ライフサイエンスコーパス: cell killing

1 ombination with G4 ligand treatment enhances cell killing.

2 body; HDPDL1) as a strategy to enhance CAR T-cell killing.

3 tumor-infiltrating CD8(+) T cells and tumor cell killing.

4 ent, MTX to tumor cells and induce effective cell killing.

5 proinflammatory cytokines, leading to target cell killing.

6 affecting IR or chemotherapy-induced cancer cell killing.

7 rucially control toxin conformation and host cell killing.

8 , NK cell activation, and influenza-infected cell killing.

9 y', causing interferon signalling and cancer cell killing.

10 fected cells may inhibit complement-mediated cell killing.

11 in, thereby leading to more effective target cell killing.

12 g radiation to achieve more efficient cancer cell killing.

13 because of copy gain and was resistant to NK cell killing.

14 resist viral cytopathic effects and CD8(+) T-cell killing.

15 additively with BRCA2 or MUS81 depletion in cell killing.

16 L/B inhibitor enhances cisplatin uptake and cell killing.

17 viral vectors encoding CAR that direct tumor cell killing.

18 ling and sensitized them to Ad-E1A12-induced cell killing.

19 ity of newborn cells to mediate Ab-dependent cell killing.

20 in each case leading to natural killer (NK) cell killing.

21 intestinal epithelial cells, which preceded cell killing.

22 cell fragments, and that this contributes to cell killing.

23 DCs protect tumor plasma cells from CD8(+) T-cell killing.

24 te antigen (HLA) class I-restricted CD8(+) T-cell killing.

25 unmethylated INS DNA are indicative of beta cell killing.

26 in control of tumor progression, but limited cell killing.

27 ence for more efficacious CTL-mediated tumor cell killing.

28 presentation, T-cell recognition, and target cell killing.

29 itizes hMSH5-deficient cells to CPT-elicited cell killing.

30 is sufficient to trigger sensitization to NK cell killing.

31 holocomplex, and this correlates with cancer cell killing.

32 the higher RBE of high LET radiation-induced cell killing.

33 action in vivo was auristatin-mediated tumor cell killing.

34 cktail or a single antibody achieved greater cell killing.

35 can provide a substantial advantage in tumor cell killing.

36 of cytotoxic mediators, and restricts tumour cell killing.

37 aB activation, caspase activation, and tumor cell killing.

38 ent mitochondrial dysfunction and subsequent cell killing.

39 he cargo is released allowing imaging and/or cell killing.

40 nase (HSV-TK) gene was introduced for cancer cell killing.

41 o engage cytotoxic T cells and trigger tumor cell killing.

42 ction, we analyzed various steps involved in cell killing.

43 on of NF-kappaB signaling and synergistic WM cell killing.

44 which elicited cellular expansion and target cell killing.

45 and evaluated its capacity to promote cancer cell killing.

46 on in vivo by facilitating NK-mediated tumor cell killing.

47 d KIR/HLA combination expected to inhibit NK cell killing.

48 hibition on ionizing radiation (IR)-mediated cell killing.

49 iller cells and macrophages, to induce tumor cell killing.

50 iated pharmacokinetics and radiation-induced cell killing.

51 crosslink tumor and T-cells to induce tumor cell killing.

52 expression in primary T cells, led to tumor cell killing.

53 le of trafficking to the tumor and mediating cell killing.

54 learance, and tissue penetration to maximize cell killing.

55 y a distinct role in amebic trogocytosis and cell killing.

56 increased TIL locomotion, and impaired tumor cell killing.

57 ion, migration toward tumor cells, and tumor cell killing.

58 e enabled higher tissue penetration and more cell killing.

59 ssessed to demonstrate on-target synergistic cell killing.

60 ssion, as a means to enhance selective tumor cell killing.

61 trigger DNA damage, genome instability, and cell killing.

62 atural killer (NK) cells for efficient tumor cell killing.

63 m, which can be exploited for tumor-specific cell killing.

64 uce K-RAS expression, and to further enhance cell killing.

65 ic trogocytosis and phagocytosis, as well as cell killing.

66 uild an immunologic synapse and induce tumor cell killing.

