ライフサイエンスコーパス: killing by

1 strains that bind C4BP require properdin for killing by 2C7, whereas strains that do not bind C4BP ar

2 mplement, eosinophils greatly increased cell killing by a complement-dependent cell-mediated cytotoxi

3 een channel inhibition and in vitro parasite killing by a family of compounds provided chemical valid

4 killing by apolactoferrin but did not block killing by a lactoferrin-derived peptide.

5 y (P<0.05) decreased intracellular bacterial killing by a mouse alveolar macrophage cell line and pri

6 G mutants, in turn, correlated with enhanced killing by a range of CAPs of diverse structure and orig

7 making them susceptible to phagocytosis and killing by a secondary phagocyte.

8 of the CPPC, dramatize the virtue of bimodal killing by a single therapeutic agent, and suggest a the

9 ntly increased capacity to mediate bacterial killing by abundant production of reactive oxygen specie

10 ome of these strains avoid contact-dependent killing by accumulating immunity genes to effectors that

11 d with the ability of the strains to survive killing by acid and oxidative agents.

12 s, those lacking OprD were more resistant to killing by acidic pH or normal human serum and had incre

13 or the DR5 agonistic antibody AMG655 or cell killing by activated T cells.

14 onal Mycobacterium bovis BCG mutant enhanced killing by ADEP unlike in other bacteria.

15 but similar to PBNs, the enhanced bacterial killing by AINs accompanied both better granule maturati

16 amma release, proliferation, and target cell killing by alphabeta CD8(+) T cells, but not CD4(+) T ce

17 dis possesses a remarkable ability to resist killing by alveolar macrophages.

18 B, C, W, and Y capsules limited CP-mediated killing by anti-fHbp, the unencapsulated group A mutant

19 of Hia, which facilitated their escape from killing by anti-Hia antisera.

20 with CF and measured their susceptibility to killing by antibiotics and host defenses.

21 Dormant persister cells that are tolerant to killing by antibiotics are responsible for this apparent

22 ow a small fraction of microbes that resists killing by antibiotics can emerge in a population of gen

23 ants of bacterial cells that are tolerant to killing by antibiotics(1).

24 , most importantly, is highly susceptible to killing by antibiotics, showing that endogenous oxidativ

25 ted targets also increased susceptibility to killing by antibiotics.

26 g aspects of human latency and resistance to killing by antibiotics.

27 on a plasmid were all susceptible to opsonic killing by antibodies to PNAG.

28 ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection b

29 n, DNA binding by BrlR, and recalcitrance to killing by antimicrobial agents of DeltasagS biofilm cel

30 taining 2-O-sulfate motifs inhibit S. aureus killing by antimicrobial factors secreted by degranulate

31 Haemophilus ducreyi resists killing by antimicrobial peptides encountered during hum

32 acterial replication and decreased bacterial killing by antimicrobial peptides.

33 echanisms to alter their surfaces and resist killing by antimicrobial peptides.

34 nd as one mechanism for H. ducreyi to resist killing by antimicrobial peptides.

35 ation by T-cell responses and to avoid rapid killing by antimycobacterial drugs.

36 lactoferrin and were relatively resistant to killing by apolactoferrin (P < 0.001).

37 erine protease inhibitors were able to block killing by apolactoferrin but did not block killing by a

38 Animals lacking DKF-2 were hypersensitive to killing by bacteria that are pathogens of C. elegans and

39 MIC but not the recalcitrance of biofilms to killing by bactericidal agents.

40 ored biofilm resistance and recalcitrance to killing by bactericidal antibiotics to wild-type levels.

41 eliminated the recalcitrance of biofilms to killing by bactericidal antimicrobial agents, a phenotyp

42 for activating TLR4 and more susceptible to killing by beta-defensins 2 and 3.

43 The lack of meningococci killing by blood containing eculizumab resulted from inh

44 Many microbial cells are highly sensitive to killing by blue light (400-470 nm) due to accumulation o

45 Cryptococcal killing by bone marrow-derived ExMs was CCR2 independent

46 even though the sifA mutant was sensitive to killing by bone marrow-derived macrophages from BALB/c.D

47 y primes the innate immune system, enhancing killing by bone marrow-derived neutrophils of two major

48 mpanzees in 15 communities and one suspected killing by bonobos.

