ライフサイエンスコーパス: -damaging

1 interstrand cross-linking inducers, and base-damaging agents.

2 inhibit Abeta aggregation and detoxify cell-damaging conformers.

3 se pathogen-secreted proteins that form cell-damaging channels in the membranes of host cells.

4 al functions, it transports potentially cell-damaging compounds out of the cell using the energy from

5 Besides their cell-damaging effects in the setting of oxidative stress, rea

6 as cellular signaling and responses to cell-damaging events.

7 Instead, a broad outlook on neural-circuit-damaging processes may yield insights into new therapeut

8 flavivirus that is associated with fetal CNS-damaging malformations during pregnancy in humans.

9 ectly responsible for the suppression of CNS-damaging autoreactive T cells.

10 DNA-damaging anticancer drugs remain a part of metastatic me

11 DNA-damaging chemotherapeutics are widely used in cancer tre

12 red cancer regimens combine a MTA with a DNA-damaging agent (DDA).

13 The addition of a DNA-damaging agent further upregulated p53 protein levels, w

14 by the sni1 mutation or treatment with a DNA-damaging agent markedly enhances SA-mediated defense gen

15 A DNA-damaging agent that induces DNA double-stranded breaks (

16 s formed in well-done cooked meats, as a DNA-damaging agent that may contribute to the etiology of pr

17 he cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes.

18 Upon addition of a DNA-damaging agent, MMSET-high cells repaired DNA damage at

19 8) that were untreated or treated with a DNA-damaging agent.

20 very to benefit cancer therapies using a DNA-damaging agent.

21 s in a clonal population to cisplatin, a DNA-damaging chemotherapeutic agent.

22 redominantly induced by treatment with a DNA-damaging drug in bladder cancer cell lines, and APOBEC3A

23 w that exposure to temozolomide (TMZ), a DNA-damaging drug used to treat glioblastoma (GBM), can supp

24 Following exposure to a DNA-damaging stimulus, the inactive pool of miR-34 is rapidl

25 Specifically, adding a DNA-damaging toxin (DNase colicin) from another strain induc

26 f pulmonary arterial vascular cells in a DNA-damaging, hostile microenvironment.

27 B4 as a marker of tumor cell death after DNA-damaging cytotoxic treatment that could be harnessed as

28 s genetically deficient in MDR1A against DNA-damaging drug-induced apoptosis.

29 at the conjugation of antiangiogenic and DNA-damaging agents can generate potential hybrid agents for

30 AZD1775 and DNA-damaging agents have displayed favorable activity in sev

31 ractions between kinase deficiencies and DNA-damaging agents that are used as chemotherapeutics.

32 istone deacetylase (HDAC) inhibitors and DNA-damaging agents were identified as novel Golgi disruptor

33 persensitivity to replication stress and DNA-damaging agents when combined with mutations in histone

34 east cancer cells to PARP inhibitors and DNA-damaging chemotherapeutics by reducing expression of the

35 treatment of cancer by radiotherapy and DNA-damaging chemotherapy is based on this principle, yet it

36 it the effectiveness of radiotherapy and DNA-damaging chemotherapy, commonly used treatment modalitie

37 ariety of DNA replication inhibitors and DNA-damaging drugs.

38 from inflammation, oxidative stress, and DNA-damaging electrophiles, requires exploration, particular

39 ptosis by expression of IAP-antagonists, DNA-damaging agents and even knockdown of the IAP diap1.

40 ) in combination with the antineoplastic DNA-damaging agents doxorubicin, cisplatin, olaparib, and ga

41 ein foci occurring in the absence of any DNA-damaging treatment.

42 and found that the most potent drugs are DNA-damaging agents.

43 e both stiffness and X-ray radiation are DNA-damaging stressors, the additive effect of these stresso

44 ngly, of several agents commonly used as DNA-damaging therapeutics, only cell death caused by cisplat

45 gly, synergism has been observed between DNA-damaging drugs and targeted inhibitors of DNA repair.

46 t also recognizes DNA adducts induced by DNA-damaging agents, and triggers cell-cycle arrest and apop

47 hypersensitive to genotoxicity caused by DNA-damaging agents.

48 -dependent manner, which is activated by DNA-damaging agents.

49 is under LexA control, being induced by DNA-damaging agents.

50 t mice (SKO) are prone to CAC induced by DNA-damaging agents.

51 ancers, confers resistance to killing by DNA-damaging agents.

