ライフサイエンスコーパス: target cell

1 athogen-infected or tumorigenic cells (i.e., target cells).

2 infected or tumorigenic cells (also known as target cells).

3 sitive disassembly switch after entry into a target cell.

4 iral membrane, blocking HIV-1 entry into the target cell.

5 release of perforin and granzymes toward the target cell.

6 hat the virus strikes within and without the target cell.

7 itional studies were conducted using a water target cell.

8 viral reverse transcription products in the target cell.

9 neously, such as in linking an effector to a target cell.

10 ny, and egress and dissemination to the next target cell.

11 which the viral genome is transferred into a target cell.

12 y of HIV-1: the requirement to bind CD4 on a target cell.

13 and hence are proficient for modulating the target cells.

14 ystems capable of delivering the catalyst to target cells.

15 tic tools for altering membrane potential in target cells.

16 display unique ability to infect nondividing target cells.

17 ributed to a vaccine-induced increase in SIV target cells.

18 VI secretion system (T6SS) against specified target cells.

19 iruses to establish infection in nondividing target cells.

20 in-converting enzyme 2 (ACE2) for entry into target cells.

21 tors against both prokaryotic and eukaryotic target cells.

22 AC polypeptide across the plasma membrane of target cells.

23 okine activation following contact with K562 target cells.

24 ), complement, and calreticulin, on distinct target cells.

25 ad to selectively deliver the warhead to the target cells.

26 lfate proteoglycan expressed by many natural target cells.

27 ive bacteria to deliver toxins into adjacent target cells.

28 these PS receptors to gain entry into their target cells.

29 varying cellular nucleotide levels in their target cells.

30 targeting, even after mRNA is delivered into target cells.

31 pos donor showed reactivity against HA-1Hpos target cells.

32 through the epithelium to infect underlying target cells.

33 asite viability, excystation, or invasion of target cells.

34 gulate the strength of Hedgehog signaling in target cells.

35 een different iPSC lines, largely due to off-target cells.

36 on to the postfusion state is independent of target cells.

37 ion of KSHV from producer iSLK cells to BJAB target cells.

38 orter for real-time separation of individual target cells.

39 elp eliminate virus-infected and transformed target cells.

40 capsid cores during subsequent infection of target cells.

41 elies on direct contact between infected and target cells.

42 ystem (Ad-CC9-LANA) into various KSHV latent target cells.

43 the coreceptor for HIV entry of HIV into new target cells.

44 lement activation by inhibitors expressed on target cells.

45 bilizing antibodies that are specific to the target cells.

46 T cells by split SEA-scFv fusion binding to target cells.

47 ntly saturate host restriction by TRIMCyp in target cells.

48 to reduce DPP4 binding and viral entry into target cells.

49 ssess the physiological impact to downstream target cells.

50 igens by using gene-edited stem cell-derived target cells.

51 a classic model of highly insulin-responsive target cells.

52 then transfer HTLV-1 virus particles to the target cells.

53 nt, such as mRNA, microRNA, and proteins, to target cells.

54 delivery of extracellular vesicle cargo into target cells.

55 capacity as well as the ability to kill IAV target cells.

56 cular attack particles (SMAPs), from CTLs to target cells.

57 thereby blocking activation of NF-kappaB in target cells.

58 enerate the proper transcriptional output in target cells.

59 specific receptors in the plasma membrane of target cells.

60 apse, to kill virus-infected and tumorigenic target cells.

61 act between immune cells and the surrounding target cells.

62 e on pathway for virion membrane fusion with target cells.

63 re degradation of the viral genome and IN in target cells.

64 rstand inflammatory signaling in on- and off-target cells.

65 slocation of HIV-2/SIV genome in nondividing target cells.

66 of Zika virus spread in clinically relevant target cells.

67 and the integrase enzyme for degradation in target cells.

68 alr association facilitates the infection of target cells.

