, which caused JE degeneration, PDL destruction, and bone resorption.

73 s, including overfishing, pollution, habitat destruction, and climate change.

74 sive tumor growth, leading to extensive bone destruction, and metastasis to the lungs.

75 bout the environment, waste accumulation and destruction, and the inevitable depletion of fossil reso

76 omplex impact on osteoclastogenesis and bone destruction, and the underlying mechanisms of which, esp

77 The immunological mechanisms of cancer cell destruction are well defined(3-5), but whether immune-me

78 rocess we describe as antibody RING-mediated destruction (ARMeD).

79 itor BOT-64 reverses the inflammatory tissue destruction associated with periodontal disease.

80 IL-10R blockade led to severe, fatal tissue destruction associated with widespread changes in the in

81 Here, we report that PP1 promotes cyclin B destruction at the onset of anaphase by removing specifi

82 ted junctional epithelium, connective tissue destruction, bacterial invasion, increased neutrophil in

83 Biologically, these changes include habitat destruction, biotic homogenization, increased species in

84 CYP24A1 has a functional destruction box (D-box) motif that allows binding with t

85 clear that viruses are not merely agents of destruction but essential components of global ecosystem

86 pithelium, cementum with alveolar bone crest destruction, but animals pretreated with Losartan (G4) d

87 pain as a result of bone metastasis and bone destruction, but how PD-1 blockade affects bone cancer p

88 cterize the mechanisms underlying CD4 T-cell destruction by analyzing the chromosome end (telomere) D

89 cterize the mechanisms underlying CD4 T-cell destruction by analyzing the telomeric DNA damage respon

90 nize foreign nucleic acids, triggering their destruction by Cas nucleases(2).

91 : (a) enzyme and the product inactivation or destruction by honey compounds; (b) non-enzymatic pathwa

92 TRAF3 limits bone destruction by inhibiting RANKL-induced NF-kappaB signal

93 ivation of TLR3 may help to attenuate tissue destruction by limiting the inflammatory process and per

94 anslocated into the cytosol and targeted for destruction by the ER--associated degradation pathway (E

95 enophagy targets intracellular pathogens for destruction by the host autophagy pathway.

96 ic circuits that allow cancer cells to evade destruction by the host immune system remain poorly unde

97 in-specific camelid nanobody mediates target destruction by the ubiquitin proteasome system, a proces

98 ntation and promotes cell death prior to its destruction by the ubiquitin-proteasome system (UPS).

99 and an E3 ubiquitin ligase component for HIF destruction called von Hippel-Lindau.

100 Despite sperm destruction caused by drive, we find no evidence that SR

101 gainst infections: microbe-directed pathogen destruction characterized by type 1 immunity(1), and hos

102 4% of the initial PFAS on GAC underwent full destruction, compared to 16% of the PFAS on soil.

103 eta-catenin pathway is the Axin/APC/GSK3beta destruction complex (DC), which, under unstimulated cond

104 We discuss new insights into destruction complex activity and regulation, highlightin

105 form by phase separation to suggest that the destruction complex acts as a biomolecular condensate in

106 otherwise posttranslationally processed by a destruction complex and degraded by the proteasome.

107 Wnt signaling operates by inhibiting the destruction complex and thereby reducing destruction com

108 creened new potent targets from beta-catenin destruction complex associated with GC progression from

109 The multiprotein destruction complex binds and phosphorylates beta-cat an

110 hat Slimb/TrCP is a dynamic component of the destruction complex biomolecular condensate, while other

111 proposed that sequestration of beta-catenin destruction complex components in multivesicular bodies

112 Destruction complex components, including Ck1alpha, GSK3

113 luence AXIN1 expression and the beta-catenin destruction complex in Wnt-driven intestinal tumorigenes

114 ithelial cells displayed similar Wnt-induced destruction complex localization which appeared to be de

