ライフサイエンスコーパス: cell killing

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

2 unmethylated INS DNA are indicative of beta cell killing.

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

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

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

6 is sufficient to trigger sensitization to NK cell killing.

7 holocomplex, and this correlates with cancer cell killing.

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

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

10 cktail or a single antibody achieved greater cell killing.

11 can provide a substantial advantage in tumor cell killing.

12 of cytotoxic mediators, and restricts tumour cell killing.

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

14 ent mitochondrial dysfunction and subsequent cell killing.

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

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

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

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

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

20 which elicited cellular expansion and target cell killing.

21 and evaluated its capacity to promote cancer cell killing.

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

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

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

25 ent needs to be elucidated for optimal tumor cell killing.

26 cin-induced mitochondrial depolarization and cell killing.

27 gh mitoferrin-2 (Mfrn2) enhanced PDT-induced cell killing.

28 ruction by cytotoxic lymphocytes upon target cell killing.

29 and secrete IFN-gamma for nonspecific tumor cell killing.

30 LA combinations in NK cell-mediated CD4(+) T-cell killing.

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

32 ion of BAG6 by ATM/ATR are also required for cell killing.

33 ritical role for macrophages in Fc-dependent cell killing.

34 nd signaling by p38 MAPK and JNK1/2 promoted cell killing.

35 growth and at least partially resistant to T-cell killing.

36 ed c-Myc induction and enhanced ADI-mediated cell killing.

37 als that lead to their own exocytosis and to cell killing.

38 are activated during alpha-TEA-induced tumor cell killing.

39 ha chain), and led to antigen-specific tumor cell killing.

40 rteen antibodies mediated cross-clade target cell killing.

41 concentrations to trigger significant tumor cell killing.

42 rtant mechanisms for CD4(+) T cell-triggered cell killing.

43 affecting IR or chemotherapy-induced cancer cell killing.

44 m of therapeutic transgenes to enhance tumor cell killing.

45 rom mCP-CML cells, which protect them from T cell killing.

46 by IFN-gamma and IL-2 secretion and by tumor cell killing.

47 tly contributing to the high level of target cell killing.

48 with HLH or MAS lack defects in cytotoxic T cell killing.

49 activation and also potentiates C93-induced cell killing.

50 ized colorectal cancer cells to 5-FU-induced cell killing.

51 enretinide and that correlated with enhanced cell killing.

52 itor rescued SPI6(-/-) MSCs from cytotoxic T-cell killing.

53 ch explains most of the observed variance in cell killing.

54 Vav-1, which is known to be implicated in NK cell killing.

55 totoxic immunological synapses and in target cell killing.

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

57 rucially control toxin conformation and host cell killing.

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

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

60 fected cells may inhibit complement-mediated cell killing.

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

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

63 g radiation to achieve more efficient cancer cell killing.

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

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

66 additively with BRCA2 or MUS81 depletion in cell killing.

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

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

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

70 intestinal epithelial cells, which preceded cell killing.

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

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

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

74 We compared the cell killing abilities of (i) a recombinant NDV (rNDV) s

75 ytic granule component and measure of target cell killing ability.

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

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

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

79 as positively correlated with its diminished cell killing activity in C. elegans.

80 T-cell killing activity of immature granulocytes was explo

81 ell permeability, proteolytic stability, and cell-killing activity in Mcl-1-overexpressing U937 cells

82 tion and demonstrate that it is critical for cell-killing activity in vivo.

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

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

85 reventive agent because of its potent cancer cell-killing activity, the molecular mechanisms by which

86 sulting in enhanced cisplatin uptake and its cell-killing activity.

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

88 mor cell types that displayed high levels of cell killing after combination treatment showed elevated

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

90 roquine and found that either drug increased cell killing after NVP-BEZ235 treatment and radiation.

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

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

93 After cell killing, amoebae detach and cease ingestion.

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

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

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

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

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

99 R induction by CPT and increased CPT-induced cell killing and histone gammaH2AX.

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

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

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

103 Both direct cell killing and indirect mechanisms related to immune a

104 ide generation plays a central role in tumor cell killing and inhibition of multiple signaling pathwa

105 wth of tumors, whereas FG-3019 increased PDA cell killing and led to a dramatic tumor response withou

106 The IgG2a mAb prevented lethal toxin cell killing and mitogen-activated protein kinase/extrac

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 ic drug treatment is shown to increase tumor cell killing and substantially enhance therapeutic activ

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

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

112 Viral tumor cell killing and the host immunologic response it engend

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

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

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

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

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

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

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

125 T-cell/B-cell associations for redirected T cell-killing applications.

126 ressed by small intefering RNA, adhesion and cell killing are blocked.

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

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

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

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

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

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

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

134 ty is a powerful approach to study selective cell killing based on genotype.

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

136 ath-1 ligands 1 and 2 (PD-L1/L2) to resist T cell killing, because only GVL against mCP-CML was augme

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

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

139 integrase inhibitor, abolished HIV-1-induced cell killing both in cell culture and in CD4(+) T cells

140 gulation, resulting in sustained logarithmic cell killing both in vitro and in xenograft models in vi

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

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

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

144 of complement, eosinophils greatly increased cell killing by a complement-dependent cell-mediated cyt

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

146 d suggest a therapeutic approach to mitigate cell killing by C. difficile toxins A and B.