67 osphorylation of MLKL did not result in host cell killing.

68 onses that led to in vitro and in vivo tumor cell killing.

69 ro-inflammatory cytokines, leading to target cell killing.

70 rate effects and intercellular signalling on cell-killing.

71 he virus-host relationship, such as enhanced cell killing, a shift toward higher virion density, and

72 burden, promotes survival, and restores the cell-killing abilities of NK cells, demonstrating the th

73 low l-glutaminase ErA variant maintained its cell killing ability.

74 etween healthy and diseased tissue, with the cell-killing ability of cytotoxic drugs.

75 transduction model based on nonlinear direct cell killing accounted for observed tumor growth pattern

76 L-24) displays potent growth suppressing and cell killing activity against a wide variety of human an

77 quadruplexes and R loops and showed a potent cell killing activity associated with the formation of m

78 T-cell killing activity of immature granulocytes was explo

79 Here we show that the cell killing activity of PAF26 is dependent on extracell

80 llular effects were different in relation to cell-killing activity and stimulation of micronuclei, a

81 The infectivity (cell-killing activity by infecting cells) of rNDV is una

82 )-mediated crosslinking increases the cancer-cell-killing activity of TRAIL-R2-specific antibodies in

83 Anthracyclines also exert cell-killing activity via TOP2-independent mechanisms, i

84 g membrane damage and exhibited more complex cell-killing activity, probably because of two different

85 ted deeper into tissue resulting in improved cell killing after a 2nd NIR-PIT session.

86 Cell killing after NIR-PIT was primarily on the surface,

87 r of sensitivity of head and neck cancers to cell killing after PDT.

88 iofilm-eradicating agent (>/=99.9% persister cell killing) against MRSA (MBEC < 10 muM), MRSE (MBEC =

89 een used in combination therapies to enhance cell killing, although their success has been limited.

90 After cell killing, amoebae detach and cease ingestion.

91 we examine theoretically different models of cell killing and analyze data from clinical trials based

92 roduced in 88hIgG1, recapitulated the direct cell killing and avidity of 88mIgG3.

93 oleate, rescued AML and e-BL cells from BaP cell killing and decreased levels of BaP-induced reactiv

94 r or superior potency in ADCC-mediated tumor cell killing and demonstrate improved stability in the C

95 NA damage model with experimentally observed cell killing and DNA damage induction via the combinatio

96 that the mechanism leading to an increase in cell killing and DNA damage is still not clear.

97 ting IgG1 mAb confers proinflammatory direct cell killing and enhanced avidity, an approach that coul

98 tion of cell competition could induce cancer cell killing and form the basis for novel anticancer the

99 rexpression of NKG2D(TR) severely attenuated cell killing and IFN-gamma release mediated by full-leng

100 cells correlated with more efficient target cell killing and improved control of viremia.

101 and payload release by 2 days, and in vitro cell killing and in vivo tumor shrinkage 2 to 3 days lat

102 e murine IgG3 residues underlying the direct cell killing and increased avidity via a series of const

103 adiation in tissues, resulting in high tumor cell killing and low toxicity to surrounding tissues.

104 adiation in tissues, resulting in high tumor cell killing and low toxicity to surrounding tissues.

105 Moreover, NK cell killing and macrophage engulfment of our engineered

106 like Prf1-/- mice, they showed normal target cell killing and normal clearance of viral RNA and antig

107 roach enables protein inactivation, targeted cell killing and rapid targeted lineage ablation in livi

108 Clonogenic cell killing and reductive metabolism of PR-104A and SN3

109 rotecting infected macrophages from CD8(+) T cell killing and suggest that other mechanisms are invol

110 ng T cell activity by promoting fratricide T cell killing and T cell exhaustion.

111 cts with dual-modality mechanisms: malignant cell killing and TAM-based immunomodulation.