115 In vivo, inhibition of the beta-catenin destruction complex or expression of a degradation-resis

116 In response, the endogenous beta-catenin destruction complex reoriented toward the local Wnt cue

117 APC and Axin are core components of a destruction complex that scaffolds GSK3beta and CK1 to e

118 between APC and Axin drives the beta-catenin destruction complex to form biomolecular condensates in

119 We explore beta-cat transfer from the destruction complex to the E3 ligase, and test models su

120 Wnt signalosomes to inhibit the beta-catenin destruction complex via recruitment of Axin.

121 the plasma membrane, which then recruits the destruction complex, eventually leading to inactivation

122 nals act though Dishevelled to turn down the destruction complex, stabilizing beta-cat.

123 the destruction complex and thereby reducing destruction complex-phosphorylated beta-catenin, but hig

124 PTPRF functions upstream of the beta-catenin destruction complex.

125 ch that in response to Wnt, the beta-catenin destruction complex: (1) maintains composition and bindi

126 ression, via ultrasound-targeted microbubble destruction, decreased ETBR phosphorylation and restored

127 Multiple Myeloma (MM) induces bone destruction, decreases bone formation, and increases mar

128 verview of the situations where MOFs undergo destruction due to external stimuli such as chemical, th

129 its co-activator Cdc20, targets cyclin B for destruction during mitotic exit.

130 te to the initiation of pancreatic beta-cell destruction during the development of autoimmune diabete

131 Substrate COD destruction efficiency reached 65%, and the methane yiel

132 light, moisture, and oxygen) and biological destruction (enzymes, metabolism, and phagocytosis).

133 ation in less than 5% of crypts and no crypt destruction, erosions, ulcerations, or granulation tissu

134 lthough there are several reports of habitat destruction following cessation of conflict, there has n

135 from the extraction of forest resources, and destruction from natural events.

136 which normally commits transcripts to their destruction, has the capacity to dynamically reshape the

137 the immune system for tumor recognition and destruction, have succumbed to resistance development.

138 ite of melatonin, could not prevent follicle destruction, implying that melatonin does not confer the

139 Autoimmune deficiency and destruction in either beta-cell mass or function can cau

140 We hypothesized PS formation/destruction in fibrillation could be modeled as self-reg

141 mmunosuppression and potentially delay graft destruction in future human islet transplantation studie

142 l drivers of mucosal inflammation and tissue destruction in IBD.

143 ing animal models, that causes cholangiocyte destruction in in-vitro models.

144 the K48- and K63-linkage, resulting in Ser5 destruction in lysosomes.

145 e cytolytic complement proteins in astrocyte destruction in NMO is well established, little is known

146 ly defined by the mechanical environment and destruction in osteoarthritis is the pathophysiological

147 ) (LV.InsB) in hepatocytes arrests beta-cell destruction in prediabetic NOD mice by generating InsB9-

148 This protects the CDK1-bound fraction from destruction in prometaphase, ensuring a period of prolon

149 cated in CD8 T cell (CTL)-mediated beta-cell destruction in type 1 diabetes (T1D).

150 Melanocytes are the target of immune destruction in vitiligo and are hypothesized to be the s

151 to beta2 microglobulin-deficient target cell destruction in vivo.

152 of cancers can encode the seeds of their own destruction, in the form of T-cell recognizable immunoge

153 pre-existing osteonecrosis, and rapid joint destruction (including bone loss) may be observed in pat

154 plications of osteonecrosis, and rapid joint destruction, including bone loss.

155 ic inflammatory cells and mediators of islet destruction, including high-mobility group box-1, tissue

156 ors likely contributed to the enhanced fiber destruction, including the action of hydrolytic enzymes

157 onstrated remarkable protection against bone destruction induced by femoral inoculation of Lewis lung

158 ed inflammatory lesions largely reduced bone destruction, inhibited inflammation, and dramatically re

159 mestic wastewater rather than deal with its "destruction" into elemental dinitrogen.