52 oteins and resistance to cell killing by DNA-damaging agents.

53 redict cellular resistance to killing by DNA-damaging agents.

54 creased after genotoxic stress caused by DNA-damaging drugs.

55 cancer therapeutic responses produced by DNA-damaging drugs.

56 nsitizes transformed cells to killing by DNA-damaging drugs.

57 from cells renders resistance to certain DNA-damaging agents.

58 e to treatment with the chemotherapeutic DNA-damaging agent temozolomide.

59 However, combined Nutlin3a and chronic DNA-damaging agent treatment is insufficient to promote sene

60 nes, providing a rationale for combining DNA-damaging agents or targeted DDR inhibitors with hormonal

61 Combining DNA-damaging drugs with DNA checkpoint inhibitors is an emer

62 In this context, combining conventional DNA-damaging chemotherapy with siRNA-based therapeutics repr

63 asured using the SOS-Chromotest (detects DNA-damaging agents).

64 To study the direct DNA-damaging effect of HDM on human bronchial epithelial cel

65 cellular responses to chronic, low-dose DNA-damaging agent treatment by maintaining MEFs in low oxyg

66 became effective when paired with either DNA-damaging therapy or with nutlin, an inhibitor of p53-Mdm

67 mon type of environmental and endogenous DNA-damaging agents.

68 o block DNA repair and therefore enhance DNA-damaging agents.

69 is exposed to a variety of environmental DNA-damaging chemicals, principal among which are polyaromat

70 ic stability in the absence of exogenous DNA-damaging agents is unclear.

71 optosis in response to certain exogenous DNA-damaging agents.

72 optosis to both endogenous and exogenous DNA-damaging agents.

73 tially improves cell viability following DNA-damaging treatments that stimulate PAR synthesis during

74 odels to assess bone marrow toxicity for DNA-damaging agents and inhibitors of the DNA damage respons

75 se inhibitors as potential adjuvants for DNA-damaging cancer chemotherapeutics.

76 A replication stress than by the general DNA-damaging agent methyl methanesulfonate.

77 te their potential as radical-generating DNA-damaging agents.

78 omen undergoing commonly used genotoxic (DNA-damaging) chemotherapy experience an accelerated loss of

79 d tolerable when combined with localized DNA-damaging therapies and thus has promising clinical poten

80 osed mice and in mice exposed to a model DNA-damaging chemical, 1,3-butadiene.

81 the current interest in monofunctional, DNA-damaging metallodrugs, these results are of likely relev

82 tors also prevent recovery from multiple DNA-damaging agents, suggesting broad applicability for thei

83 tumors to the effects of taxanes but not DNA-damaging agents.

84 tumors utilizing a regimen consisting of DNA-damaging agents and mutp53 acetylators, which is current

85 e show that infection in the presence of DNA-damaging agents enhances infection and triple-negative b

86 may be exploited to optimize the use of DNA-damaging agents in patients with high-risk MM.

87 HuR's role in the efficacy of DNA-damaging agents in PDA cells was, in part, attributed to

88 scherichia coli grows in the presence of DNA-damaging agents such as methyl methanesulphonate (MMS),

89 o provide resistance to a broad range of DNA-damaging agents while also contributing to mismatch repa

90 sogenic cell lines to a diverse panel of DNA-damaging agents, enriched for chemotherapeutics.

91 HPOB enhances the effectiveness of DNA-damaging anticancer drugs in transformed cells but not n

92 systemic resistance to a broad range of DNA-damaging chemotherapeutics.

93 ns identified here imply rational use of DNA-damaging chemotherapy in some patients with BL and targe

94 ity of lower concentrations (IC20-50) of DNA-damaging drugs (doxorubicin, dacarbazine, temozolamide)

95 activate p53 and enhance the efficacy of DNA-damaging drugs.

96 ng proliferation despite the presence of DNA-damaging insults, eventually leading to PAH.

97 Millions of DNA-damaging lesions occur every day in each cell of our bod

98 Cancer cells can resist the effects of DNA-damaging therapeutic agents via utilization of DNA repai

99 ChK1 might enhance the effectiveness of DNA-damaging therapies in the treatment of cancer.

100 nsitize PDAC and improve the efficacy of DNA-damaging treatment.

101 ly, the utility tracked independently of DNA-damaging treatments and instead with different tumor met

102 merase inhibitors and a variety of other DNA-damaging agents.

