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1 gment holoreceptors that remain bound at the cell surface.
2 ses at least some of these proteins from the cell surface.
3 phate receptor-mediated endocytosis from the cell surface.
4 indicate that receptors can function at the cell surface.
5 ch are required for MHC-I trafficking to the cell surface.
6 -driven interaction of RET with GFRAL on the cell surface.
7 stress that breaks the mature F-pilus at the cell surface.
8 ed ability to anchor latent TGF-beta1 on the cell surface.
9 A-B*57:01 altering peptides displayed on the cell surface.
10 SCUBE and SHH, recruiting the complex to the cell surface.
11 ia expression of LDL receptors (LDLR) at the cell surface.
12 and key virulence factor PfEMP1 to the host cell surface.
13 for those that enhance TREM2 protein at the cell surface.
14 bserved when the channel is expressed at the cell surface.
15 utants in presenting latent TGF-beta1 to the cell surface.
16 ndosomes to a PI3K amplification loop at the cell surface.
17 esulted in the accumulation of IFITM3 at the cell surface.
18 n export by destabilizing ferroportin on the cell surface.
19 jor route for cargo internalisation from the cell surface.
20 in the abundance of cognate receptors on the cell surface.
21 enhance pertactin secretion to the bacterial cell surface.
22 hether LapA is retained or released from the cell surface.
23 d by assembly of curli amyloid fibres on the cell surface.
24 iated lipids and proteins from the bacterial cell surface.
25 ften modulate growth factor signaling on the cell surface.
26 g high-avidity molecular interactions on the cell surface.
27 zing intact non-MHC proteins on the opposing cell surface.
28 of large clathrin-containing "scars" on the cell surface.
29 ar fluid, potentially enabling action at the cell surface.
30 ibition of the TMK1 signaling pathway at the cell surface.
31 rely on global or local deformations of the cell surface.
32 ipids and E-cadherin molecules at the living cell surface.
33 nse sequence diverse peptide hormones at the cell surface.
34 o help direct 34 different proteins onto the cell surface.
35 me 2), which is expressed on the endothelial cell surface.
36 s often wrap membrane extensions around stem cell surfaces.
37 charge interactions with negatively charged cell surfaces.
38 g of FHR5 oligomers to C3b deposited on host cell surfaces.
39 in the 2D plane of the cortex can pattern 3D cell surfaces.
40 ein families are expressed on infected blood cell surfaces.
43 ation, yet therapy-mediated removal from the cell surface activates cancer-protective beta-arrestin-b
46 CS-assisted shRNA screens, we identified the cell-surface adhesion receptor CD44 as a key positive re
48 ificant investments in the identification of cell surface Ags, there is a paucity of targets that mee
49 aling pathways by forming a complex with its cell surface alpha-receptor, IL-11Ralpha, and the beta-s
50 actin-rich protrusions that extend from the cell surface and are important for cell-cell communicati
51 ependent IFN-I signaling originates from the cell surface and depends on MyD88; it involves combined
52 encoded RNAs that are stably attached to the cell surface and exposed to the extracellular space, her
53 glycoprotein promotes attachment to the host cell surface and fusion of the viral and host membranes.