49 When killing by bortezomib (an agent whose cytotoxicity in Ju

50 eptide at 0.1 nM are completely resistant to killing by C. albicans The peptide also protects macroph

51 nificant increase in the level of macrophage killing by C. albicans.

52 gest a therapeutic approach to mitigate cell killing by C. difficile toxins A and B.

53 with bortezomib) resulted in increased cell killing by C93, indicating that the NF-kappaB response i

54 phosphorylation and sensitized the cells to killing by carboplatin.

55 s, but deleting arnT decreased resistance to killing by cationic antimicrobial peptides, such as poly

56 that the potentiation of PARP inhibitor cell killing by CCT241533 was due to inhibition of CHK2.

57 at likely permitted CD22(+) cell escape from killing by CD22-CAR T cells.

58 Here, we show that suppression of CTL killing by CD4(+)CD25(+)Foxp3(+) regulatory T cell (Treg

59 eath, Bax(-/-)Bak(-/-) DCs were resistant to killing by CD4(+)Foxp3(+) T regulatory cells (Tregs) com

60 fine mechanisms of pathogen recognition and killing by CD8(+) T cells.

61 reactive epitopes to escape recognition and killing by CD8+ T cells.

62 t affect WLBU2 killing compared to decreased killing by cefazolin.

63 We found a significant decrease in bacterial killing by CF alveolar macrophages compared with control

64 replication rate, total tumor population, or killing by chemotherapy of mouse or human leukemia cells

65 reviously proposed adaptive explanations for killing by chimpanzees, whereas the human impact hypothe

66 = 58 observed, 41 inferred, and 53 suspected killings) by chimpanzees in 15 communities and one suspe

67 ide (LPS) synthesis as uniquely required for killing by colicin N, but not by other colicins.

68 This renders the organism resistant to killing by complement in normal human serum.

69 es showed that both were resistant to direct killing by complement, although B. thailandensis acquire

70 acteremia because of their ability to resist killing by complement.

71 pression of COPZ2 protected tumor cells from killing by COPZ1 knockdown, indicating that tumor cell d

72 Enhanced bacterial killing by CPPD-induced NETs demonstrates their ability

73 aberrant growth and was more susceptible to killing by crystal violet, osmotic shock, and select car

74 heless, the reported kinetics for tumor cell killing by CTLs in vivo is surprisingly low as it takes

75 ion augmented pore formation by perforin and killing by CTLs.

76 oth granzyme B- and Fas-mediated pathways of killing by CTLs; however, the kinetics of caspase activa

77 ll surface, PDHc is an important mediator of killing by CXCL10.

78 e myeloid leukemia (AML) cells for cytotoxic killing by cytarabine (Ara-C).

79 cells were significantly more susceptible to killing by cytotoxic chemotherapy following androgen dep

80 ng schemes optimized to sustain and maximize killing by cytotoxic immune effector systems.

81 d no effect on susceptibility of melanoma to killing by cytotoxic T cells, blocking SD-4 function enh

82 ive to Ca-dependent and Fas ligand-dependent killing by cytotoxic T lymphocytes.

83 lsion, renders E. faecalis more resistant to killing by defensins and less susceptible to focal targe

84 Antibodies to TNF-alpha reversed the 95% killing by Deltaisp2/isp3, whereas they grew normally in

85 system, GraRS, is involved in resistance to killing by distinct host defense cationic antimicrobial

86 e pathways to predict cellular resistance to killing by DNA-damaging agents.

87 ntly in human cancers, confers resistance to killing by DNA-damaging agents.

88 L4A and GET4 proteins and resistance to cell killing by DNA-damaging agents.

89 s capsule was shown to mediate resistance to killing by Drosophila antimicrobial peptides (Imd pathwa

90 the impact of EGFR expression on tumor cell killing by EGFR mAb.

91 tinib with obatoclax caused synergistic cell killing by eliciting autophagic cell death that was depe

92 response, participating directly in parasite killing by encapsulating and clearing the infection.

93 e a promising strategy to improve tumor cell killing by enhancing the interaction between humoral and

94 protecting M. catarrhalis from intracellular killing by epithelial cells.

95 ts of Escherichia coli are hypersensitive to killing by exogenous cytidine, adenosine, or guanosine,

96 rain of M. catarrhalis was very resistant to killing by exogenous hydrogen peroxide (HO).

97 cellular H2O2 threshold to enable more rapid killing by exogenous sources of H2O2.