160 Avoiding immune destruction is a hallmark of cancer.

161 The primary cause of cartilage destruction is considered to be the presence of elevated

162 Avoiding immune destruction is essential for tumorigenesis.

163 The legacy of 20th-century destruction is evident-more than a third of these likely

164 Myelin destruction is followed by resident glia activation and

165 ; whereas in photodynamic therapy, the tumor destruction is mainly caused by highly reactive singlet

166 e creative evolutionary radiations (creative destruction) is central to classic concepts of macroevol

167 hritis (TMJ OA) leads to permanent cartilage destruction, jaw dysfunction, and compromises the qualit

168 ntropy theory, and rates of PS formation and destruction (lambda(f)/lambda(d)) determined.

169 Autoimmune beta-cell destruction leads to type 1 diabetes, but the pathophysi

170 previously unrecognized TMPRSS2-ERG protein destruction mechanism and demonstrate that intact PTEN a

171 Furthermore, we discuss possible destruction mechanisms and their varying derived product

172 m and possesses two putative APC/C-dependent destruction motifs.

173 Thus, pathological bone destruction not only relies on increased osteoclast diff

174 ndings indicate that NE participates in lung destruction not only through direct proteolytic degradat

175 nment at unprecedented rates through habitat destruction, nutrient pollution and the application of a

176 ion and complement cascades and leads to the destruction of 25% of all transplanted islets within min

177 cated strands, followed by Hi-C and then the destruction of 5-bromodeoxyuridine-containing strands vi

178 cs and main mechanism(s) responsible for the destruction of aflatoxins in pure water and assesses the

179 MMP-12 activity in turn causes the destruction of alveolar walls leading to emphysema, maki

180 P suggests that quantum entanglement-not the destruction of antiferromagnetism-is the common driver o

181 sease resulting in irreversible, progressive destruction of articular cartilage(1).

182 gineering, imaging, and ganciclovir-mediated destruction of B7H3 CAR T cells incorporating a mutated

183 brought conflict, mass displacement, and the destruction of basic infrastructure to Northeast Nigeria

184 is an autoimmune condition that results from destruction of beta cells in the pancreas.

185 cells have been implicated in the autoimmune destruction of beta cells.

186 somal degradation of axin, reducing targeted destruction of beta-catenin and promoting beta-catenin-m

187 aditionally been characterized by a complete destruction of beta-cell mass (BCM); however, there is g

188 al of ubiquitin, as well as the delivery and destruction of both the mono- and polyubiquitinated form

189 lity platform that can be used for efficient destruction of brain tumor by a combination of photodyna

190 a major hurdle for inducing immune-mediated destruction of cancer cells.

191 s are especially appropriated to the thermal destruction of cancer in the case of photothermal therap

192 o a hyperplastic invasive tissue that causes destruction of cartilage and bone.

193 mass species extinction is the result of the destruction of component populations leading to eventual

194 Dephosphorylation requires APC/C-dependent destruction of cyclin B and was resolved into PP1-depend

195 ansition by promoting APC/C(CDC20)-dependent destruction of cyclin B in human cells.

196 phosphatase domains capable of synthesis and destruction of D-1 PP-IPs.

197 drial homeostasis by signalling the targeted destruction of damaged mitochondria, however, how disrup

198 igo is a complex disease in which autoimmune destruction of epidermal melanocytes results in patches

199 ed oxidative stress, to avoid overeating and destruction of essential cellular components.

200 iabetes results from the autoimmune-mediated destruction of functional beta-cell mass, whereas T2D re

201 mmune-mediated disorder characterized by the destruction of gastric parietal cells, leading to the lo

202 re the conflict has contributed to a massive destruction of health facilities.

203 These molecules accelerate the destruction of IgG, reducing pathogenic IgG and IgG immu

204 influence cellular processes leading to the destruction of insulin producing pancreatic beta cells.