54 expression of envelope (Env) trimers at the cell surface and increased Env incorporation into virion
55 regulate the translocation of CD107a to the cell surface and kill cellular targets, while NKG7 also
56 s required for sialic acid expression on the cell surface and mediate reovirus infection of microglia
57 ate, NV18.1, that down-regulate MR1 from the cell surface and retain MR1 molecules in the endoplasmic
59 ubiquitous glycosaminoglycan located on the cell surface and tethered to proteoglycans such as synde
60 us iRhom1 and -2 proteins are present on the cell surface and that iRhom2 also is present on the surf
61 As a result of unequal ion fluxes across cell surface and TT membranes, limited diffusion may gen
62 lative to that of wild-type SERINC5 from the cell surface and with enhanced exclusion of the mutant p
66 ulting in significantly increased NIS at the cell-surface and markedly increased RAI uptake in mouse
67 ion of antigenic cargo, final release to the cell surface, and engagement with their cognate receptor
68 providing a first anchor of the virus to the cell surface, and further facilitate high-affinity bindi
69 ative LGR4 and LGR5 existed as dimers on the cell surface, and LGR5 interacted with both FZD and LRP6
70 or to areas of E2 expression on the infected cell surface, and LIF enhanced the antiviral effects of
71 f Salmonella Typhimurium to hydrophobic host cell surfaces, and contributes to efficient gut coloniza
72 d exhibit enhanced interactions with plasma, cell-surface, and intracellular proteins, which facilita
76 y of adoptive T cell therapies targeting the cell surface antigen CD19 has been demonstrated in hemat
77 ings identify ALPP2 as a true tumor-specific cell surface antigen whose tissue specificity enables th
78 e a Gram-negative cell envelope and a unique cell surface antigen; therefore, this approach should be
80 eagent can directly be used for detection of cell surface antigens obviating the laborious steps of p
85 eshwork in the cells' interior, MTs near the cell surface are preferentially aligned with the PM.
87 cell, and ACE2, its docking site on the host cell surface, are extensively glycosylated, making them
90 Alternatively, polysaccharides hydrolyzed by cell-surface attached or free extracellular enzymes (ext
95 natural transformation by extending from the cell surface, binding to exogenous DNA, and retracting t
96 we show that endogenous iRhom1 and -2 can be cell surface-biotinylated on mouse embryonic fibroblasts
98 of the endoplasmic reticulum (ER) and to the cell surface, but not to mitochondria, endosomes, or lip
99 f Nef is to remove the CD4 receptor from the cell surface by hijacking clathrin- and adaptor protein
100 ce to a soluble form of PrP(C) shed from the cell surface by proteases in the A Disintegrin And Metal
102 ylated PrPC that had been liberated from the cell surface by the metalloproteinase, ADAM-10, in combi
103 signal transduction ligand that activates a cell surface calreticulin-mediated, proarthritogenic, bo
105 ing non-natural amino acid incorporation and cell surface click chemistry in bacteria with high-throu
108 use outer membrane vesiculation to exchange cell surface components, thereby increasing survival dur
113 ntrolling TPP formation and transport to the cell surface, enabling us to propose an updated model of
117 edures required for phosphoflow often affect cell surface epitopes or mAb conjugates, precluding the
120 94 x 10(-13)) and was associated with HLA-DP cell surface expression in healthy individuals (p = 2.04
122 lammatory cytokine stimulation increased the cell surface expression of ICAM-1 and induced cell surfa
123 the mature protein, alpha1(Lys374Serfs)*(25) Cell surface expression of mutant murine GABA(A)Rs is se
125 y revealed that chlamydial infection induced cell surface expression of T-cell homing and activation
127 T cells (TCR-T cells) are not restricted by cell surface expression of their targets and are therefo
128 ubset is IgM(+), but due to low/negative IgD cell surface expression, it was named B-cell IgD low (BD
129 virus from host cells by down-regulating the cell-surface expression of the host restriction factor t
130 cells may therefore utilize their TCR like a cell-surface Fab repertoire, somewhat analogous to engin
131 ese dynamic FtsZ assemblies is to sample the cell surface for the proper location for the Z-ring.