69 become targets through which pathogens enter target cells.

70 ngineered T cells potentiated the killing of target cells.

71 he ability of cryopreserved NK cells to kill target cells.

72 d ErbB4 receptor tyrosine kinases on various targets cells.

73 ne synapse formation to trigger apoptosis of targeted cells.

74 binding directs doxorubicin into the aptamer-targeted cells.

75 2 receptor and mediate entry of virions into target cells(2-6).

76 cate that GRAP enables efficient noninvasive target cell ablation with high temporal and spatial prec

77 ma receptors were observed and suppressed by targeted cell ablation and/or gene knockout.

78 in plants) and are also efficient tools for targeted cell ablation in genetics, developmental biolog

79 system will be widely used for optogenetics, targeted cell ablation, subcellular manipulation, and im

80 oordinated daily waves of GABAergic input to target cells across the paraventricular hypothalamus and

81 te, compensatory adaptations which stabilise target cell activity through activity-dependent global s

82 esynaptic and postsynaptic sides to maintain target cell activity.

83 especially impacts the synthesis of membrane-targeted cell adhesion molecules (CAMs), measured by pul

84 Our virus-mimetic NPs showed outstanding target-cell affinity with picomolar avidities and were a

85 These HIV target cells also often appeared in large focal accumula

86 r function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promot

87 Fusion of HIV-1 with the membrane of its target cell, an obligate first step in virus infectivity

88 at bile salts enhance cell attachment to the target cell and increase the intrinsic affinity between

89 the cellular nuclear import pathways of the target cell and mediate their nuclear translocation thro

90 by NK cells can lead to direct lysis of the target cell and production of the signature cytokine IFN

91 sulted in a significantly reduced killing of target cells and a >50% reduction in CG fusion in total

92 ociated with reduced IAV-specific killing of target cells and a reduction in the number of IAV-specif

93 epertoires of proteins directly presented on target cells and cross-presented by professional APC, sp

94 HIV-1 integrates into the genome of target cells and establishes latency indefinitely.

95 context of 80% donor chimerism in total HIV target cells and greater than 99% probability of remissi

96 cribed suppressor of YAP activity in insulin target cells and provide insight into cross-talk between

97 otein complexes from untimely degradation in target cells and provide the first causal link between h

98 otects the vRNP from untimely degradation in target cells and provide the mechanistic basis of how CA

99 te target cells, enabling isolation of these target cells and sequencing of the cognate TCR ligand.

100 ial role in subsequent T-cell recognition of target cells and the specificity of the immune response.

101 , that will allow them to be taken up by the target cells and then released in the appropriate cellul

102 se ADAM10 on the surface of a broad range of target cells and tissues(2,5,6).

103 iated with a decrease of viral attachment to target cells and viral entry due to diminished exposure

104 through a membrane to efficiently colocalize target cells and virus particles.

105 lose cell-cell contact (between effector and target cell) and formation of immunological synapses are

106 ape and intensity, opsin distribution in the target cell, and cell morphology, which affect the spati

107 s of activation depending on sEV population, target cell, and the function of the endosomal sorting c

108 producing T-cell uropods contacting putative target cells, and (iii) macrophages engulfing HIV-1-prod

109 YT cells loaded with GrB attacked MDA-MB-231 target cells, and active GrB influenced its target cell-

110 ments and C5b-9 are deposited on TF1PIGAnull target cells, and complement factor Bb is increased in t

111 e cognate HLA class I molecules on potential target cells, and recent studies imply that an HLA-B dim

112 opriate model for these viruses because many target cells are present, including basal keratinocytes,

113 sion of complement inhibitory proteins on MM target cells as well as DARA-induced depletion of CD38hi

114 Delivering the transgene of interest to target cells at levels high enough to be therapeutically

115 molecular cargo from bacterial membranes to target cells at the host-pathogen interface.

116 the Enterobacteriaceae, has evolved a second target cell attachment mechanism.