103 itor camptothecin and a variety of other DNA-damaging anticancer agents.

104 Cisplatin and other DNA-damaging chemotherapeutics are widely used to treat a br

105 d sensitizes cells to UV light and other DNA-damaging drugs.

106 t G4 stabilization synergizes with other DNA-damaging therapies, including ionizing radiation, in the

107 evels and by exposing cells to oxidative DNA-damaging agents.

108 luminescence the presence of potentially DNA-damaging sample components separated on the plate.

109 olites (MTZ or oxygen) before they reach DNA-damaging levels.

110 Acetaldehyde is a highly reactive, DNA-damaging metabolite that is produced upon alcohol consum

111 ns may be a useful strategy for rescuing DNA-damaging chemotherapeutics in TP53-mutant cancers.

112 t experimental evidence for colibactin's DNA-damaging activity.

113 dition, we have counter-screened several DNA-damaging agents and demonstrate that the Topo2a-dependen

114 B. subtilis sensitized cells to several DNA-damaging agents that can block or impair replication for

115 er, it is still unclear how CSCs survive DNA-damaging agent treatment.

116 ndency on the p38/MK2 pathway to survive DNA-damaging chemotherapy.

117 olaparib PARP inhibitor and temozolomide DNA-damaging agent as an effective therapy for rhabdomyosarc

118 ion at two asparaginyl residues and that DNA-damaging antineoplastic agents as well as other stimuli

119 Here, we demonstrate that DNA-damaging modalities used during cancer therapy lead to t

120 h Ptpn11 GOF mutations and cautions that DNA-damaging treatments in Noonan syndrome patients with ger

121 use cortical neurons, treatment with the DNA-damaging agent camptothecin (CPT) resulted in elongated

122 own exacerbated apoptosis induced by the DNA-damaging agent camptothecin.

123 e used to investigate the effects of the DNA-damaging agent cumene-hydroperoxide (cum-OOH) and a chem

124 toward the induction of apoptosis by the DNA-damaging agent etoposide.

125 is not necessary for the response to the DNA-damaging agent methyl methanesulfonate.

126 -rich nucleoli in cells treated with the DNA-damaging agents cisplatin and etoposide.

127 r genes are regulated in response to the DNA-damaging agents methyl methanesulfonate (MMS) and hydrox

128 ced their viability upon exposure to the DNA-damaging agents mitomycin C and Irofulven, but not etopo

129 strate that following treatment with the DNA-damaging agents, etoposide or camptothecin, BRCA1 is req

130 nhibition compared to treatment with the DNA-damaging anti-cancer agent TMZ.

131 cies under aerobic conditions and of the DNA-damaging byproducts of nitrate respiration under anaerob

132 le checkpoint kinase inhibitors with the DNA-damaging chemotherapeutic agent gemcitabine offers clini

133 The relevance of this finding to the DNA-damaging properties of phenanthriplatin and its biologic

134 Laboratories, Abbott Park, IL), and the DNA-damaging topoisomerase I inhibitor camptothecin-11 (CPT-

135 chondria and nucleus in response to this DNA-damaging agent.

136 ked to the resistance of cancer cells to DNA-damaging agents (DDAs).

137 ficantly reduces cellular sensitivity to DNA-damaging agents and decreases cellular DNA mismatch repa

138 sed to sensitize hypoxic cancer cells to DNA-damaging agents and inhibitors of DNA repair.

139 CCR5 reexpression augments resistance to DNA-damaging agents and is sufficient to induce cancer metas

140 eostat that determines susceptibility to DNA-damaging agents and other death stimuli.

141 genes and subsequent hypersensitivity to DNA-damaging agents and PARP1/2 inhibitors.

142 id of Set2/H3K36me are hypersensitive to DNA-damaging agents and site-specific DSBs, fail to properly

143 stablished predicted hypersensitivity to DNA-damaging agents and were associated with mutations in cr

144 ent tumors in order to sensitize them to DNA-damaging agents by eliminating Chk1-mediated checkpoint

145 est that BRN2 may impact the response to DNA-damaging agents in BRN2-expressing cancers.

146 e phenotypic effects with sensitivity to DNA-damaging agents in fission yeast and reduced viability i

147 The causes of sensitivity to DNA-damaging agents in nondividing cell populations, such as

148 -1 and CTLA-4 and greater sensitivity to DNA-damaging agents in representative cell line models; (ii)

149 mESCs are fully viable and resistant to DNA-damaging agents in those conditions.

