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1                                              DC-SIGN (dendritic cell-specific intercellular adhesion
2                                              DC-SIGN (SIGN-R1) is present on mouse lung epithelial ce
3                                              DC-SIGN also was shown to play a role in the infection o
4                                              DC-SIGN and CD206 nanodomains are randomly distributed o
5                                              DC-SIGN forms remarkably stable microdomains on the plas
6                                              DC-SIGN has high affinity for fucosylated glycans in sev
7                                              DC-SIGN is a dendritic cell surface structure which part
8                                              DC-SIGN is a major receptor for infection of both monocy
9                                              DC-SIGN is thought to be crucial for the development of
10                                              DC-SIGN nanoclusters exhibited free, Brownian diffusion
11                                              DC-SIGN, a Ca(2+)-dependent transmembrane lectin, is fou
12                                              DC-SIGN-blocking assays were performed by incubating DCs
13                                              DC-SIGN-targeted transduction occurs in the presence of
14  frequency and microbiome of CD19(-)BDCA-1(+)DC-SIGN(+) blood myeloid DCs (mDCs) were analyzed in CP
15            We found that cocaine activates a DC-SIGN mediated 'signalosome' complex by enhancing its
16 tion and decreased T cell proliferation in a DC-SIGN-, glycosylation-, and Raf1-dependent manner.
17 alpha, production by LPS-stimulated DCs in a DC-SIGN-dependent fashion.
18 tDNA, which induces platelet activation in a DC-SIGN-dependent manner.
19            Finally, M2 macrophages induced a DC-SIGN-dependent adhesion of highly mannosylated IgM(+)
20  mtDNA induces platelet activation through a DC-SIGN dependent pathway.
21                                      Using a DC-SIGN-Fc chimera, food extracts were tested for bindin
22          Our data suggest that SAP activates DC-SIGN to regulate the innate immune system differently
23                                 In addition, DC-SIGN expression was sufficient to cause a significant
24                                 In addition, DC-SIGN-mediated endocytosis provided a minor alternativ
25                   A polycyclic aminothiazole DC-SIGN ligand and anti-DC-SIGN antibodies mimic SAP eff
26 nnose, Fc receptor, CD11c/CD 18, DEC-205 and DC-SIGN on DC for active targeting is reviewed.
27  inhibiting gp120 interactions with 2G12 and DC-SIGN and blocking 2G12-mediated neutralization of HIV
28            Antibodies specific for SR-BI and DC-SIGN/L-SIGN reduced B-cell transinfection, supporting
29 g antibodies against CD18, CD11a, CD11b, and DC-SIGN as well as TLR4.
30 nd CD68 expression), polarization (CD206 and DC-SIGN expression), and IL-10 secretion.
31 f HCV-induced CD68 and M2 markers (CD206 and DC-SIGN) in normal monocytes was further enhanced in the
32 mong the inflammatory markers, only CD68 and DC-SIGN were significant prognostic factors in univariat
33 nhibitory receptors (FcRL5, FcgammaRIIb, and DC-SIGN) with high avidity and specificity, whilst elimi
34  cell line decreases PU.1 protein levels and DC-SIGN at both the mRNA and protein levels.
35 ity to invade DCs, alveolar macrophages, and DC-SIGN-expressing transfectants.
36 yte-derived DCs (Mo-DCs) develop in mice and DC-SIGN/CD209a marks the cells.
37 ifically to the lectin domains of the MR and DC-SIGN and blocked signaling.
38 s indicate that the CRDs of both SIGN-R1 and DC-SIGN bind to a restricted set of primarily oligomanno
39        Mutations in dectin-1 (rs7309123) and DC-SIGN (rs11465384 and rs7248637), allogeneic stem cell
40     The genes encoding OAS1, OAS2, TLR3, and DC-SIGN, which mediate antiviral innate immunity, were w
41                                         Anti-DC-SIGN monoclonal antibody (MAb) inhibited HHV-8 infect
42 cyclic aminothiazole DC-SIGN ligand and anti-DC-SIGN antibodies mimic SAP effects in vitro.
43 ceptors because only the combination of anti-DC-SIGN and low-molecular-weight heparin prevented bindi
44 blocked, in part, by Raf-1 inhibitor or anti-DC-SIGN antibodies and was significantly reduced in cell
45 food extracts followed by staining with anti-DC-SIGN antibody.
46 with C-type lectin receptors (CLRs), such as DC-SIGN (DC-specific ICAM-3-grabbing nonintegrin) result
47  of HIV-1 attachment factors (HAFs), such as DC-SIGN, heparan sulfate proteoglycan (HSPG), and alpha4
48 es can be mediated by C-type lectins such as DC-SIGN.