98 etic targets that can sensitize AML cells to killing by FLT3 inhibitors, we performed a genome-wide R

99 t MHC-I downregulation did not promote rapid killing by freshly isolated CD8(+) T cells.

100 udged from flow cytometric assays, bacterial killing by GA occurred within minutes.

101 Efficient killing by GA was also demonstrated in Acinetobacter bau

102 ants of Gal3-binding sugar moieties, escaped killing by Gal3.

103 ormal and cancer stem cells are resistant to killing by genotoxins, but the mechanism for this resist

104 utant were more sensitive than the parent to killing by H2O2.

105 olated an ALL cell line that is resistant to killing by HA22.

106 , resulting in an increase in sensitivity to killing by HO in disk diffusion assays and a concomitant

107 sceptibility of NC101 and NC101DeltagadAB to killing by host antimicrobial peptides and their translo

108 edly increased the resistance of bacteria to killing by host defenses and antibiotics, and reduced th

109 tion plays in circumventing detection and/or killing by host defenses.

110 odalis glossinidius, requires PhoP to resist killing by host derived antimicrobial peptides.

111 stent disease, the bacterium must circumvent killing by host innate immune factors, such as cationic

112 etemcomitans displays enhanced resistance to killing by host innate immunity.

113 of adenosine in sPLA2-IIA-mediated S. aureus killing by host is still unknown.

114 ed to RAG hosts suggesting that avoidance of killing by host NK cells might be essential for autoanti

115 s, and resistance to bacterial ingestion and killing by host phagocytes.

116 lement evasion that allows for resistance to killing by human complement and persistence in mice.

117 ement pathways, T. forsythia is resistant to killing by human complement, which is present at up to 7

118 ensitive than the wild-type parent strain to killing by human lysozyme in the presence of human apola

119 least 2-fold more resistant to SP-A-mediated killing by human macrophages than their respective early

120 d that SOK contributes to both resistance to killing by human neutrophils and to oxidative stress.

121 ptides, which correlated with increased MRSA killing by human neutrophils and within neutrophil extra

122 mutant was also more susceptible than BG2 to killing by human neutrophils in vitro.

123 related with higher resistance to nonopsonic killing by human neutrophils in vitro.

124 eumoniae has enhanced capacity to circumvent killing by human neutrophils, the primary cellular defen

125 tant to complement-mediated opsonophagocytic killing by human neutrophils, whereas the acapsular muta

126 ex vivo, which was associated with increased killing by human neutrophils.

127 fluence complement-mediated opsonophagocytic killing by human neutrophils.

128 nt C3 on these bacteria for opsonophagocytic killing by human neutrophils.

129 enhanced the susceptibility of S. aureus to killing by human neutrophils.

130 Differences in sensitivity to killing by human nLc4 LOS IgG may account for the fact t

131 ant was more susceptible to phagocytosis and killing by human polymorphonuclear cells (P = 0.01 and P

132 tant strain is more susceptible to oxidative killing by human polymorphonuclear leukocytes and displa

133 his toxin gene region increase resistance to killing by human polymorphonuclear leukocytes, increase

134 is severely attenuated in ability to resist killing by human polymorphonuclear leukocytes.

135 nt mutants demonstrate reduced resistance to killing by human serum.

136 st vertebrates are most threatened by direct killing by humans.

137 HSV-1 was found to be more sensitive to killing by hydrogen peroxide in the presence of a catala

138 hyloxanthin production and susceptibility to killing by hydrogen peroxide, respectively.

139 g that the luxS mutant was more sensitive to killing by hydrogen peroxide, suggesting a potential req

140 oxidative PMN-mediated killing and oxidative killing by hydrogen peroxide.

141 ree of fluidity and unique susceptibility to killing by hydrophobic peptides and is therefore a targe

142 acellular killing within NETs and phagocytic killing by incoming neutrophils, due to oligosaccharide

143 rium is able to resist antimicrobial peptide killing by induction of the PhoP-PhoQ and PmrA-PmrB two-

144 confirmed a role for PorB2 in resistance to killing by infant rat serum.

145 ne B4 (LTB4), which are involved in parasite killing by infected macrophages.

146 Chi3l1 augments macrophage bacterial killing by inhibiting caspase-1-dependent macrophage pyr

147 echanisms by which bacterial pathogens avoid killing by innate host responses, including autophagy pa

148 s, the esx-3 region, in evasion of bacterial killing by innate immunity.