205 s a chronic autoimmune disease that leads to destruction of insulin-producing beta cells and dependen

206 sis of Type 1 diabetes (T1D) arises from the destruction of insulin-producing beta-cells by islet-spe

207 Type 1 diabetes arises from the autoimmune destruction of insulin-producing beta-cells of the pancr

208 ated disease that culminates in the targeted destruction of insulin-producing beta-cells.

209 at is associated with effector T cell (Teff) destruction of insulin-producing pancreatic beta-islet c

210 ammatory reaction (IBMIR) causes significant destruction of islets transplanted intraportally.

211 s a chronic autoimmune disease that leads to destruction of joint tissues.

212 The selective destruction of large-scale brain networks by pathogenic

213 targeting of cancer cells would allow immune destruction of malignancies in all individuals.

214 and the E3 CTLH ligase are required for the destruction of ME31B, TRAL, and Cup.

215 Despite the apparent destruction of most tumor cells by VSV-EBOVDeltaMLD, the

216 -range chemotactic attraction, trapping, and destruction of motile pathogens.

217 synergistic drug-induced and phagolysosomal destruction of Mtb.

218 omes for synergistic lysosomal and Isoniazid destruction of Mtb.

219 Thus, Pin1 inhibitors promote SPOP-mediated destruction of Nanog, which provides the molecular insig

220 , herbaceous communities that assemble after destruction of old-growth grasslands).

221 Destruction of oligodendrocytes and myelin sheaths in co

222 chain reaction responsible for the oxidative destruction of organic molecules in biological cells, fo

223 valuate the probability of avoiding the self-destruction of our civilisation.

224 In order to allow the destruction of our institute's stocks of RPV while maint

225 While T cells play a major role in the destruction of pancreatic beta cells, molecular underpin

226 1 diabetes mellitus results from autoimmune destruction of pancreatic beta cells.

227 n CD8(+) T cells alone was able to drive the destruction of pancreatic beta-cells and the onset of di

228 diabetes (T1D) results from the progressive destruction of pancreatic beta-cells in a process mediat

229 activation, production of NO, and subsequent destruction of parasites.

230 disease is characterized by inflammation and destruction of periapical tissues, leading to severe bon

231 responsible for the continuous formation and destruction of phase singularities (PS) in cardiac fibri

232 tress, thus attenuating the mutually assured destruction of PIF3-phyB.

233 niversal framework to quantify formation and destruction of rotational events in cardiac fibrillation

234 the DNA damage-dependent ubiquitylation and destruction of Rpb1.

235 eories compete, and some lose, incentivizing destruction of seemingly opposing views.

236 response drive chronic inflammation, causing destruction of soft tissue and alveolar bone supporting

237 nylase and decapping complexes to accelerate destruction of target mRNAs.

238 alysts offers precise recognition and potent destruction of targeted RNA, hitherto not found in natur

239 ndirectly by T-cell-mediated inflammation or destruction of targets within the nociceptive pathways.

240 Destruction of the alveolar bone in the jaws can occur d

241 ted cells, NucC activation leads to complete destruction of the bacterial chromosome, causing cell de

242 ple cycles simply by addition and subsequent destruction of the cage.

243 esponse and augmented CD8(+) T cell-mediated destruction of the cancer cells in vitro and in vivo.

244 This synergy caused membrane depolarization, destruction of the cell wall, and eventually growth inhi

245 tion leads to damaged axons and irreversible destruction of the central nervous system (CNS).

246 at the chlorinated TP296 (generated from the destruction of the CFC piperazine ring) maintained 41%,

247 Destruction of the endothelial glycocalyx has been obser

248 ts into the host cytosol often without overt destruction of the infected cell.

249 diabetes mellitus is believed to result from destruction of the insulin-producing beta-cells in pancr

250 revotella in the gut, thereby preventing the destruction of the intestinal barrier.

251 monary fibrosis is a fatal disease involving destruction of the lung alveolar structure.

252 e distillation, and can lead to the physical destruction of the membrane material.

