ライフサイエンスコーパス: target cell

1 emagglutinin protein-mediated binding to the target cell.

2 enhanced inhibition of HIV-1 fusion with the target cell.

3 cal synapse (IS) between the NK cell and the target cell.

4 cell and short pulses for interrogating the target cell.

5 le effector proteins into the cytosol of the target cell.

6 totic granzymes, thereby rapidly killing the target cell.

7 sulted in accelerated detachment from an old target cell.

8 to activate receptors in the membrane of the target cell.

9 nship between HSV-1 and its relevant in vivo target cell.

10 ivering this cargo from donor to acceptor or target cell.

11 as IFITM subcellular localization within the target cell.

12 ially to the receptors, CD4 and CCR5, on the target cell.

13 ytotoxic machinery of the NK cell toward the target cell.

14 sponses to HIV-1-infected and peptide-loaded target cells.

15 LysRS that is relocalized to the nucleus of target cells.

16 the delivery of naked siRNA predominantly to target cells.

17 ut increasing capsid antigen presentation in target cells.

18 y, molecules known to be chemotactic for HIV-target cells.

19 om premature degradation before reaching the target cells.

20 ns that comprise the translocon itself, into target cells.

21 eptor by ligands expressed on the surface of target cells.

22 d at an early reverse transcription stage in target cells.

23 h hematopoietic target cells as well as GVHD target cells.

24 totoxic effector (TEFF) cells that eliminate target cells.

25 ines could induce resistance to the virus in target cells.

26 s able to interact with HIV-1 viral cores in target cells.

27 jugated and unconjugated oligonucleotides in target cells.

28 virus) to promote their internalization into target cells.

29 d at an early reverse transcription stage in target cells.

30 the duration of contacts between T cells and target cells.

31 del, in both cases describing CTLs that kill target cells.

32 and that can induce Fas-induced apoptosis in target cells.

33 stion, while protecting the integrity of the target cells.

34 132 receptor to deliver their signals within target cells.

35 apsid assembly and/or impair its function in target cells.

36 T-deficient NK cells to degranulate and kill target cells.

37 routes to invade and replicate within their target cells.

38 to modify the phenotype and function of the target cells.

39 y to a diverse array of molecularly distinct target cells.

40 g of a small natural cystine-rich peptide by target cells.

41 seases, and exert a wide range of effects on target cells.

42 can inhibit mycobacterial growth in infected target cells.

43 pressed CCR5 and therefore are potential HIV target cells.

44 for HIV-1 capture and infection of bystander target cells.

45 ia increase HIV risk by inducing mucosal HIV target cells.

46 ll activation responses toward hematopoietic target cells.

47 bound to specific antigens expressed on the target cells.

48 ntly infected primary B cells, EBV's natural target cells.

49 igrate from the site of infection and invade target cells.

50 c toolbox that enable neuronal inhibition in target cells.

51 nd strengthening insulin signal reception in target cells.

52 pathogens alike, breach this barrier to lyse target cells.

53 Jak) and phosphorylation of STAT proteins in target cells.

54 by regulating protein-trafficking events in target cells.

55 1 TDB was well tolerated and able to deplete target cells.

56 atively from both the starting cells and the target cells.

57 lular cholesterol in the entry of HSV-1 into target cells.

58 e unrelated to the binding of the MAb to the target cells.

59 establishment or reversal of latency in the target cells.

60 and kinetics of virus entry and fusion with target cells.

61 alized EBV infection of cultured and primary target cells.

62 argo, and subsequent inefficient delivery to target cells.

63 ll as new rounds of infection of susceptible target cells.

64 increase in NK cell activation against said target cells.

65 on whether the injured axons can find their target cells.

66 e, metabolic pathways and persistence of HCV target cells.

67 se transcription and productive infection in target cells.

68 se transcription and productive infection in target cells.

69 een used, aiming for higher efficacy against target cells.

70 y regulate gene expression and activation of target cells.

71 embrane attack complex (C5b-9) and opsonizes targeted cells.

72 ILY and developed a model of conditional and targeted cell ablation by generating floxed STOP-CD59 kn

73 nes that are up to 1,000-fold more potent on target cells, allowing specific signaling in selected ce

74 tem delivers effector proteins directly into target cells, allowing the bacterium to modulate host ce

75 ow that SitA is transferred serially between target cells, allowing the toxins to move cell-to-cell l

76 capable of transfer of therapeutic gene into target cells, along with long-term expression that avoid

77 es and compromise their ability to fuse with target cells, an effect that is antagonized by the viral

78 between the biochemical reaction networks of target cell and host, a drug can limit the flux of the s

79 environment that limits drug delivery to the target cell and therefore renders the therapy ineffectiv

80 gens, altering the biophysical nature of the target cell and thus reducing a critical energy barrier

81 proteins deter HIV-1 entry when expressed in target cells and also impair HIV-1 infectivity when expr

82 ansmission, and may increase HIV-susceptible target cells and alter epithelial integrity.