149 pecies is thought to contribute to bacterial killing by interaction with diverse targets and nitratio

150 Rapid parasite killing by intravenous artesunate might obscure the effe

151 ans, its absence sensitizes the bacterium to killing by ionizing radiation (IR).

152 thracis, which is known to escape phagocytic killing by its pXO2 encoded poly-d-gamma-glutamic acid (

153 in 3 (Prdx3) that render them susceptible to killing by K-Ras(G12V)-mediated ROS production.

154 ial function plays an essential role in cell killing by lapatinib and obatoclax, as well as radiosens

155 ncy of CMG2 protected macrophages from rapid killing by large toxin doses (>50 ng/mL), by 24 h the to

156 ll portion of a culture which is tolerant to killing by lethal doses of bactericidal antibiotics.

157 est (BIAT)) for investigating illegal badger killing by livestock farmers across Wales.

158 greater sensitivity than the sapA mutant to killing by LL-37.

159 the cellular mechanism through which failed killing by lymphocytes causes systemic inflammation invo

160 ed and displayed increased susceptibility to killing by lysosomal SF and the antimicrobial peptide LL

161 chanisms which B. subtilis utilizes to avoid killing by lysozyme.

162 We observed 100% complement-dependent killing by mAb 2C7 of a mutant that expressed lactose (G

163 ered effective FcalphaRI-mediated tumor cell killing by macrophages already at low effector to target

164 s pathogenic in mice and more susceptible to killing by macrophages in vitro than are wild-type cells

165 sitive phenotype and was more susceptible to killing by macrophages than the WT strain.

166 gnaling protects through enhancing bacterial killing by macrophages, which is independent of the infl

167 acting in part via a modulation of bacterial killing by macrophages.

168 y tandem repeats are relatively resistant to killing by macrophages.

169 of infection by opsonization, ingestion, and killing by macrophages.

170 ve the capacity to evade DC (and macrophage) killing by manipulation of autophagic pathways.

171 N-gamma sensitizes these leukemias to T cell killing by mechanisms other than MHC upregulation.

172 nvironment may impair NK-mediated tumor cell killing by mechanisms that are not fully understood.

173 anner which affects MIC and recalcitrance to killing by microbicidal antimicrobial agents.

174 he MICs and the recalcitrance of biofilms to killing by microbicidal antimicrobial agents.

175 p53 inhibition boosts bacterial killing by mouse neutrophils and oxidant generation by h

176 ch in turn leads to a reduction in bacterial killing by moxifloxacin, a substrate of the NorB efflux

177 Bacterial killing by MSC was found to be mediated in part by secre

178 tein, is required for Mtuberculosis to evade killing by NADPH oxidase and LAP.

179 ha resulted in their increased resistance to killing by natural cytotoxic cells.

180 Killing by NET-forming cells is ascribed to these struct

181 nables N. gonorrhoeae to escape trapping and killing by NETs during symptomatic infection, highlighti

182 ith bacteria, and are deficient in bacterial killing by NETs.

183 n and biofilm formation, decreases bacterial killing by neutrophil extracellular traps, and modulates

184 ies showed significantly enhanced uptake and killing by neutrophils after critical levels of C3 were

185 oxidative stress, febrile temperatures, and killing by neutrophils and also had defects in filamenta

186 ggregatibacter actinomycetemcomitans resists killing by neutrophils and is inhibited by azithromycin

187 criptional regulator of genes directing AP53 killing by neutrophils and regulates the levels of the r

188 ous M1 protein rescues M1-deficient GAS from killing by neutrophils and within neutrophil extracellul

189 MPO) is important in intracellular microbial killing by neutrophils but extracellularly causes tissue

190 oxygen species, and intracellular bacterial killing by neutrophils remains intact.

191 r-mediated changes protect S. aureus against killing by neutrophils, and Fur is required for full sta

192 s, and phagocytosis, and succeeds in evading killing by neutrophils.

193 reased susceptibility to complement-mediated killing by neutrophils.

194 B-negative staphylococci more susceptible to killing by neutrophils.

195 se against S. pneumoniae is opsonophagocytic killing by neutrophils.

196 o a secondary stimulus, preventing oxidative killing by neutrophils.

197 but does not affect intracellular phagocytic killing by neutrophils.

198 degrades NETs to help N. gonorrhoeae resist killing by neutrophils.

199 veloped strategies to evade phagocytosis and killing by neutrophils.