253 Antibiotic-mediated destruction of the microbiota enables Enterobacteriaceae

254 DNA to date has been limited to the targeted destruction of the mitochondrial genome by designer nucl

255 D8 activators induce the proteasome-mediated destruction of the N-terminal fragment, liberating the C

256 The knockout of this cluster causes the destruction of the outer segment of the photoreceptors,

257 acid, although a minor channel could lead to destruction of the perfluorinated backbone.

258 Treatments have evolved from destruction of the peripheral avascular retina to inhibi

259 incubation of spike with CR3022 Fab leads to destruction of the prefusion trimer.

260 mical response decreases; this is due to the destruction of the sheet integrity and lack of electrica

261 in most instances due mainly to competitive destruction of the substrates.

262 recruitment of immunity-related GTPases and destruction of the vacuole.

263 ll fusion, a process that contributes to the destruction of the virus-infected cell.

264 oduction method for isots prevents excessive destruction of their color attributes and contributes to

265 s a well-established role in immune-mediated destruction of tumors.

266 Within the primary {332} <113> type twin, "destruction" of the prior quenched-in athermal omega pha

267 reduced pancreatic beta-cell number (due to destruction or defective development) or impaired beta-c

268 er security applications requiring immediate destruction or vanishing features.

269 impacts on the environment, such as habitat destruction or wildlife fatalities.

270 lence mechanisms enabling CDI and epithelial destruction outweigh the relatively minor impact of less

271 mits the ligature-induced periodontal tissue destruction (P <0.01).

272 SAR), but decreased percentage of aggregates destruction (PAD) than CC treatment.

273 egeneration of injured axons involves a self-destruction pathway whose components and mechanism are n

274 juries and occurs via a cell autonomous self-destruction pathway whose mechanism is poorly understood

275 These results indicate that cyclin C destruction pathways are fine tuned depending on the str

276 The nature of the disease lies in the CNS destruction process disseminated in time and space.

277 tream of RSP5, where it acts to initiate the destruction process.

278 pathway as a central component in beta-cell destruction processes and as a potential target for the

279 Histological analyses of joint destruction provided evidence for a significant reductio

280 K1 to control CDK1 activity; early cyclin B1 destruction reflects the loss of an excess of non-CDK1-b

281 Bone destruction relies on interactions between bone and immu

282 e molecular mechanisms leading to myocardial destruction, remodelling and arrhythmic predisposition r

283 on proved to be less protective in cartilage destruction than [-1A]TIMP3 at late stages of OA.

284 ts through a process of extracellular matrix destruction that is strongly associated with inflammator

285 tributed to massive hepatocyte infection and destruction that results in a defect in clotting factor

286 e, or prevent, autoimmune mediated beta-cell destruction, thus preserving endogenous insulin producti

287 vide a perspective on the utilization of MOF destruction to develop advanced materials with a superio

288 ivity of MDM2 homodimer and promote its self-destruction to enable rapid p53 stabilization and resolv

289 However, MOFs are prone to destruction under external stimuli, considerably hamperi

290 We used ultrasound-targeted microbubble destruction (UTMD) to locally deliver microRNA-loaded na

291 causing overt metastasis, which causes bone destruction via activation of osteoclast-mediated osteol

292 However, the bone destruction was almost completely alleviated, suggesting

293 whereas the inflammation area and cartilage destruction was comparable to wild-type mice.

294 The severity of periodontal destruction was determined by measuring alveolar bone lo

295 Safety of US-triggered MB destruction was evaluated by physiologic monitoring, cha

296 ment, and the severe emphysema-like alveolar destruction was prevented.

297 a gradient of actin network compression and destruction, which is controlled by myosin contraction a

298 be used to target heterologous proteins for destruction with IMiDs in a time- and dose-dependent man

299 genic microRNA-21 (pre-miR-21) for enzymatic destruction with selectivity that can exceed that for pr

300 essed only by tumor cells-might enable tumor destruction without causing undue damage to vital health