83 explicitly considering the heterogeneity of target cells and analysed datasets of cell-free HIV-1 si

84 for trafficking of HIV-1 in the cytoplasm of target cells and evasion of innate sensing mechanisms in

85 rus (ZIKV) rapidly establishes viraemia, the target cells and immune responses, particularly during p

86 Using primary effector and target cells and primary virus isolates, we studied the

87 These neurons communicate with target cells and regulate their long-term activity by po

88 oss this thin barrier, and to gain access to target cells and tissues, leading to systemic infection.

89 By transferring their cargoes into target cells and tissues, they now emerge as novel regul

90 VLVs triggered differentiation signaling in targeted cells and facilitated viral lytic infection via

91 o deliver active and therapeutic proteins to targeted cells and organs is an important tool for many

92 are bound to the biotinylated surface of the target cell, and anti-IL-22 and IL-17A detection antibod

93 that mediates virus attachment and fusion to target cells, and also facilitates HIV infection in vari

94 maging of cellular NO signal transduction in target cells, and the use of ultrasensitive detector cel

95 account the different susceptibility of the target cells as a continuous distribution.

96 vely, effectively eliminating drug-sensitive target cells as quickly as possible.

97 s II molecules recognized both hematopoietic target cells as well as GVHD target cells.

98 fates of these immobilized viral proteins in targeted cells as well as to isolate and enrich GAGs-ass

99 formance, ranging from the whole body to the target cells, as well drug retention in the nanoparticle

100 cells failed to produce IFN-gamma and lysed target cells at one third the capacity of Zap70(hi)Syk(h

101 bility of developed devices prior to that of targeted cells because most of the devices contact the b

102 ement cannot be performed while trapping the target cell, because the current method uses long ultras

103 n lead to different outcomes in terms of the target cell behavior and function.

104 cell conjugate formation between the NK and target cells but decreased NK cell cytolytic activity an

105 adhesion and fusion of viral particles with target cells but not their aggregation.

106 sing the amount of payload delivered to each targeted cell but increasing the number of cells that re

107 es the precise delivery of siRNA to specific target cells by controlling multiple parameters, thus pa

108 MV infects its target cells by coordinated action of the MV hemagglutin

109 These viruses enter target cells by endocytosis and low pH-dependent membran

110 resulting in reduced recognition of infected target cells by HIV-1-specific CD8(+) effector cells in

111 facilitate nanoparticle delivery to multiple target cells by measuring the uptake of biotinylated nan

112 fast communication between neurons and their target cells by propagating action potentials in a salta

113 Cytotoxic T lymphocytes (CTLs) kill target cells by the regulated release of cytotoxic subst

114 luded improved cytotoxic protein expression, target cell conjugation, and LFA-1-, CD2-, and NKG2D-dep

115 that are engaged during natural killer (NK)-target cell contact remains undefined.

116 ellular vesicles that move to the synapse on target cell contact.

117 ed tenofovir by metabolism more rapidly than target cells convert to pharmacologically active drug.

118 To kill multiple target cells, CTLs use endocytosis of membrane component

119 companied by altered expression of the c-Myc-targeted cell cycle regulators CCND1, CDKN1A and CDKN2D

120 d atherosclerosis through, at least in part, targeting cell cycle regulator cyclin A and connective t

121 (APC/C), a multisubunit E3 ubiquitin ligase targeting cell-cycle factors for destruction.

122 In that case, target cell damage appeared marginal compared with the e

123 xumab prevented the association of TcdA with target cells demonstrating that actoxumab neutralizes to

124 ltistage killing saturates at higher CTL and target cell densities.

125 se this dilution effect is strongest at high target cell densities; this can result in a peak in the

126 dependence of the total killing rate on the target cell density.

127 ting cells, as well as vesicle deposition on target cells, depend on interactions with macrophages.

128 In monkeys, assessment of safety and target cell depletion by the high- and low-affinity TDBs

129 the phosphatidylserine-binding sites on HIV target cells did not affect SERINC5 restriction or Nef a

130 o non-productive internalization pathways in target cells, did not change upon expression of SERINC5

131 activation, particularly Lck, downstream of target cell engagement or NKp30 ligation.

132 icity and cytokine production in response to target cell engagement or receptor ligation.