112 of the mechanisms that limit effective tumor cell killing and the identification of apoptotic vulnera

113 myriad of cellular responses, such as target cell killing and the secretion of different cytokines, t

114 esults show a significant additive effect in cell killing and they provide initial evidence for a nov

115 ity of S. aureus strains to evade phagocytic cell killing and to survive temporarily within phagocyte

116 G-NT elicited increased NTR-selective cancer cell killing and transduction efficiency when compared w

117 s, compromises c-NHEJ and markedly increases cell killing and translocation-formation compared to sin

118 e and replicative stress and increased tumor cell killing and tumor control by DNA damage therapies i

119 ibition and achieved both efficient in vitro cell killing and tumor regression in Mcl-1 dependent can

120 ified Ham (mHam) assay (complement-dependent cell killing) and cell-surface deposition of C5b-9 to te

121 tion of human cell fragments is required for cell killing, and also contributes to invasion of intest

122 T cells reduced tumor infiltration and tumor cell killing, and altered tumor vascularization.

123 This allows for potent tumour cell killing, and an overall decreased metastatic burden

124 Ribotoxins cleave essential RNAs for cell killing, and RNA repair neutralizes the damage infl

125 erferon (IFN-gamma) release, specific target cell killing, and suppression of HIV-1 pseudovirus produ

126 n of cultures, autoimmunity or self-targeted cell killing, and the engineering or control of metaboli

127 granules involved in T cell-mediated target cell-killing, and monomeric teal fluorescent protein fro

128 ve synergistic or additive effects in cancer cell killing are outlined.

129 rred mechanisms of anti-proliferation and/or cell-killing are consistent with the published mechanism

130 The study highlights the regulation of beta-cell killing as a potential point for therapeutic contro

131 ed INS DNA serves as a marker of active beta cell killing as the result of T1D-associated autoimmunit

132 Furthermore, E4orf4 inhibited JNK-dependent cell killing as well.

133 damage and appear to play redundant roles in cell killing, as depletion of either one has no effect b

134 emia target cells toward late apoptosis in a cell killing assay.

135 th CRISPR/Cas9-KO cell lines, natural killer cell-killing assays, and RNA-Seq experiments, we now dem

136 Widespread tumor cell killing at 5 days was prevented by depletion of CD8

137 ous cell responses and results in fractional cell killing at low levels of receptor stimulation.

138 lethality is an approach to study selective cell killing based on genotype.

139 Here, exosomal BAG6 was essential for tumor cell killing because BAG6-deficient cells evaded immune

140 We also show marked synergy in tumor cell killing between MEK inhibitors (trametinib) and ret

141 he same colicin N molecule and later, during cell killing, binding to two different receptors, OmpF a

142 sitizes paclitaxel-resistant prostate cancer cells, killing both cancer stem-like cells (CSC) and bul

143 r reveal that these peptides not only induce cell killing but also potently sensitize PEL to the proa

144 CPs are required for amebic trogocytosis and cell killing but not phagocytosis.

145 nti-apoptotic signaling responses that limit cell killing, but also primes cells for inhibitors of an

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

147 iew focuses on three different mechanisms of cell killing by checkpoint kinase I inhibitors (CHK1i).

148 th UBL4A and GET4 proteins and resistance to cell killing by DNA-damaging agents.

149 titute a promising strategy to improve tumor cell killing by enhancing the interaction between humora

150 ostimulation plays a critical role in target cell killing by freshly isolated human CD8(+) T cells, w

151 at IFN-gamma sensitizes these leukemias to T cell killing by mechanisms other than MHC upregulation.

152 icroenvironment may impair NK-mediated tumor cell killing by mechanisms that are not fully understood

153 Ex vivo and in vivo tumor cell killing by NK cells were significantly reduced in s

154 lls isolated from the same individual escape cell killing by NK cells.

155 event macrophage pyroptosis, attenuated both cell killing by p30 in a 293T transient overexpression s

156 It is, therefore, apparent that cell killing by PAF26 is complex and unusually dependent

157 infection and triple-negative breast cancer cell killing by reovirus.

158 lude that mitochondrial damage and ROS drive cell killing by SFB, while glycolytic cell reprogramming

159 ns2 in endothelium increased immune-mediated cell killing by T cells and natural killer (NK) cells, t

160 7 lines lacking pAKT (P = .024) and exceeded cell killing by the PI3K-delta-specific inhibitor idelal

161 Through synergistic cell killing by these distinct reactive oxygen species,

162 gy in which CAR T cell activation and cancer cell killing can be sensitively regulated by adjusting t

163 trials using ZOL for improving gammadelta T-cell killing capacity against leukemia cells.