49 DC-SIGN and DC-SIGNR (collectively termed as DC-SIGN/R) using a sensitive, ratiometric Forster resona
50 oprotein from Sindbis virus engineered to be DC-SIGN-specific.
51        To understand the differences between DC-SIGN and L-SIGN that affect HIV-1 interactions, we de
52 polymers to inhibit the interactions between DC-SIGN and the HIV envelope glycoprotein gp120.
53         In THP-1 cells and human MDDCs, BG60-DC-SIGN interaction led to the activation of Raf-1 and E
54              The QD probes specifically bind DC-SIGN, but not its closely related receptor DC-SIGNR,
55 of glycomimetic compounds were able to block DC-SIGN-dependent HIV infection in cervical explant mode
56                                     Blocking DC-SIGN signaling allows RLR activation and suppresses M
57                                     Blocking DC-SIGN with HIV-1 gp120 prevents the uptake of minor fi
58       However, combination targeting to both DC-SIGN and BDCA3(+) DCs led to significantly greater ac
59 led to endocytosis in vitro as expected, but DC-SIGN, even when cross-linked, did not lead to signifi
60  further intracellular pathways activated by DC-SIGN in a range of primary FL cells with detection of
61                                Activation by DC-SIGN occurred in both IgM(+) and IgG(+) cases and led
62 t internalization of virus-like particles by DC-SIGN.
63 rom DCs to T cells was mediated primarily by DC-SIGN.
64 alled MDDC differentiation, as quantified by DC-SIGN/CD14 expression ratios, showing cooperative invo
65 ht differences between pathogen targeting by DC-SIGN and receptors in which binding sites at fixed sp
66 ing factor (M-CSF)-dependent, CD14(+)CD11b(+)DC-SIGN(+) monocyte-derived DCs.
67 eclampsia, both CD14(+)DC-SIGN(+) and CD14(+)DC-SIGN(-) APCs induced iTreg cells poorly.
68     Conversely, in preeclampsia, both CD14(+)DC-SIGN(+) and CD14(+)DC-SIGN(-) APCs induced iTreg cell
69                 We show that decidual CD14(+)DC-SIGN(+) APCs are closely associated with Foxp3(+) Tre
70   These results suggest that decidual CD14(+)DC-SIGN(+) APCs may play important roles in iTreg cell i
71                          Furthermore, CD14(+)DC-SIGN(+) cells display a distinct phenotype compared w
72 s significantly more efficiently than CD14(+)DC-SIGN(-) APCs.
73 istinct phenotype compared with their CD14(+)DC-SIGN(-) counterparts.
74                             In vitro, CD14(+)DC-SIGN(+) APCs from healthy pregnant women induced iTre
75  there is a complete deficiency of CD209(+) (DC-SIGN) human dendritic cells.
76  CD206/macrophage mannose receptor and CD209/DC-SIGN, as well as costimulatory molecules CD86 and CD4
77 -SIGN (CD209) or its isoform L-SIGN (CD299) (DC-SIGN/R).
78 HIV-1 gp120-specific attachment factors CD4, DC-SIGN, and syndecans, were attenuated in their ability
79 s of DCs is based on the expression of CD83, DC-SIGN, and DC-LAMP, which are nonspecific markers of D
80                    We sought to characterize DC-SIGN-binding glycoproteins in a panel of allergenic a
81                             On the contrary, DC-SIGN enhances HIV trans-infection of T lymphocytes.
82           Both BDCA3(+) and monocyte-derived DC-SIGN(+) NP-loaded DCs were equally effective at gener
83 loped Raji B cell lines expressing different DC-SIGN/L-SIGN chimeras.
84 ing of gp120 to 2G12 and recombinant dimeric DC-SIGN with IC(50) in the nanomolar range.
85 core LPS is naturally exposed, might exploit DC-SIGN to invade APCs.
86                      Dendritic cells express DC-SIGN, a C-type lectin (CTL) that binds a variety of p
87 ut not in B-cell lines transduced to express DC-SIGN lacking the transmembrane domain, demonstrating
88 es from peripheral blood and tonsils express DC-SIGN and that this expression increases after B-cell
89 dendritic cells (DCs), many of which express DC-SIGN (DC-specific ICAM-3 grabbing nonintegrin; CD209)
90  of feline monocyte-derived cells expressing DC-SIGN, indicating a role for FIPV infection in vivo.
91       Although human B cell lines expressing DC-SIGN efficiently capture and transmit HIV-1 to suscep
92 ood myeloid DCs, and B-cell lines expressing DC-SIGN.
