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 agents (DDAs) constitute the backbone of treatm

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

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 results suggest that Al likely acts as a DNA-damaging agent in vivo and that Al-dependent root growth

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

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

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

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

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

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

21 nhibitors alone or in combination with a DNA-damaging agent.

22 1beta (CAS 865070-37-7), consisting of a DNA-damaging aniline mustard linked to an androgen receptor

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

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

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

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

27 n the level of PCNA ubiquitination after DNA-damaging treatments, whereas no such effect was observed

28 ible for the acquired resistance against DNA-damaging agents.

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

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

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

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

33 to structurally diverse antibiotics and DNA-damaging chemicals, we studied this gene (MSMEG_2631) in

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

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

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

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

38 diate risk patients with APL without any DNA-damaging chemotherapy.

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

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

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

42 ient tumor cells to apoptosis induced by DNA-damaging agents and suggests that disruption of cryptoch

43 Rad3-related (ATR) gene is activated by DNA-damaging agents that are frequently used as anticancer t

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

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

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

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

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

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

50 hypersensitive to genotoxicity caused by DNA-damaging agents.

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

52 the cell size checkpoint is inducible by DNA-damaging chemotherapeutic agents as well as by ionizing

53 cancer therapeutic responses produced by DNA-damaging drugs.

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

55 eficient tumors to cell death induced by DNA-damaging therapeutic agents, by targeting strategies tha

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

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

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

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

60 o its extreme resistance to conventional DNA-damaging chemotherapeutics.

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

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

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

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

65 o its role in promoting apoptosis during DNA-damaging stress, p53 can promote cell survival during me

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

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

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

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

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

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

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

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

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

77 7 (ALKBH7) gene plays a pivotal role in DNA-damaging agent-induced programmed necrosis by triggering

78 s and is required for resistance to many DNA-damaging and replication stress-inducing agents.

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

80 r drug candidates using a monofunctional DNA-damaging strategy.

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

82 Most DNA-damaging agents are weak inducers of an anticancer immun

83 ly S phase and are sensitive to multiple DNA-damaging agents, indicating impaired DNA replication and

84 display sensitivity to a broad range of DNA-damaging agents and cell wall-targeting antibiotics.

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

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

87 potentiates the efficacy of a variety of DNA-damaging agents in preclinical models.

88 repair and enhances the genotoxicity of DNA-damaging agents such as benzo[a]pyrene and ultraviolet r

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

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

91 m cells showed sensitivity to a range of DNA-damaging agents, highlighting its role in replication an

92 at is sufficient, even in the absence of DNA-damaging agents, to increase the expression of proapopto

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

94 very from adverse hematologic effects of DNA-damaging cancer therapies, and development of radioprote

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

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

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

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

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

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

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

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

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

104 fferentially to doxycycline, hypoxia, or DNA-damaging agents.

105 lls were exposed to mitomycin C or other DNA-damaging agents.

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

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

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

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

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

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

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

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

114 -null cells are not sensitive to several DNA-damaging agents that sensitize Xrcc1-deficient cells.

115 Treatment of plants with several DNA-damaging drugs further showed that RECA3 is required for

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

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

118 Since we previously showed that DNA-damaging agents (including chemotherapy and irradiation)

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

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

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

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

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

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

125 oximately 20%) following exposure to the DNA-damaging agent etoposide.

126 hen assessed for hypersensitivity to the DNA-damaging agent hydroxyurea (HU).

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

128 e activity, and affects tolerance to the DNA-damaging agent mitomycin C, argue that this prototypic e

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

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

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

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

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

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

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

136 Treatment of cells with the DNA-damaging drug doxorubicin or the p53 stabilizing agent N

137 artial activation of CAD may explain the DNA-damaging effects of diverse cellular stresses that do no

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

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

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

141 This results in sensitivity to DNA-damaging agents and chromosomal instabilities.

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

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

144 mutant conferred cellular sensitivity to DNA-damaging agents and led to defective repair of DNA doubl

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

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

147 to confer yeast cells with resistance to DNA-damaging agents and play a role in activation of DNA dam

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

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

150 this complex confers hypersensitivity to DNA-damaging agents by undefined mechanisms.