164 uction, CTL/regulatory T cell ratio, and per-cell killing capacity of CD8 T cells without increasing

165 L2, and CXCL12 and activation of their tumor cell killing capacity through IFNgamma and IL4, which le

166 istinguishing residues are important for its cell-killing capacity and antagonism by pro-survival pro

167 a direct correlation between persistence and cell-killing capacity.

168 sistence is related to virus replication and cell-killing capacity.

169 contrast, no intereference was seen in tumor cell killing, caspase activation, or mitochondrial membr

170 the apoptosome, which recruits and activates cell-killing caspases.

171 Unlike specific target cell killing, CD4-mediated bystander injury required tis

172 ynthase kinase 3 (GSK3) phosphorylation, and cell killing correlated with reduced activity of AKT and

173 with possible implications for mechanisms of cell killing during cancer chemotherapy.

174 cell migration, vessel sprouting, and cancer cell killing effect compared to naked KOX or KOX/PEGbPHF

175 noparticles significantly enhance the cancer cell killing effect of radiation therapy.

176 from stored chemical energy may enhance the cell-killing effect and boost the therapeutic effect.

177 Relative to BPS alone, an enhanced cell-killing effect is seen under hypoxic conditions bot

178 ression of this pathway could potentiate the cell-killing effect mediated by proteasome inhibitor dru

179 rand break (DSB) repair, and (ii) the strong cell-killing effect of carbon-ion beams due to poor repa

180 Mechanistically, the cell killing effects of PP were a result of inhibition o

181 The cell killing effects of two representative voxels (isoce

182 d/ABP-PEG-HCBP1 demonstrated enhanced cancer cell killing efficacy in comparison to oAd/ABP complex.

183 ence in 5-10 s) and display a summary of the cell killing efficacy measurements.

184 results in 10-fold improvement of its cancer cell-killing efficacy.

185 cells, and active GrB influenced its target cell-killing efficiency.

186 ties, but that may function to promote tumor cell killing either alone or in association with apoptos

187 -MPL signaling also enables sequential tumor cell killing, enhances the formation of effective immune

188 f tissue rejection through individual target cell-killing events in vivo.

189 N in human CD8+ T cells reduced direct tumor cell killing ex vivo.

190 The serum cell killing factor was shown to be an enzyme with L-asp

191 drug screen identified agents that enhanced cell killing following reduction of IL6 signaling.

192 l protease-resistant platform with selective cell-killing functionality.

193 mutations can restore and sometimes enhance cell-killing functions while still retaining protease re

194 o resulted in a profound loss of Fc-mediated cell-killing functions.

195 operty consistent with that possessed by the cell-killing guinea pig serum enzyme.

196 The mechanism of human cell killing has been unclear, although the accepted mod

197 gnition but at increased risk of NKG2A(+) NK cell killing.IMPORTANCE For almost two decades, it was t

198 cer can be robustly leveraged for anticancer cell killing in a heterogeneous population of cells with

199 Cl-amidine (compound 13), exhibits enhanced cell killing in a PAD4 expressing osteosarcoma bone marr

200 L chemotherapeutics and found this augmented cell killing in AML cell lines that overexpress GATA2, b

201 ombined inhibition of MKP1 and HER2 enhanced cell killing in breast cancer.

202 ADCs demonstrate specific cell killing in clinic, but the basis of their antitumor

203 by DSS-BEN/miR-34a not only enhanced cancer cell killing in cultured human colon cancer cells, but a

204 clinical models of human cancers and induced cell killing in leukemia cells.

205 es in activating macrophages to induce tumor cell killing in mice.