200 e extent of S. aureus opsonophagocytosis and killing by neutrophils.

201 fied by Tn-seq in A. baumannii resistance to killing by NHS but not by normal mouse serum, highlighti

202 C4b deposition, and increased resistance to killing by NHS.

203 tion of C4b, and increased susceptibility to killing by NHS.

204 Killing by NK cells is mediated by a small family of act

205 Ex vivo and in vivo tumor cell killing by NK cells were significantly reduced in surgic

206 g receptor 2B4, thereby leading to decreased killing by NK cells.

207 well as Fas/Fas ligand-dependent pathways of killing by NK cells.

208 cer cells more susceptible to NKG2D-mediated killing by NK cells.

209 apy, suggesting a decrease in TRAIL-mediated killing by NK cells.

210 owing T. spiralis larvae were susceptible to killing by NO in vitro, whereas mature larvae were highl

211 ype and the mutant strains were resistant to killing by normal and heat-inactivated sera.

212 levant A. baumannii strains are resistant to killing by normal human serum (NHS), an observation supp

213 eptibility of an lptA null strain of FA19 to killing by normal human serum (NHS).

214 correlated with enhanced protection against killing by normal human serum.

215 gonococcal resistance to complement-mediated killing by normal human serum.

216 ased microbial ROS production can potentiate killing by oxidants and antibiotics.

217 capacity may selectively enhance cancer cell killing by oxidative stress-generating agents through st

218 guinis protects Drosophila melanogaster from killing by P. aeruginosa in a nitrite-dependent manner.

219 elegans and human lung epithelial cells from killing by P. aeruginosa.

220 were screened for altered susceptibility to killing by P. gingivalis.

221 macrophage pyroptosis, attenuated both cell killing by p30 in a 293T transient overexpression system

222 es not induce serotype 3 (ST3) S. pneumoniae killing by phagocytes in vitro, protects mice from death

223 ing cytokine levels, promoting extracellular killing by phagocytes, and generating a granulomatous re

224 ram-negative bacteria and supports bacterial killing by phagocytes.

225 ella by directly coating bacteria to promote killing by phagocytes.

226 We confirmed the cell shape-specific killing by photothermal colloid antibodies in a mixture

227 in MICs tracked with increased resistance to killing by platelet-derived but not neutrophil-derived H

228 g Gram-negative pathogen in CGD that resists killing by PMN of CGD patients (CGD PMN) and inhibits PM

229 B. parapertussis is able to avoid bacterial killing by polymorphonuclear leukocytes (PMN) if specifi

230 operty as an evasion-type mechanism to avoid killing by polysaccharide-targeting factors in the ecosy

231 ast cancer and melanoma cells susceptible to killing by PR1-specific CTLs (PR1-CTL) and the anti-PR1/

232 TDE0471 protects T.denticola from serum killing by preventing the deposition of membrane attack

233 Therefore, we examined phagocytic killing by primary human monocytes and monocyte-derived

234 rs of innate immunity against fast paralytic killing by Pseudomonas.

235 -induced apoptosis and no protection against killing by Puma or ABT-737 plus Noxa overexpression.

236 an neutrophils susceptible to LukAB-mediated killing by purified LukAB as well as during S. aureus in

237 coli with engineered bacteriophage enhances killing by quinolones by several orders of magnitude in

238 er-transporting ATPase was hypersensitive to killing by RAW264.7 macrophages, and this phenotype was

239 hages and exposed the bacteria to uptake and killing by reactive oxygen species in neutrophils.

240 is usually resists complement-mediated serum killing by recruiting to its surface a complement inhibi

241 ibiotics, P. gingivalis can evade antibiotic killing by residing within gingival keratinocytes.

242 ith mutations of phoPQ are hypersensitive to killing by RNS generated in vitro.

243 G. bethesdensis resists killing by serum, CGD polymorphonuclear leukocytes (PMN)

244 that mitochondrial damage and ROS drive cell killing by SFB, while glycolytic cell reprogramming may

245 in protecting SIV-infected macrophages from killing by SIV-specific CD8(+) T cells.

246 membrane of these organisms is a target for killing by small hydrophobic peptides that increase the

247 linical GBS isolates are highly sensitive to killing by sPLA2-IIA but not by human antimicrobial pept

248 erminating spores become more susceptible to killing by stressors, induction of germination has been

249 potently and specifically inhibit S. aureus killing by synthetic CRAMP.