117 From a pathway-targeted cell-based screen, we identified a non-nucleoti

118 arrier-mediated delivery, including receptor-targeted, cell-based, blood-brain-barrier disrupting and

119 rom vMC021L-HA exhibit a marked reduction in target cell binding and an increase in dissolution, both

120 During HIV-1 entry into target cells, binding of the virus to host receptors, CD

121 reshold dose in vivo, resulting in decreased target cell burden, decreased serum and tissue-bound aut

122 cted killing activity against Env-expressing target cells but began to decline after 3 to 6 weekly do

123 ting receptors to discriminate and eliminate target cells but they can also produce immunoregulatory

124 hod for delivering gene-editing machinery to target cells, but a major challenge remaining is that mo

125 activates caspase-independent pyroptosis in target cells by directly cleaving GSDME at the same site

126 inhibitors to trap HIV-1 virions attached to target cells by Envs in an extended pre-hairpin intermed

127 elope glycoprotein mediates virus entry into target cells by fusing the virus lipid envelope with the

128 e Mycobacterium tuberculosis or infection of target cells by HIV elicited TFEB activation in an IRGM-

129 ) proteins induce transcriptional changes in target cells by inhibiting the proteolytic processing of

130 ells often identify their correct partner or target cells by integrating information from multiple re

131 ytotoxic CD8(+) T cells can effectively kill target cells by producing cytokines, chemokines, and gra

132 hat affect numerous viruses at two steps: in target cells by sequestering incoming viruses in endosom

133 associated invariant T cells, recognition of target cells by the TCR was independent of bacterial loa

134 This approach assumes that off-target cells cannot incorporate these analogs.

135 aled that step by step increase in bacterial target cells caused to gradually increased fluorescence

136 ), two Tec-family kinases expressed in HIV-1 target cells (CD4 T cells and macrophages, respectively)

137 ion of T cells expressing an orphan TCR with target cells collectively presenting a library of peptid

138 herapeutic that more accurately mimics HIV-1 target cells compared with monomeric sCD4 and dimeric CD

139 ia, was observed in all macrophage, mAb, and target cell conditions tested in vitro and was also seen

140 Target cell contact reduced intracellular GrzB and perfo

141 s suggest that therapeutics that mimic HIV-1 target cells could prevent viral escape by exposing a un

142 cell types use multiple strategies to induce target cell death including Fas/CD95 activation and the

143 re secreted into the synaptic cleft inducing target cell death.

144 s the completion of reverse transcription in target cells, demonstrating that reverse transcription i

145 contributed to beta2 microglobulin-deficient target cell destruction in vivo.

146 nteraction mediated between a T cell and its target cell dictates its function and thereby influences

147 ir inability to migrate, plant cells rely on targeted cell division and expansion to regenerate wound

148 ize viral glycoproteins to efficiently enter target cells during infection.

149 Targeting cells early during the infection cycle would b

150 ide-MHCs led to specific labeling of cognate target cells, enabling isolation of these target cells a

151 ning antigen 1 (LFA-1) on the surface of the target cell engaging with its ligand, ICAM-1, on the sur

152 cargos originating from the source cells to target cells, EVs can also be used as a therapeutic mean

153 and are compatible with robust infection of target cells expressing large amounts of the viral recep

154 We find that IL-2C targeting cells expressing IL-2 receptor beta cause an a

155 generated a viral construct that selectively targets cells expressing promoter IV-derived Bdnf transc

156 mutant Haloferax strains with enhanced self-targeting, cell fitness decreases and microhomology-medi

157 as a unique yet unidentified role within the target cell for FSGS, the kidney podocyte.

158 s, in combination with the separation of the target cells for downstream analyses, provide powerful n

159 we confirmed that CD68+ macrophages are the target cells for EBOV in affected ganglia.

160 llular degradation in the two most important target cells for HIV infection.