150 sensitized p53-deficient cancer cells to DNA-damaging agents in vitro and in vivo.

151 nd show that REV3-mediated resistance to DNA-damaging agents is independent of the replication damage

152 BRCA-associated cancers are sensitive to DNA-damaging agents such as cisplatin.

153 ion (HR) DNA repair and are sensitive to DNA-damaging agents such as platinum and PARP inhibitors.

154 ins unchanged after cells are exposed to DNA-damaging agents such as UV light (generating UV photopro

155 homologous end joining, and tolerance to DNA-damaging agents when other resection enzymes are absent.

156 esponse and to sensitize cancer cells to DNA-damaging agents without affecting other functions of RPA

157 mes, DNA repair capacity, sensitivity to DNA-damaging agents, and iron homeostasis.

158 ects genomic instability, sensitivity to DNA-damaging agents, and migration of tumor cells by recipro

159 ent cells, do not exhibit sensitivity to DNA-damaging agents, but do display shortened (but stably ma

160 s resistance to apoptosis in response to DNA-damaging agents, causing BRCA1 wild-type tumours to be s

161 SETD2 mutations led to resistance to DNA-damaging agents, cytarabine, 6-thioguanine, doxorubicin,

162 and rendered parasites more sensitive to DNA-damaging agents, including ART.

163 n and consequently are hypersensitive to DNA-damaging agents, including cisplatin and poly(ADP-ribose

164 Upon exposure of human cells to DNA-damaging agents, NUCKS1 controls the resolution of RAD54

165 uses either sensitivity or resistance to DNA-damaging agents.

166 genome and showed higher sensitivity to DNA-damaging agents.

167 pericentromere expands after exposure to DNA-damaging agents.

168 flies or their survival upon exposure to DNA-damaging agents.

169 oliferation and confers sensitization to DNA-damaging agents.

170 growth advantage, following exposure to DNA-damaging agents.

171 cells display heightened sensitivity to DNA-damaging agents.

172 resistance of BRCA1 wild-type tumours to DNA-damaging agents.

173 d the deletion strain for sensitivity to DNA-damaging agents.

174 stream function of WEE1 upon exposure to DNA-damaging agents.

175 instability and enhanced sensitivity to DNA-damaging agents.

176 ng normal replication and in response to DNA-damaging agents.

177 e DSBs, and increased the sensitivity to DNA-damaging agents.

178 mic instability and drives resistance to DNA-damaging agents.

179 tion of mTOR results in sensitization to DNA-damaging agents; however, the molecular mechanism is not

180 nd amino acids, which rapidly convert to DNA-damaging carcinogens.

181 ppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents.

182 rabilities and resistances of kinases to DNA-damaging chemotherapeutics have not been possible, parti

183 w) splenocytes mediate the resistance to DNA-damaging chemotherapeutics induced by two platinum-induc

184 nt of the sensitivity of cancer cells to DNA-damaging chemotherapeutics, which may induce certain rep

185 tors to alter the biological response to DNA-damaging chemotherapy and enhance the efficacy of chemot

186 Resistance to DNA-damaging chemotherapy is a barrier to effective treatmen

187 le to sensitize p53-deficient cancers to DNA-damaging chemotherapy is through the use of ATP-competit

188 teration as a mechanism of resistance to DNA-damaging chemotherapy, consistent with a local loss of D

189 eukemia, a disease caused by exposure to DNA-damaging chemotherapy.

190 MCF-7 cells, and causes sensitization to DNA-damaging drug etoposide and DNA repair inhibitor olapari

191 1is) sensitize most cancer cell lines to DNA-damaging drugs and also elicit single-agent cytotoxicity

192 Resistance to DNA-damaging drugs such as temozolomide has been related to

193 cer cell lines results in sensitivity to DNA-damaging drugs, which is further exacerbated by poly-ADP

194 ng of AXL may sensitize these cancers to DNA-damaging drugs.

195 sealing activity and were sensitized to DNA-damaging drugs.

196 lective of exposure of the human body to DNA-damaging molecules and their metabolic pathways.

197 quick measurement of cell sensitivity to DNA-damaging reagents and for lentivirus-based complementati

198 ibroblasts (MEFs) were more sensitive to DNA-damaging reagents, such as methyl methanesulfonate (MMS)

199 levels normally increased in response to DNA-damaging reagents.

200 enomic instability and were sensitive to DNA-damaging reagents.