147 ating with bortezomib) resulted in increased cell killing by C93, indicating that the NF-kappaB respo

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

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

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

151 lapatinib with obatoclax caused synergistic cell killing by eliciting autophagic cell death that was

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

153 hondrial function plays an essential role in cell killing by lapatinib and obatoclax, as well as radi

154 triggered effective FcalphaRI-mediated tumor cell killing by macrophages already at low effector to t

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

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

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

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

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

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

161 oach in cancer treatment has been to trigger cell killing by targeting microtubule dynamics or spindl

162 7 lines lacking pAKT (P = .024) and exceeded cell killing by the PI3K-delta-specific inhibitor idelal

163 antibacterial and anticancer drugs initiate cell killing by trapping the covalent complexes formed b

164 ntial for T6SS-mediated secretion and target cell killing by Vibrio cholerae and Acinetobacter baylyi

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

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

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

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

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

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

171 We show that E4orf4 induced low levels of cell killing, caused by both caspase-dependent and -inde

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

173 fficient cell killing, whereby the extent of cell killing correlated strongly with the respective num

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

175 Cell killing depended on two properties of 6-TG: its inc

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

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

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

179 The cell killing effects of two representative voxels (isoce

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

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

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

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

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

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

186 onses, and antibodies engineered with potent cell-killing functions that are also resistant to hinge

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

188 nge of IgG1 results in a loss of Fc-mediated cell-killing functions without a concomitant loss of ant

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

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

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

192 anisms of caspase-dependent and -independent cell killing have been examined extensively, how these p

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

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

195 ubstitute for CED-9 in mediating HBx-induced cell killing in C. elegans, suggesting that CED-9 and Bc

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

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

198 cysteine completely reversed BSO+AUR-induced cell killing in FaDu and Cal-27 cells, while catalase an

199 pplementation only inhibited BSO+AUR-induced cell killing in FaDu cells.

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

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

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

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

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

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

206 with PMEL17 exhibits target-dependent tumor cell killing in vitro and in vivo.

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

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

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

210 Ribotoxins cleave essential RNAs for cell killing in vivo, and the bacterial polynucleotide k

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

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

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

214 ltiple PARP1 inhibitors to cause transformed cell-killing in short-term viability assays and synergis

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

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

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

218 ized FaDu, Cal-27, SCC-25 and SQ20B cells to cell killing induced by the EGFR inhibitor Erlotinib in

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

220 The mechanism of cell killing involves the induction of reactive oxygen s

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

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

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

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

225 duced cell death in lymphoma cells, and this cell killing is regulated by the Bcl-2 family of protein

226 Here we show that virus-induced cell killing is triggered by viral integration.

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

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

229 possible mechanism for CD8-LV enhanced tumor cell killing may be based on activation of the effector

230 Moreover, the mechanism of Het-S cell killing may be similar to the mechanism by which so

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

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

233 dysregulation of apoptosis through multiple cell-killing mechanisms.

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

235 Tumor cell killing mediated by Th-1-activated killer DCs was d

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

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

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

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

240 Consequently, maximal B cell killing of an initial and secondary B cell challeng

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

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

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

244 ly transferred tumor antigen-specific CD8+ T cell killing of cognate antigen-expressing melanoma cell

245 rolongation of the response by preventing NK cell killing of donor dendritic cells nor prior immuniza

246 nhibition of GSH and Trx metabolism enhanced cell killing of human head and neck squamous cell carcin

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

248 Thus, perforin-dependent CD4(+) T-cell killing of infected cells is an important mechanism

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

250 n of protein kinase D3 (PRKD3) could enhance cell killing of RAF and MEK inhibitors across multiple m

251 arides, which independently promote effector cell killing of S. aureus in vitro and protection agains

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

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

254 Sensitivity is essential in CD8+ T-cell killing of virus-infected cells and tumor cells.

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

256 in PDA tumors without stimulating neoplastic cell killing or decreasing the growth of tumors, whereas

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

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

259 e transcription factor controls two distinct cell-killing programs that act in parallel to drive apop

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

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

262 Mechanistic studies reveal that iNKT cell killing requires the tyrosine kinase Fyn, a known S

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

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

265 Cell killing studies determined that bacteriochlorins ar

266 s triggered similar levels of indirect tumor cell killing such as antibody-dependent cell-mediated cy

267 t1-Cre-activated diphtheria toxin fragment-A cell-killing system was employed.

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

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

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

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

272 rget gene expression and demonstrated potent cell killing that was selective for acute leukemia lines

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 expression in these cells restores infected-cell killing to 68% (P < 0.05), with similar levels of v

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

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

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

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

280 However, virus-induced cell killing was greatly enhanced in PyV-infected adar1(

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

282 Complete cell killing was observed for the PEG polysulfanes at 4

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

284 CD8(+)alphabetaT or gammadeltaT cells; tumor cell killing was partially restored by treating RS cells

285 Efficient cell killing was possible at nanomolar concentrations of

286 ls are known to induce granzyme B-mediated B-cell killing, we decided to evaluate the regulatory capa

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

288 Efficient replication and virus-mediated cell killing were rescued by the addition of exogenous d

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

290 ''-DTPA-cetuximab also resulted in efficient cell killing, whereby the extent of cell killing correla

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

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

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

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

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

296 ctivation of AKT and resulted in synergistic cell killing with AZD6244.

297 h anti-Gli1 shRNA resulted in supra-additive cell killing with cisplatin; shifting the cisplatin IC50

298 therapies hold promise of enhanced leukaemia cell killing with non-overlapping toxicities.

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.