133 ed astrocytes only), offering advantages for targeted cell engineering.

134 capacities upon MR1-dependent recognition of target cells expressing physiological levels of surface

135 as fibroblasts progressively convert to the target cell fates remain unclear.

136 tes is characterized by insulin tolerance in target cells followed by a reduction of pancreatic beta-

137 g involves the formation of a synapse with a target cell, followed by delivery of perforin and granzy

138 Identification and selection of target cells for an in vivo live-manipulation are genera

139 inding to heparan sulfate on the surfaces of target cells for attachment and infection.

140 e implicated mast cells (MCs) as the primary target cells for DS.

141 Through the spatial positioning of RTKs in target cells for EGF and insulin action, the temporal ex

142 and the theoretical possibility that natural target cells for HIV and SIV in vivo could potentially c

143 re of GalNAc transferase isoforms in natural target cells for HIV and SIV in vivo could result in O-g

144 e cytokines can activate CD4(+) T cells, the target cells for HIV infection.

145 ys were validated in primary CD4(+) T cells, target cells for HIV-1.

146 ch is used to automate the identification of target cells for perturbation, as well as to validate th

147 ells in intestinal tissues are major primary target cells for SIV/HIV infection, and massive depletio

148 selected membrane proteins and small RNAs to target cells for the control of cell migration, developm

149 ivated CD4(+) T cells that are the preferred target cells for this virus in the infected host.

150 T-cell activation to avoid the generation of target cells for viral infection.

151 ffective immune response, also represent the target cells for viral infection.

152 Our studies identify IPCs as the main target cells for ZIKV.

153 mediate progenitor cells (IPCs) are the main target cells for ZIKV.

154 dvances include a variety of new methods for targeting cells for translating ribosome affinity purifi

155 survival and polarization signals or to kill target cells, for example in the form of antibody-drug c

156 Target cells from fixed preparations can be extracted an

157 netration induces tissue deformation, moving target cells from their initial location.

158 gnaling proteins and noncoding RNAs to alter target cell function.

159 oating) before it can be integrated into the target cell genome.

160 3s, in the presence of human T cells, killed target cells grown as monolayers at subnanomolar concent

161 -terminal toxin domains (CdiA-CT) to inhibit target-cell growth.

162 act between the bacterium and its eukaryotic target cell has been established, and the T3SS proteins

163 he molecular mechanism of GnIH action in the target cells has not been fully elucidated.

164 After invasion of a susceptible target cell, HIV-1 completes the early phase of its life

165 atory cytokine production and the killing of target cells; however, much less is known about its role

166 2 points of contact between the effector and target cell (ie, HA and sialic acid, respectively, and t

167 Our system keeps the target cell in focus while iteratively adjusting the pip

168 plasma, and that PIP2 on HDL is taken up by target cells in a scavenger receptor-BI-dependent manner

169 of the CRISPR-Cas9 genome-editing system to target cells in human body.

170 pecific CTLs producing cytokines and killing target cells in vivo at levels seen when using VLPs cont

171 iator of the effects induced by SW620Exos in target cells, in which we also found a significant incre

172 can elicit a number of mechanisms to delete target cells, including complement-dependent cytotoxicit

173 s rapidly shed in tissue culture and primary target cells, independent of entry pathway.

174 ell rounding and detachment of A549 cells by targeting cell integrin-extracellular matrix connections

175 apses, in which the sCAR-T cell, switch, and target cell interact in a structurally defined and tempo

176 ibronectin and dramatically inhibits exosome-target cell interaction.

177 with close cell-cell contacts at the NK cell-target cell interface that are required for NK cell acti

178 iral material is efficiently translocated to target cells into heterogeneous, protease-resistant, ant

179 dentify sites in TcdB that are essential for target cell intoxication, we identified a region at the

180 phocyte (CTL) and an infected or transformed target cell is a physically active structure capable of

181 e efficient and precise delivery of siRNA to target cells is critical to successful gene therapy.

182 The message delivered to the target cells is dependent on EV composition, which, in t

183 The entry of HIV-1 into target cells is mediated by the viral envelope glycoprot

184 tinin is also present in the membrane of the target cell, it can be cocaptured with MOG by MOG-specif

185 the total killing rate (i.e., the number of target cells killed by all CTLs) is well described by th

186 perforin, thereby leading to more effective target cell killing.

187 TAPs) approach enables protein inactivation, targeted cell killing and rapid targeted lineage ablatio

188 munization of cultures, autoimmunity or self-targeted cell killing, and the engineering or control of

189 Additionally, vigilin downregulation in target cells led to a significant increase in NK cell ac

190 ert distinct and differential effects at the target cell level.