206 Treatment with hIFNbeta promoted cell killing in neighboring, non-transduced cells, thus

207 aling mechanisms underlying incomplete tumor cell killing in oncogene-addicted cancer cells, we inves

208 immunodeficiency syndrome, is involved in NK cell killing in part through its effects on MT organizin

209 ces widespread CD8(+) T-cell-dependent tumor cell killing in primary tumors and metastases, and that

210 G3 glycan-targeting mAb often induces direct cell killing in the absence of immune effector cells or

211 Drug targeting AXL induces a significant cell killing in the glycolytic cells without affecting t

212 f transcription3 inhibitor provided enhanced cell killing in triple-negative breast cancer cell lines

213 cells by Ly49C resulted in both decreased NK cell killing in vitro and reduced rejection in vivo.

214 antigen-dependent CD8(+) CTL-mediated tumor cell killing in vitro.

215 synapse, which correlates with reduced tumor cell killing in vitro.

216 Our data highlight striking differences in cell killing in vivo, depending on the cell subset and o

217 For effective lymphoma cell killing in vivo, we further functionalized CD22 lig

218 based assay and suppressed antibody-mediated cell killing in vivo.

219 meostatic proliferation and for Ag-dependent cell killing in vivo.

220 lpha, CD47, are more susceptible to CD8(+) T cell-killing in vivo.

221 ma secretion, granule exocytosis, and target-cell killing, in part by inhibiting the PIP(3) effector-

222 y, USP7 inhibition induces significant tumor-cell killing independently of ATM and p53 through the ac

223 ssue damage that may explain the inefficient cell killing induced by E4orf4 in normal cells in tissue

224 g one of the major mechanisms of cytotoxic T cell killing, inhibits B cell receptor-mediated gammaher

225 ition in vitro resulted in caspase-dependent cell killing irrespective of p53, ATM, NOTCH1, or SF3B1

226 enhanced it, indicating that E4orf4-induced cell killing is a distinctive form of cell death that di

227 We further demonstrate that LukED-dependent cell killing is blocked by CCR5 receptor antagonists, in

228 This cancer cell killing is due to noncovalent association between F

229 The mode by which the pores achieve cell killing is elucidated with confocal microscopy.

230 onsisting of a modest increase in fusion and cell killing, lower neuraminidase activity, and reduced

231 s into 129hIgG1, converting it into a direct cell killing mAb with enhanced avidity and significant i

232 itro and in vivo, along with efficient tumor cell killing makes it an attractive oncolytic virus cand

233 ic cells but not healthy cells suggests that cell killing may play a rate-limiting role in the proces

234 ination of both selectivity and an effective cell killing mechanism.

235 mode of action drives two orthogonal cancer-cell killing mechanisms with temporal and spatial contro

236 and leveraging on several synergistic cancer cell killing mechanisms.

237 dysregulation of apoptosis through multiple cell-killing mechanisms.

238 ion inhibitory activity studies and promoted cell killing mediated by caspase-3 activation.

239 r cytotoxic immunoconjugates (ICs), in which cell-killing moieties, including toxins, drugs, or radio

240 ulature, produce immune activation and tumor cell killing more widespread than the infection, and sup

241 ordination of transient competence with cell-cell killing, observed in multiple species, was found to

242 ther, the data support the concept that beta cell killing occurs sporadically during the years prior

243 rial clearance, and iv) increased phagocytic cell killing of bacteria compared with tail trauma.

244 hting how these steps in turn influence host cell killing of bacteria.

245 release to the cytosol, enhanced PDT-induced cell killing of both resistant and sensitive cells.

246 e CD44-targeted conjugate demonstrated acute cell killing of breast cancer cells with high CD44 expre

247 Fc engineering enhances avidity and direct cell killing of cancer-targeting anti-glycan antibodies

248 n expected to allow licensed missing self NK cell killing of index partners' cells.

249 ative binding mode; consequently, the direct cell killing of mouse IgG3 mAb is lost upon chimerizatio

250 is was associated with greater-than-additive cell killing of pancreatic tumor cells.

251 forin and granzyme B confirmed that CD8(+) T cell killing of parasitized cells is dependent on granul

252 lls to the peritoneum, or improve phagocytic cell killing of pathogens.

253 (X), which may account for the enhanced host cell killing of that mutant.

254 and that this may be due to alloreactive NK cell killing of the HIV-1-infected partner's cells.