161 lymphoid tissues by reducing the numbers of target cells for infection and persistence.IMPORTANCE Al

162 ge plasmablasts and macrophages as principal target cells for SFTSV infection in fatal SFTS.

163 t transport of morphogen from source cell to target cell, for example, via cytonemes.

164 re, we show that these compounds inhibit HIV-target cell fusion independently of viral tropism.

165 ts isomer, thymol, were shown to block virus-target cell fusion while not perturbing other stages of

166 The targeted cells generate glucocerebrosidase-expressing ma

167 r other than the virus receptor expressed by target cells has been found to accelerate the loss of an

168 However, the source, route, and function in target cells have not been formally established for spec

169 ic extracellular vesicle-associated cargo on target cells have stoked interest in extracellular vesic

170 RNA sequencing, we show that Gli1- and Ascl1-targeted cells have highly similar yet distinct transcri

171 cs for synchronous upconversion-mitochondria-targeted cell imaging, in vivo NIR-II osteosarcoma imagi

172 delineation of the underlying biology of the target cell in INS - the glomerular podocyte - has trans

173 problem: if injected toxins can quickly lyse target cells in addition to killing them, the T6SS becom

174 and high-throughput genetic modification of target cells in cellular therapy manufacturing applicati

175 d therefore be harnessed to deliver drugs to target cells in diseases such as cancer.

176 ding, half-life, or their ability to deplete target cells in FcgammaR/FcRn humanized mice.

177 Some TCR Vdelta1 clones recognized target cells in the absence of parasite-derived Ags, thu

178 t influence the granularity and dimension of target cells in the flow cytometry system.

179 layer and a more apical distribution of HIV target cells in the human ectocervix, which could confer

180 +) T-cell-mediated killing of antigen-loaded target cells in vivo.

181 miR-127, which is functionally activated in target cells, inhibits growth and spontaneous metastasis

182 stemically administered drugs to reach their target cells inside the nucleus pulposus (NP), the centr

183 ugh fusion of cytotoxic granules (CG) at the target cell interface, the immune synapse, to kill virus

184 nes (e.g., IL-2) are polarized to the T cell-target cell interface, whereas the other cytokines are d

185 , BETP degradation by ARV-825 simultaneously targets cell intrinsic signaling, stromal interactions a

186 genomic RNA and regulates steps essential to target-cell invasion(1).

187 The delivery of therapeutic agents into target cells is a challenging task.

188 cells, effective delivery to the appropriate target cells is a major challenge of siRNA-based therapy

189 ch ectoenzymatic hemagglutinin activation by target cells is a mandatory prerequisite for binding to

190 taining safety by minimizing delivery to off-target cells is a prevalent challenge in the field of ge

191 delivery of multiple nucleic acid probes to target cells is critical for nucleic acid-based methods

192 affinity by KSHV.IMPORTANCE Virus entry into target cells is the first step for virus infection.

193 sitizer, molecular oxygen, and light to kill target cells, is a promising cancer treatment method.

194 Unlike Prf1-/- mice, they showed normal target cell killing and normal clearance of viral RNA an

195 icit a myriad of cellular responses, such as target cell killing and the secretion of different cytok

196 t CD2 costimulation plays a critical role in target cell killing by freshly isolated human CD8(+) T c

197 B and proinflammatory cytokines, leading to target cell killing.

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

199 ation of tissue rejection through individual target cell-killing events in vivo.

200 totoxic granules involved in T cell-mediated target cell-killing, and monomeric teal fluorescent prot

201 pores in the plasma membrane of pathogens or targeted cells, leading to osmolysis.

202 Manipulation of miR-128 levels in HIV-1 target cell lines and in primary CD4(+) T-cells by overe

203 However, its practicality can be limited if target cell lines are difficult to transfect and do not

204 or high concentrations of cholesterol in the target cells' lipid membrane.

205 the ectocervical tissue architecture and HIV target cell localization.