191 th human PBMC in 3D spheroids generated from target cell lines to mimic the in vivo behavior and micr

192 HMBPP-induced Hill coefficients of 0.69 for target cell lysis and 0.68 in interferon secretion.

193 This bispecific antibody efficiently induces targeted cell lysis in the presence of effector cells at

194 al tasks with extensive neuronal mapping and targeted cell manipulations in mice, we explored how age

195 This suggests that UAG is subject to target cell-mediated activation - a novel mechanism for

196 transition, extending and inserting into the target cell membrane and then refolding into a postfusio

197 airpin structure can be activated on site at target cell membrane by reacting with two aptamers as 'd

198 of the peptides, while integration into the target cell membrane increases fusion inhibitor potency.

199 ecifically address whether distance from the target cell membrane influences the aforementioned effec

200 us viral fusion proteins (F) insert into the target cell membrane, and form a transient intermediate

201 e virus to facilitate membrane fusion with a target cell membrane.

202 diate that inserts the fusion loops into the target-cell membrane; and (iii) folding back of a cluste

203 strategy for HPV-associated malignancies by targeting cell metabolism.

204 reverse transcriptase inhibitor tenofovir to target cells more efficiently at a lower dose than tenof

205 rmulated to deliver the active metabolite to target cells more efficiently than TDF at lower doses, t

206 Targeting cell motility, which is required for dissemina

207 ression of these factors likely reflects the target cell of transformation rather than being required

208 analyzed the adaptation of IAV-H9N2 virus to target cells of a new host by passaging the virus three

209 ts and colocalized with neurons, the primary target cells of BDV infection.

210 Dendritic cells (DCs) are the main target cells of DENV, and we investigated their role in

211 RNAi) revealed that B cells were the primary target cells of rapamycin for the impaired humoral immun

212 However, the major target cells of the MF are the interneurons of CA3.

213 Target cells of TSLP in Th2 responses include CD4 T cell

214 inflammation, DCs have also been shown to be target cells of TSLP.

215 imilar to other arteriviruses, EAV primarily targets cells of the monocyte/macrophage lineage, which,

216 sing physical and chemical properties of the target cell or microorganism, are highlighted.

217 asses, reducing chemokine receptor levels on target cells or eliminating competent chemokine receptor

218 ly target the virus as it seeks to enter new target cells, or as it is expressed from previously infe

219 Stress-induced changes in target cell PAg levels are specifically detected by buty

220 diting via homology-directed repair (HDR) in targeted cells, particularly in vivo, provides an invalu

221 within a single fusion protein for mediating targeted cell penetration and non-covalent self-assembly

222 separation with single cell arraying of the target cell population, enabling direct on-chip tumor ce

223 of biological pathways and the isolation of target cell populations.

224 adient during compartmental transport within target cells, potential K28 oligomerization in the ER lu

225 sed gene clusters upon encountering hepatoma target cells presenting endogenously expressed HCV prote

226 uced reprogramming require the activation of target cell programs and silencing of donor cell program

227 IGF signaling is active, and NG2 inhibition targets cell proliferation and apoptosis.

228 Ligand binding in target cells promotes activation of Vgamma9Vdelta2 T cel

229 f pHLIP gets exposed to the cytoplasm of the target cell, providing a means to translocate membrane-i

230 d approximately linearly with the increasing target cell ratio.

231 monstrated that for mixed cells with various target cell ratios, the transit time delay increased app

232 and coated with adhesive ligands specific to target cell receptors.

233 ing cells, and second after virus binding to target-cell receptors.

234 ting that at least some LITRs have a role in target cell recognition and/or cytotoxicity.

235 aracter and TNF and IFNgamma production upon target-cell recognition.

236 with barrier protection and facilitating HIV-target cell recruitment.

237 nt for decades, the mechanism of action, and target cell, remain poorly understood.

238 respiratory tract and blanket alveoli where target cells reside.

239 stimulation in the presence of K562 or P815 target cells, respectively.