201 when it was induced by p53 subjecting to DNA-damaging stimuli such as treatment with doxorubicin, was

202 hat mutant SPOP may increase response to DNA-damaging therapeutics.

203 t to induce tumour-cell sensitization to DNA-damaging therapies and thus inhibit tumour growth in mic

204 ng chemosensitization of tumour cells to DNA-damaging therapies in vitro and in vivo.

205 ulloblastomas are typically sensitive to DNA-damaging therapies, because they retain apoptosis compet

206 e the basis for a tumor's sensitivity to DNA-damaging therapies.

207 mutations in relapsed CLL, refractory to DNA-damaging therapy, suggests that accurate detection of su

208 combination of inflammation, exposure to DNA-damaging toxins, and failed DNA repair promote the accum

209 d to increased genomic instability under DNA-damaging conditions.

210 omotes the survival of these cells under DNA-damaging conditions.

211 division is critical for viability under DNA-damaging conditions.

212 an be exploited for cancer therapy using DNA-damaging agents.

213 s (FCIC) lysogeny proxy determined using DNA-damaging mitomycin C inductions.

214 f cancer could be exploited by utilizing DNA-damaging molecules.

215 > Zn(II)], which is mirrored in in vitro DNA-damaging outcomes.

216 cumulates significant vehicle from which DNA-damaging Pt payload gradually releases to neighbouring t

217 ve WEE1 inhibitor MK-1775 synergize with DNA-damaging agent to inhibit cancer cell growth.

218 at AZD1775 alone and in combination with DNA-damaging agents (e.g., cisplatin and radiation) decrease

219 PARGi synergized with DNA-damaging agents (i.e., oxaliplatin and 5-fluorouracil),

220 rapeutically exploited by treatment with DNA-damaging agents and PARP inhibitors.

221 d cell survival following treatment with DNA-damaging agents and, as such, may play roles in modulati

222 ation of allosteric PARP inhibitors with DNA-damaging agents in genomically unstable cancer cells (re

223 a clinical application for AZD1775 with DNA-damaging agents in KRAS/LKB1 NSCLC.

224 urn, cellular response to treatment with DNA-damaging agents such as cisplatin, ionizing radiation (I

225 of ARPE-19 diploid epithelial cells with DNA-damaging agents, etoposide or zeocin, induces HSATII RNA

226 preclinical activity in combination with DNA-damaging agents, including radiotherapy and topoisomeras

227 f patients with NPC who are treated with DNA-damaging agents.

228 NA, which is altered upon treatment with DNA-damaging agents.

229 treatment alone and in combination with DNA-damaging and antimitotic agents on human cancer cells.

230 ocarcinoma (PDA) cells by treatment with DNA-damaging anticancer agents (mitomycin C, oxaliplatin, ci

231 NA damage repair, promoting synergy with DNA-damaging chemotherapy and PARP inhibitors.

232 M loss) as monotherapy and combined with DNA-damaging drugs such as carboplatin.

233 d infection and following treatment with DNA-damaging drugs.

234 ever, are not expected to cooperate with DNA-damaging or antimitotic chemotherapies as the former pre

235 poor prognosis of patients treated with DNA-damaging therapies.

236 blastomas as such or in combination with DNA-damaging therapies.

237 n protects against double-strand DNA (dsDNA)-damaging events, and show that this protective function

238 co-culture system visualized the epithelial-damaging effect of PSC-derived K. pneumoniae that was as

239 indicates cheetah fixation of five function-damaging amino acid variants distinct from AKAP4 homolog

240 lt in significant cross-resistance to genome-damaging disinfectants.

241 s to reduce ambient concentrations of health-damaging pollutants such as ozone and fine particulate m

242 come Americans exposed to potentially health-damaging concentrations of HAP.

243 everal risk factors that promote this health-damaging phenotype, including infections, physical inact

244 Host-damaging and immunostimulatory oral bacteria cooperative

245 MRSA possesses an arsenal of secreted host-damaging virulence factors that mediate pathogenicity an

246 ontitis development, depending on their host-damaging and immunostimulatory activities.

247 rine functional tests for patients with IRF6-damaging mutations.

248 and do not allow any conclusion about kidney-damaging effects of long-term, high-protein intake.

249 in, sustains continuous activation of kidney-damaging macrophages by DM components, thus creating chr

250 colitis and, less commonly, a serious kidney-damaging sequela called the hemolytic uremic syndrome (H

251 formation of structurally different and less-damaging aSyn aggregates.