132 vivo chemico-genetic approach that applies a cell-surface fragment complementation strategy, Split-Tu
133 with C-terminal truncations showed increased cell surface Frizzled and Wnt/beta-catenin signaling and
135 ls exhibited significantly reduced levels of cell-surface Gb3, and both AHR knockout HeLa cells and t
136 ognostically associated secreted factors and cell surface genes, and computationally reconstruct cros
137 rease in cellular GLUT4 protein and enhanced cell surface GLUT4 levels in response to AMPK activation
138 glycosylation but does not enter other major cell surface glycan types including Asn(N)-linked glycan
145 gically extracellular compartments or on the cell surface; hence, diverse secretion systems evolved t
146 of the C-terminal domains of OPG is to bind cell surface heparan sulfate (HS), but the in vivo evide
148 y altering the number of transporters on the cell surface, however there is some disagreement on just
149 u interacted with human BST-2, downregulated cell surface human BST-2 expression, and facilitated HIV
152 expression of TMPRSS13 protein on the cancer cell surface in CRC patient samples; in contrast, the ma
153 strocytes resulted in their retention at the cell surface in the form of functional gap junctions ind
154 antibody bound to HLA antigens on the donor cell surface in their native conformation that is not im
158 signaling (MAVS)-dependent remodeling of the cell surface, increasing surface presentation of HLA pro
160 on and increased alphavbeta3 and alphavbeta5 cell surface integrin expression as a result of combined
161 nesis and remodeling or by signaling through cell-surface integrin receptors to promote cell adhesion
162 gnaling is generated and transduced from the cell surface into the intercellular space and will aid i
165 factor signalling is also controlled at the cell surface level via binding to heparan sulfate proteo
168 -associated, gingipain-dependent decrease in cell surface levels of the intercellular adhesion molecu
169 eover, RalGAPA1 deficiency clearly increased cell-surface levels of lipid raft components in detached
171 that modulate the biophysical properties and cell-surface localization of VGSC alpha subunits and par
172 lar trilineage differentiation potential and cell surface marker expression as bone marrow hMSCs.
173 eceptor superfamily member OX40 (CD134) is a cell surface marker that is highly specific for activate
174 single skeletal stem cell population through cell surface markers and the development of single-cell
176 rences between these profiles, we identified cell surface markers, CD69 and CD36, whose genes were di
177 blood frequencies of MAIT cells, defined by cell surface markers, decline during tuberculosis (TB) d
179 nd proteomic approaches to identify specific cell-surface markers for cardiac PW1(+) cells and found
180 ytosis activity, viability and expression of cell-surface markers, from tens of thousands of single i
181 lar, the levels of antigen expression at the cell surface may determine antibody-mediated cell death.
182 stic insight into how O-glycan structures on cell surface modulate their sensitivity to apoptotic sti
183 ponses, regardless of cell type and targeted cell surface molecule, suggest the Type I and II curves
188 eome-instructed in vivo screen identified 20 cell-surface molecules regulating neural circuit assembl
191 to a C-end rule (CendR) motif that binds to cell surface neuropilin-1 (NRP1) and NRP2 receptors.
192 identification and quantification of unique cell surface O-glycans from different cell lines and the
194 sults demonstrate that glioblastomas exploit cell surface O-linked glycans for local and distant immu
195 ormal tissues, but which is expressed on the cell surface of human embryonic stem cells and many canc
199 e protein that is highly up-regulated on the cell surface of several human cancers, making it a promi
200 may mediate host-parasite interaction at the cell surface, offering promising targets for blocking th
203 structural homology searches reveal no other cell-surface or secreted domains in vertebrates that res
208 ne phosphorylation motifs to the promiscuous cell-surface phosphatase CD45(2,3), which results in the
210 of its coding gene dramatically reduced the cell surface poly-N-acetyl-lactosamine and led to hypers
212 iosynthesis and processing lead to decreased cell surface presence of GPI-anchored proteins (GPI-APs)
213 l non-amyloidogenic processing of APP at the cell surface promotes ferroportin stabilization to decre
214 We have investigated the utility of the cell surface protein CD26 to identify functionally disti
216 Here we report that mice lacking CD137, a cell surface protein used in several studies as a marker
221 lls (MSCs) are characterized by their unique cell surface proteins and aberrant signaling pathways.