206 Targeted cell loss in whole organisms has been typically

207 we identified the sialic acid content of the target cell membrane as an important inhibitory factor f

208 urface glycoproteins to bind and fuse with a target cell membrane.

209 ) protein catalyzes fusion between viral and target cell membranes to initiate infection.

210 ated multiprotein nanomachines that puncture target cell membranes.

211 implicated in effector translocation across target cell membranes.

212 s chemokine receptor CCR5) to fuse viral and target-cell membranes.

213 deoxy-d-glucose (2DG), a pharmaceutical that targets cell metabolism.

214 ibroblasts and the expression of profibrotic targets, cell migration, and soft agar colony formation

215 In the target cells, miR-274 down-regulates Sprouty (Sty) throu

216 transcriptional activity in classic insulin target cells, namely HepG2 and C2C12.

217 In contrast, Cyp24a1 regulation in nonrenal target cells (NRTCs) is limited to induction by 1,25(OH)

218 es not affect Cyp27b1 expression in nonrenal target cells (NRTCs).

219 3(+) regulatory T cells (Tregs) are the main target cells of IL-27, mediating its immunoregulatory fu

220 expression and a more basal location for HIV target cells of the control group.

221 other cell types, including VPAC2-expressing target cells of VIP, are, however, not understood.

222 We characterized the primary target cells of ZIKV infection and the subsequent mucosa

223 e of the toxin-induced growth retardation of target cells only weakly impacts the composition of the

224 ory and enact downstream responses; and 3) a target cell or tissue to receive the signal and convert

225 This nanogel does not recognize target cells or disrupt endosomal vesicles in its unmodi

226 This phenomenon provided Env to target cells prior to de novo Env expression, resulting

227 b inhibits FGFR signaling and its downstream targets, cell proliferation, the angiogenic rescue progr

228 convertase furin, reducing its dependence on target cell proteases for entry.

229 y, while most mutations concomitantly affect target cell protection and negative imprinting, a region

230 uestration of incoming virions in endosomes (target cell protection) and with the production of virio

231 p between negative imprinting of virions and target cell protection.

232 ty by IFITMs and about its relationship with target cell protection.

233 In the presence of target cell receptors, an immunocomplex was formed betwe

234 of human immunodeficiency virus (HIV-1) bind target cell receptors, triggering changes in the shape o

235 ollably generate reactive oxygen species for targeted cell regulation.

236 ivities reprogram the immunological state of target cells remains poorly understood.

237 our major steps: attachment and entry into a target cell, replication of the viral genome, maturation

238 The penetration of enveloped viruses into target cells requires the fusion of the lipid envelope o

239 nalization of the pathogen by remodeling the target cell's plasma membrane and recruiting sorting nex

240 Virion-packaged Vpr is released in target cells shortly after entry, suggesting it is requi

241 in biosensor conformation that accompany the targeted cell signaling event.

242 l cells, and this joint mechanism leads to a target cell size where cellular proliferation capacity i

243 proliferation capacity being maximized at a target cell size.

244 Despite growing interest in targeting cell softening to impede invasion and metastas

245 h mechanisms of Raf activation, and point to targeting cell-specific, chromatin-accessible, and paral

246 Poor target cell specificity is currently a major shortcoming

247 upture, which may facilitate engineering the target-cell specificity of pore-forming proteins.

248 CD83 CAR T cells eradicate pathogenic CD83+ target cells, substantially increase the ratio of regula

249 NK cells can recognize target cells such as virus-infected and tumor cells thro

250 xogenous sequences into valuable therapeutic target cells, such as hematopoietic stem cells or T cell

251 can act as cofactors for antitumor Abs that target cell surface proteins, suggesting that the MARCH

252 these responses, regardless of cell type and targeted cell surface molecule, suggest the Type I and I

253 Antibody combinations targeting cell surface receptors are a new modality of c

254 uated a novel tumor penetrating peptide that targets cell surface p32, LinTT1 (AKRGARSTA), as a GBM t

255 icity, and highly selective binding to their target cell-surface receptors.