240 initiation of a contact to a new susceptible target cell resulted in accelerated detachment from an o

241 arises from a series of mutations in single target cells, resulting in defects in cell renewal and d

242 PD/CMM-targeted cells share neural crest origin and melanogenes

243 HLA-C typing of target cells showed that KIR2DS2 recognition was indepen

244 ation in liver, which indicates that Agt-ASO targets cell signaling pathways that specifically suppre

245 IL-15:IL-15Ralpha molecules are presented to target cells significantly affects its function as a vac

246 thalamic activation of cortical postsynaptic target cells, so called spike-trigger-averaged LFP (stLF

247 However, the killing of target cells sometimes requires multiple engagements (i.

248 ied immunohistochemically by antibodies that target cell-specific antigens in the cytosol or plasma m

249 man lung NK cells were hyporesponsive toward target cell stimulation, even after priming with IFN-alp

250 etic protein-2 (BMP-2) protein to responsive target cells, such as bone marrow-derived mesenchymal st

251 es on cellular membranes, may play a role in target-cell surface recognition or stabilization of the

252 nt production of immunoglobulin G antibodies targeting cell surface antigens expressed in multiple cG

253 we demonstrate that these anti-GRP78 AutoAbs target cell-surface GRP78, activating the unfolded prote

254 ating platelets were used in vivo to remodel target cell surfaces.

255 liferative and metabolic pathways as the HCV target cells survived.

256 approaches demonstrated that differences in target cell susceptibility can explain the non-randomnes

257 resistance factors, or molecules inside the target cell that fight HIV infection.

258 exhibited a basal alloreactivity against Bw4 target cells that increased upon activation, thus trigge

259 ay in the clinical management of asthma, the target cells that mediate their therapeutic effects are

260 ent inflammatory genes, as well as the major target cells that respond to IL-17 signaling.

261 dependent of the HLA C1 or C2 group, whereas targets cells that were only recognized by KIR2DL3 expre

262 reverse transcription of the viral genome in target cells, the mechanism by which uncoating is initia

263 RNA transcripts, microRNAs, and even DNA to target cells, thereby altering their function.

264 less of which subcellular compartment in the target cell they happen to be delivered to by the T6SS a

265 tes the selection of mAbs designed to delete target cells through specific effector mechanisms and pr

266 h delivers cytotoxic drugs specifically into targeted cells through internalization and lysosomal tra

267 It acts in the nucleus of vitamin D target cells to regulate the expression of genes whose p

268 A second, open design allows many non-targeted cells to pass through.

269 in vivo evidence that migratory DCs execute targeted cell-to-cell interactions with stationary MCs b

270 and shifted amounts of susceptible leukemia target cells toward late apoptosis in a cell killing ass

271 te infusion and recognition of donor-derived target cells transduced with the mismatched patient vari

272 ng substrate turnover for rapid depletion of target-cell tRNA.

273 engagement of erythrocyte receptors defines target cell tropism, activating downstream events and re

274 ce of the IL-10 signal and adipocytes as the target cell type mediating these effects.

275 Target cell type-dependent differences in presynaptic re

276 Our results point toward a postsynaptic target cell type-dependent regulation of Ca(2+) channel

277 unctional differences.SIGNIFICANCE STATEMENT Target cell type-dependent variability in presynaptic pr

278 Our results indicate target cell type-specific modulation of voltage-gated Ca

279 o CD40, leading to many effects depending on target cell type.

280 al cell-type-specific genes while activating target cell-type-specific genes is unclear.

281 acellular responses of the main postsynaptic target cell types and with biologically plausible assump

282 ng micro-RNA switch technologies that purify target cell types are also outlined.

283 These miRNAs can be transferred to insulin target cell types through mechanisms of paracrine or end

284 ransgenic mice, which express this sensor in targeted cell types.

285 mpounds exerted a rapid bactericidal effect, targeting cell wall synthesis.

286 e antibiotics in the beta-lactam family that target cell-wall biosynthesis.

287 nd efficient siRNA decomplexation inside the target cells was developed for tumor-targeted delivery o

288 on events involving the hepatocyte: the only target cell where HBV infection and replication take pla

289 mble into nanoparticles until they reach the target cells, where they are integrated into cell membra

290 -treated virions are prematurely degraded in target cells, whereas reverse transcriptase remains acti

291 nfection, cytotoxic lymphocytes must destroy target cells while avoiding nonspecific killing of surro

292 atterns of strong, weak, or noninhibition by target cells with defined HLA-B subtypes, which translat

293 effector molecules mediated the clearance of target cells with kinetics and efficacy comparable to th

294 ng via affinity approaches, particularly for target cells with reduced EGFR expression levels.

295 Target cells with reduced membrane-localized Flt1 (mFlt1

296 molecule inhibitors have been developed that target cells with specific DNA repair defects, providing

297 M CD4+ and CD8+ T cells, including the HIV-1-targeted cells with CD4+beta7hi/CCR5+ coexpression, as w

298 dscape of HIV-1 proviruses by preferentially targeting cells with specific types of defective proviru

299 ient in delivering full-length dystrophin to target cells, within a total genomic load of more than 1

300 Upon in vitro stimulation with target cells, Zap70(low)Syk(low) NK cells failed to prod