255 Here, we have shown that natural killer (NK) cell killing of various tumors is inhibited in the prese

256 diated virus neutralization or cytotoxic CD8 cell killing of virus-infected cells and may be mediated

257 virus, in deflecting antigen-specific CD8 T cell-killing of infected cells.

258 n poise HSCs for apoptosis but induce direct cell killing only upon active proliferation, thereby est

259 ch as ascorbic acid, have exhibited distinct cell killing outcomes between cancer and normal cells wh

260 DOTATATE was significantly more efficient in cell killing per cumulated decay than (111)In- and (177)

261 induce tumor cell cytotoxicity by way of the cell killing proteins perforin and granzyme.

262 , our group and others demonstrated that the cell-killing RBE is involved in the interference of high

263 hallmark of cancer and of radiation-induced cell killing, reflecting joining of incongruent DNA-ends

264 and a potential target for selective cancer cell killing.See related article by Seo et al., p.

265 PRISM revealed the expected patterns of cell killing seen in conventional (unpooled) assays.

266 ed on combinations of colloid antibodies and cell-killing strategies which can be applied in new anti

267 fraction used in SBRT increases direct tumor cell killing, suggesting that disruption of the tumor va

268 otoxic activity against various human cancer cells, killing SW48 colon cancer cells in particular wit

269 se deposited by (64)Cu is less effective for cell killing than gamma-rays.

270 ake throughout tumors, leading to sub-lethal cell killing that can impart treatment resistance, and c

271 The beta cell killing that characterizes type 1 diabetes (T1D) is

272 lude that DD exerts functions beyond CD25(+) cell killing that may affect their clinical use and coul

273 all groups was a sequence motif critical for cell-killing that is generally not found in bacteriocins

274 The cell culture conditions did not affect cell killing, the ability of cells to survive in a colon

275 hages, and activation of natural killer (NK) cell killing through TNF-related apoptosis-inducing liga

276 aving the way for the proinflammatory direct cell killing to promote antibody-dependent cellular cyto

277 n translation, to ATRA sharply increases APL cell killing to the extent that cures in this disease ar

278 -Env antibodies for their ability to deliver cell-killing toxins to HIV-infected cells and to perform

279 e mechanism of effector cell-mediated target cell killing triggered by Fc-engineered antibodies and e

280 and endothelial cells demonstrated selective cell-killing under therapeutic perfusion versus episodic

281 renders the infected cell susceptible to NK cell killing upon missing self recognition.

282 mpeting hypotheses of increased direct tumor cell killing versus indirect effects on stroma including

283 differential degrees of drug effect on tumor cell killing versus inhibition of cell division, which m

284 ndings suggest that Tai promotes competitive cell killing via Spz-Toll and that this killing mechanis

285 However, cell killing was immediate upon re-polarization.

286 infection spread to tumor cells, where tumor cell killing was much more widespread than the infection

287 response occurred in p53-defective cells and cell killing was not blocked by a pan-caspase inhibitor.

288 No cell killing was observed for UTSCC15 cells with low EGF

289 Efficient cell killing was possible at nanomolar concentrations of

290 ring the lytic cycle become sensitized to NK cell killing, we observed that cells in the late lytic c

291 with cell density, revealing more effective cell killing when more cancer cells are present.

292 anulation at the mcIS associated with target cell killing, whereas icIS is characterized by failure o

293 oxide release by neutrophils promotes cancer cell killing, which abates tumour growth and metastasis.

294 m induced pluripotent stem cells triggered T-cell killing, which was due to recognition of an unrelat

295 nhanced CD8(+) T-cell infiltration and tumor cell killing while decreasing myeloid-derived suppressor

296 AR-T cells in cytokine production and cancer cell killing, while expressing lower levels of exhaustio

297 associated with acquired sensitization to NK cell killing, while progress through the late lytic cycl

298 tiomer, the VC(R) isomer, mediated effective cell killing with a cysteine-VC(R)-MMAE catabolite gener

299 terial behaviours of transformation and cell-cell killing within clonally related populations, as the

300 ellent dose localization and thus maximising cell-killing within the tumour.