250 n endothelium increased immune-mediated cell killing by T cells and natural killer (NK) cells, thereb

251 vivo because of inefficient recognition and killing by T cells.

252 nity proteins that render protection against killing by T6SS predatory cells.

253 in cancer treatment has been to trigger cell killing by targeting microtubule dynamics or spindle ass

254 ngly suggest that Spiroplasma initiates male killing by targeting the dosage compensation machinery d

255 ion mutant of MG_427 was highly sensitive to killing by tert-butyl hydroperoxide and H2O2 compared to

256 portant contributor to periodontitis, evades killing by the alternative complement cascade by binding

257 ureus biofilms showed less susceptibility to killing by the antimicrobial peptide LL-37 when compared

258 37 and increased bacterial susceptibility to killing by the antimicrobial peptide.

259 class I C/E16 were highly susceptible to the killing by the CD8alphaalpha(+) AP-NK cell.

260 ain FA19 results in increased sensitivity to killing by the classical pathway of complement.

261 Evasion of killing by the complement system, a crucial part of inna

262 toaggregation and protects the pathogen from killing by the complement system.

263 he RecQ helicase Blm are highly sensitive to killing by the DNA replication stressor hydroxyurea.

264 and enhances the susceptibility of NC101 to killing by the host antimicrobial peptide cryptdin-4 but

265 ormed less biofilm and was less resistant to killing by the host complement.

266 Mtb requires the proteasome to resist killing by the host immune system.

267 Higher IFN-beta levels in vivo increase GBS killing by the host.

268 , forming drug-tolerant biofilms that resist killing by the immune system.

269 LA class II and restored recognition but not killing by the LANA-specific clones.

270 conditions, including antibiotic stress and killing by the mouse-derived macrophage cell line J774.

271 ctively, more susceptible than the parent to killing by the neutrophil cell line HL-60 cells.

272 es lacking pAKT (P = .024) and exceeded cell killing by the PI3K-delta-specific inhibitor idelalisib.

273 Many human cancer cells are sensitive to killing by the proapoptotic ligand TNF-related apoptosis

274 R system, thereby defending the cell against killing by the Sn1-type methylating agent.

275 Killing by the T6SS results from repetitive delivery of

276 lls, dendritic cell (DCs) are susceptible to killing by these activated T cells that involve perforin

277 tibacterials, leading to the hypothesis that killing by these agents can involve ROS-mediated self-de

278 air and checkpoint signaling pathways affect killing by these agents individually and in combination.

279 that contributes to effective DNA damage and killing by these agents.

280 a trophozoites were found to be resistant to killing by these antimicrobial peptides, and LL-37 and C

281 Perforin-mediated killing by these densely granulated NK cells was essenti

282 with decreased metabolic rate, refractory to killing by these drugs, and able to generate drug-resist

283 bination with rTNF restores phagocytosis and killing by TNF-deficient macrophages to that of unstimul

284 t the dividing cells are more susceptible to killing by tobramycin and ciprofloxacin.

285 th rMIF is associated with reduced bacterial killing by tobramycin.

286 Acquisition of androgen-independent killing by TPA correlates with activation of p38(MAPK),

287 n MIC of 1 mg/L exhibited significantly less killing by tPMP, compared with strains with an MIC of </

288 Noxa from cells, and protected cells against killing by transfected Noxa to a greater extent.

289 bacterial and anticancer drugs initiate cell killing by trapping the covalent complexes formed by top

290 nd apoptosis in vivo and increased bacterial killing by treated cells.

291 -thiothymidine (S(4)TdR) sensitizes cells to killing by ultraviolet A (UVA) radiation.

292 TF combinations that potentiated antibiotic killing by up to 10(6)-fold and delivered these combinat

293 FANCJ-deficient cells are not sensitive to killing by UV irradiation, yet we find that DNA mutation

294 XP cells are hypersensitive to killing by UV radiation, and XP cancers have characteris

295 Resistance to killing by Verde2, by means of alterations in host surfa

296 for T6SS-mediated secretion and target cell killing by Vibrio cholerae and Acinetobacter baylyi.

297 ile M. tuberculosis is highly susceptible to killing by vitamin C, other Gram-positive and Gram-negat

298 In the presence of erythrocytes, bacterial killing by VPO1 is slightly reduced.

299 Susceptibility of HNSCC lines to killing by VSV varied.

300 of Nrf1 in human cancer cells enhanced cell killing by YU101.