151 NBS1, mTR or hMLH1) or cells exposed to DNA-damaging agents had elevated IGF-1 expression, resulting

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

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

154 -1 and CTLA-4 and greater sensitivity to DNA-damaging agents in representative cell line models; (ii)

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

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

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

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

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

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

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

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

163 are more tolerant than the wild type to DNA-damaging agents, and show constitutive induction of gene

164 Cells lacking CHIP are hypersensitive to DNA-damaging agents, but DNA repair and cell viability are r

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

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

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

168 cells and their effect on sensitivity to DNA-damaging agents, homologous recombination and genomic in

169 lls leads to an increased sensitivity to DNA-damaging agents, in particular interstrand cross-linking

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

171 n is required for the normal response to DNA-damaging agents, the nuclear localisation of RAD51 and B

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

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

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

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

176 instability and enhanced sensitivity to DNA-damaging agents.

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

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

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

180 deubiquitinating enzyme upon exposure to DNA-damaging agents.

181 taining genomic integrity in response to DNA-damaging agents.

182 gene displayed increased sensitivity to DNA-damaging agents.

183 ir genes and enhanced cell resistance to DNA-damaging agents.

184 ar foci patterns observed in response to DNA-damaging agents.

185 formation and survival after exposure to DNA-damaging agents.

186 to resensitize PRMT7 knock-down cells to DNA-damaging agents.

187 ) that sensitizes p53-deficient cells to DNA-damaging agents.

188 tin after DNA damage or to resistance to DNA-damaging agents.

189 oes not trigger apoptosis in response to DNA-damaging agents.

190 pericentromere expands after exposure to DNA-damaging agents.

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

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

193 oliferation and confers sensitization to DNA-damaging agents.

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

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

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

197 ights into the resistance of melanoma to DNA-damaging chemotherapeutics, which is one of the major ob

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 improve the response of these tumors to DNA-damaging therapy.

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

220 sting cells at G2/M phase in response to DNA-damaging treatment.

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

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

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

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

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

226 ommon cancer in the United States, where DNA-damaging ultraviolet B (UVB) radiation from the sun rema

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

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

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

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

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

232 rn, cellular response to treatments with DNA-damaging agents such as cisplatin (cis-dichlorodiammine

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

234 hen fission yeast cells are treated with DNA-damaging agents, Chk1 is activated and phosphorylates Cd

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

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

237 nt for survival of cells challenged with DNA-damaging agents.

238 and (ii) treatment of cancer cells with DNA-damaging agents.

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

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

241 ogenic signaling pathways, combined with DNA-damaging chemotherapy, we report that time-staggered EGF

242 e of breast cancer patients treated with DNA-damaging chemotherapy.

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

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

245 ogenic following an inflammatory endothelium-damaging event.

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

247 an frameshifting indels predicted to be gene-damaging is negatively correlated with allele frequency.

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

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

250 Host-damaging and immunostimulatory oral bacteria cooperative

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

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

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

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

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

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

257 In autoimmune hepatitis (AIH), liver-damaging CD4 T cell responses are associated with defect

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

259 novel therapeutic approach to minimize lung-damaging inflammation in CF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 er regulators of transcription under protein-damaging conditions, acting in an environment where the

279 nslation to provide an accurate and not self-damaging response to host infection, and our data show t

280 w contemporary Anglophone literature on self-damaging behaviour negotiates serious conceptual difficu

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

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

283 en suggested as a cause of associated tissue-damaging inflammation.

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

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

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

287 roduction and increased production of tissue-damaging molecules in response to D/UW-3/Cx relative to

288 mature neutrophils and high levels of tissue-damaging molecules were still detectable in the upper ge

289 ially influence the impact of ongoing tissue-damaging responses to a viral infection and imply that t

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

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

292 , IFN-gamma-induced M1 cells suppress tissue-damaging inflammation during acute schistosomiasis throu

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

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

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

296 8 serves as a versatile receptor for vesicle-damaging pathogens.

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

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

299 ifically by lysozyme but not other cell wall-damaging agents.

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