223 own, and especially the identity and role of cell surface proteins that are responsible for sperm-egg
224 PORTANCE Human leukocyte antigens (HLAs) are cell surface proteins that regulate innate and adaptive
227 is invaluable for studying cell populations, cell-surface proteins are often integral markers of cell
229 1 (NEGR1) and neurotrimin (NTM) are abundant cell-surface proteins found in the brain and form part o
230 ic KRAS alters the expression of a myriad of cell-surface proteins implicated in diverse biological f
231 PC population is proliferative and marked by cell-surface proteins, including PDGFRalpha, Sca1, and C
232 These data point to N-MADD-4B processing and cell-surface proteoglycan binding as two possible mechan
233 ic analysis reveals that Rab11b controls the cell surface proteome, recycling proteins required for s
236 ght the power of temporally resolved in situ cell-surface proteomic profiling in discovering regulato
237 s in surface ultrastructure with the loss of cell surface protrusions and poor aggregation, resulting
238 ich is up-regulated by HCC cells, stabilizes cell surface PVR, which interacts with TIGIT, an inhibit
239 tivating mutations in the type I BMP/TGFbeta cell surface receptor ACVR1, which over-activates signal
243 asis, mechanisms underlying the role of this cell surface receptor in CRC have not been defined.
245 ceptor (ADR) selectively recognizes 4-1BB, a cell surface receptor temporarily upregulated by activat
246 s a molecular target; an epithelium-specific cell surface receptor that is low or undetectable in hea
247 gnal triggers cell polarization by promoting cell surface receptor-mediated nanoclustering of signali
248 sent an alternative approach for attenuating cell-surface receptor signalling, termed receptor inhibi
253 d Flo11A domains, provide a rationale of how cell surface receptors have evolved in microorganisms to
254 on adjacent cells, stabilization of adjacent cell surface receptors on the same cell, and interaction
255 ntegrins are a large family of heterodimeric cell surface receptors that bind prototypic ligands on n
263 ect relevance to the interaction of HCV with cell-surface receptors and neutralising antibodies.
267 2) is initiated by virus binding to the ACE2 cell-surface receptors(1-4), followed by fusion of the v
268 meable, making them useful for modulation of cell-surface receptors, while monosulfonated BODIPY reta
269 tate high-affinity binding to virus-specific cell-surface receptors, while other glycans function as
273 ual recycling of beta1 integrins back to the cell surface, resulting in defective FA reformation.
278 sugar and its subsequent incorporation into cell-surface structures is implicated in a variety of ba
279 ge suggest that ALPPL2 could be an excellent cell surface target for therapeutic development against
280 1 (TFR1) is common across cancer and permits cell-surface targeting of specific therapies in preclini
281 verage other hallmarks of cancer or specific cell-surface targets are gradually finding a niche in th
283 , and additional interacting proteins at the cell surface that influence the fidelity of insulin rele
284 ained introns can be presented on the cancer cell surface, the development of personalized cancer vac
285 ates the recycling of MR1 molecules from the cell surface through endosomal trafficking compartments
288 ent attachment of targeting ligands at the T-cell surface through the application of SpyCatcher-SpyTa
289 18 regulates kinectin-1 transport toward the cell surface to form ER-FA contacts, thus promoting FA g
291 e endo-O-sulfatases are transported onto the cell surface to liberate the 6-sulfate groups from the i
292 -induced, sterol-dependent nanoclustering of cell surface transmembrane receptor kinase 1 (TMK1) is c
293 that in MDA-MB-231 breast cancer cells, the cell-surface transporter density (n) may decay with cell
295 lent tool for the discovery of overexpressed cell surface tumour antigens and the development of targ
296 mulated remodeling of peritoneal mesothelial cell surface ultrastructure via induction of tunneling n
297 and MMP-2,9 gelatinase activity adjacent to cell surfaces was quantified using in vivo zymography.
298 n causes endogenous agrin to localize to the cell surface, where it co-clusters with beta-dystroglyca
299 beyond regulating protein trafficking to the cell surface, whether and if so how these N-glycans cont
300 ss-of-function (LOF) mutations that increase cell surface Wnt receptor abundance cause sensitivity to