252 tinal bleeding, vitamin deficiency, or liver-damaging diseases, such as infection and alcohol intoxic

253 re relevant in MS than in other white matter-damaging diseases.

254 y red blood cell membranes, absorbs membrane-damaging toxins and diverts them away from their cellula

255 in pathways that protect cells from membrane-damaging agents.

256 l, was combined with comparably low membrane-damaging effects toward keratinocytes, as established by

257 ontributes to autophagic control of membrane-damaging microbe Mycobacterium tuberculosis.

258 holerae cytolysin (VCC) is a potent membrane-damaging cytolytic toxin that belongs to the family of b

259 V and limits plasmid transfer under membrane-damaging conditions.

260 id transporter, was associated with missense-damaging DNVs.

261 To test the hypothesis that mtDNA-damaging agents induce mtDNA mutations, we exposed Muta(

262 to and at 3, 24, and 72 h following a muscle-damaging exercise in young and old individuals.

263 ed microtrauma. kg(-1) . d(-1)) after muscle-damaging exercise (300 eccentric contractions).

264 role in inflammation by enhancing neutrophil-damaging activities while supporting the activation and

265 tiation of agonistic behaviour (display, non-damaging aggression, biting and mutual fighting) is infl

266 of ~0.78 mN, rendering itself ideal for non-damaging manipulation of soft, fragile micro-objects.

267 eezing tolerant during exposure to mild, non-damaging sub-zero temperatures after cold acclimation.

268 he technique opens up the possibility of non-damaging compositional analyses of organic functional gr

269 ement of nsEP cytotoxicity by subsequent non-damaging chilling may find applications in tumor ablatio

270 modality offers a promising approach to non-damaging control of bleeding during surgery, and to effi

271 er in response to exposure to sub-toxic, non-damaging, signalling molecules or events, or the removal

272 w growth and developmental defects under non-damaging conditions.

273 and chronic, triggers immune-protective or -damaging responses, including increases in systemic GC l

274 eptor (FcRn) or CAMK4 prevented the podocyte-damaging effects of IgG from patients with TG.

275 Interestingly, rare, predicted-damaging LRP2 variants were enriched in a HLHS cohort; h

276 Rare, predicted-damaging MYH6 variants were identified in 10% of proband

277 rozygous de novo and rare-inherited presumed-damaging variants were characterized in ASD risk genes/l

278 e presence of host stresses, such as protein-damaging oxidants.

279 spring trios identified an excess of protein-damaging de novo mutations, especially in genes highly e

280 that gene-disruptive and putatively protein-damaging URVs (but not synonymous URVs) were more abunda

281 and trunk, and identified a single, protein-damaging p.Gly45Glu GJB2 mutation present in tissue samp

282 patterns of ancestral admixture and putative-damaging and novel variation, both within and between po

283 synthesis takes place even when the telomere-damaging conditions persist, in which case the accessory

284 zed when cells are removed from the telomere-damaging environment.

285 lea to brainstem that is activated by tissue-damaging noise and does not require glutamate release fr

286 rial burden and are unable to control tissue-damaging, pulmonary neutrophilic inflammation.

287 er, as well as to prevent deleterious tissue-damaging bystander effects.

288 cance of acute pain (to withdraw from tissue-damaging or potentially tissue-damaging external stimuli

289 e (Phox) may contribute by generating tissue-damaging reactive oxygen species.

290 ARS-CoV-2-triggered hyperinflammatory tissue-damaging and immunothrombotic responses are thought to b

291 w from tissue-damaging or potentially tissue-damaging external stimuli, and to enhance the salience o

292 urons to detect and avoid potentially tissue-damaging stimuli in the environment.

293 nimals to sense and avoid potentially tissue-damaging stimuli, is critical for survival.

294 d eicosanoids, which we correlated to tissue-damaging immune responses.

295 ripheral nerve injury attributable to tissue-damaging inflammatory responses.

296 red for the treatment of uncontrolled tissue-damaging and thrombotic responses in COVID-19.

297 ting in the extracellular space under tissue-damaging or pathological conditions.

298 so showed increased sensitivity to cell wall-damaging agents and to osmotic stresses.

299 to osmotic and oxidative stresses, cell wall-damaging agents, and to rapamycin, while showing increas

300 ion of Ser(780) is up-regulated by cell wall-damaging drugs.