256 ion in acute models of HS through mechanisms targeting cell swelling-induced microcirculatory failure

257 ntify these cells in the presence of 90% off-target cells that carried only the AT1R.

258 n significantly higher concentrations of HIV target cells that may be susceptible to HIV infection.

259 ane proteins are transferred specifically to target cells that present cognate peptide-major histocom

260 n mature osteoclasts compared to the primary target cell, the macrophage, but is able to impair the m

261 ntially to the receptors CD4 and CCR5 on the target cell, the metastable Env trimer is triggered to u

262 When the probes are delivered into target cells, the nanogel shells are degraded in acidic

263 Upon entry into target cells, the viral core undergoes a process termed

264 d science, tissue engineering, and spatially targeted cell therapies.

265 tween cytotoxic T lymphocytes (CTLs) and the target cells they aim to destroy is accompanied by reori

266 a natural killer or T cell has identified a target cell, they form a tight contact zone, the immunol

267 The sensing of target cells, thought to be mediated by the distal tip o

268 CD8(+) cytotoxic T cells kill target cells through direct cell-cell contact.

269 veals cell-intrinsic responses of a key lung target cell to SARS-CoV-2 infection and should facilitat

270 In mice, iv8 induced target cells to expand and mature in the context of a po

271 apies that eliminate DTCs and/or effectively target cells transitioning to proliferation promises to

272 If a target cell triggers NK cell cytotoxicity, lytic granule

273 We find that high glucose in EV-targeted cells triggers pro-inflammatory stimuli via mTO

274 ctors to both introduce fate programs of the target cell type and erase the identity of starting cell

275 These studies establish the main target cell type and region of the gut for productive mu

276 the specification of progenitors toward the targeted cell type.

277 galy, viral loads, and infection of multiple target cell types in the spleen and the bone marrow.

278 ion of causal genes, functional variants and target cell types.

279 ation and promote early infection in natural target cell types.

280 dation and clearance; 2) selective homing to target cell types; and 3) cytoplasmic release of the siR

281 expression, synaptic targeting (identity of targeted cell types), activity pattern during distinct b

282 inactivates small GTPases in the cytosol of target cells, ultimately leading to cell death.

283 A solution would be to target cells using specific combinations of proteins pre

284 y selection, we evaluated internalization by target cells using streptavidin-linked antibodies conjug

285 eillance for signatures of "altered self" on target cells, via a membrane-linked gammadelta TCR recog

286 ence of a coordinated signaling network that targets cell wall structure and is regulated in part via

287 Activity against CMV-infected target cells was assessed by release of cytokines (inter

288 ADCC against HIV-infected target cells was elicited in rabbits but not in RM, and

289 Infection of 293FT target cells was possible only if the cells were enginee

290 presented by HSV-1-infected HLA-DR-positive target cells were recognized mainly by effector memory C

291 by cells, the signal probes rather than the target cells, were directly combined with the electrode.

292 ies-the Fab domains bind the antigens on the target cell, whereas the Fc domain binds to the activati

293 o premature dissociation of CA from vRNPs in target cells, which was accompanied by proteasomal-indep

294 ithout sacrifice of animals, labeling of the target cells with a nontoxic and stable contrast agent i

295 te a novel viral gene expression strategy to target cells with specific miRNA expression using miRNA-

296 In contrast, co-treatment of CBD-targeted cells with inhibitors of PI3K-AKT-NF-kappaB, IK

297 s for sensitive detection and enumeration of targeted cells with minimally invasive methods, have the

298 Preclinical studies targeting cells with an antibody to "activated" matripta

299 nd preventing the virus from reaching immune target cells within the mucosa.

300 ave the unique ability to recognize and lyse target cells without prior exposure.