93 D) displayed the highest binding avidity for DC-SIGN.
94                   Thus, selectivity gain for DC-SIGN versus langerin is observed with pseudo-1,2-mann
95 play multiple copies of mannoside ligand for DC-SIGN, yet differ in length and size.
96 minor peanut allergen, is a novel ligand for DC-SIGN.
97 ligomannose glycans are also the ligands for DC-SIGN, a C-type lectin found on the surface of dendrit
98 ssentially undetectable lateral mobility for DC-SIGN but an appreciable mobility for HA within their
99 ange similar to that previously observed for DC-SIGN.
100 ereas oligomannose-type glycans required for DC-SIGN-dependent cellular attachment are predominant on
101 ther, our data support an important role for DC-SIGN-expressing infiltrating cells in the biology of
102 described for Lewis X, a ligand specific for DC-SIGN among the C-type lectin family.
103 ment of the cells with antibody specific for DC-SIGN or with mannan but not antibody specific for xCT
104  high-resolution structure of a glycomimetic/DC-SIGN complex by X-ray crystallography.
105 which are CD11b(+)F4/80(+)CD11c(+)MHCII(high)DC-SIGN(high)Ly6c(+) and express high levels of CCR5, CX
106                               To explore how DC-SIGN directs larger particles, such as pathogens, we
107 ls can be rescued by the expression of human DC-SIGN (hDC-SIGN) and that infection of a permissive fe
108 ependent on SignR3 (murine ortholog of human DC-SIGN).
109                  This study shows that human DC-SIGN is a receptor for Y. pestis that promotes phagoc
110  (LPS) as ligands to interact with the human DC-SIGN.
111      In this study, stably transfected human DC-SIGN(+/-) Raji cell lines and monocyte-derived DCs (M
112 taining glycopolymers to interact with human DC-SIGN and the ability of these glycopolymers to inhibi
113 and can be restored by a knock-in with human DC-SIGN.
114 s response in detail, we generated humanized DC-SIGN mice (hDC-SIGN), and demonstrate that the anti-i
115               Using retagging, we identified DC-SIGN as a novel receptor involved in the initial reco
116 fects of costimulatory blockade and identify DC-SIGN(+) suppressive macrophages as crucial mediators
117                                 Importantly, DC-SIGN nanocluster dissolution exclusively compromised
118 ests how CRDs may be disposed differently in DC-SIGN compared with DC-SIGNR and in variant forms of D
119  C-terminal C-type CRDs, the neck domains in DC-SIGN and DC-SIGNR act as autonomous tetramerization d
120 s of the carbohydrate-recognition domains in DC-SIGN and DC-SIGNR result from variations in the seque
121 Further, LARG was observed to participate in DC-SIGN mediated internalization of HIV-1 in DCs.
122           Comparison of the binding sites in DC-SIGN and langerin, two other pathogen-binding recepto
123 -glycans can potently and completely inhibit DC-SIGN-mediated augmentation of Ebola virus glycoprotei
124  used gene silencing to specifically inhibit DC-SIGN expression by DCs followed by allergen uptake st
125           Thus, approaches aiming to inhibit DC-SIGN, without blocking langerin, represent attractive
126 DC-specific ICAM-3 -: grabbing non integrin (DC-SIGN) and macrophage mannose receptor 1 (MMR-1).
127  to DC-specific ICAM3-grabbing non-integrin (DC-SIGN) and its related receptor, L-SIGN, were found.
128 r adhesion molecule-3 grabbing non-integrin (DC-SIGN) and mannose receptor, bound to FL surface immun
129 r adhesion molecule-3-grabbing non-integrin (DC-SIGN) on DCs as early as day 2 and continuing through
130 r adhesion molecule-3 grabbing non-integrin (DC-SIGN), after directly targeting the transcription fac
131 r adhesion molecule-3-Grabbing Non-integrin (DC-SIGN), CD123, neutrophil elastase, CD31, and carbonic
132 -cell-specific ICAM-3 grabbing non-integrin (DC-SIGN; also known as CD209).
133                               Interestingly, DC-SIGN was found within the FL cell niche in situ.
134 by the internalization of P. gingivalis into DC-SIGN-rich intracellular compartments, and MoDCs secre
135 ore, we asked whether RSV infection involves DC-SIGN (CD209) or its isoform L-SIGN (CD299) (DC-SIGN/R
136  of the feline homologue to the human lectin DC-SIGN and show that it is a coreceptor for virulent st
137 tion domain (CRD) of the cell-surface lectin DC-SIGN (dendritic cell-specific intercellular adhesion
138 ty binding to the human transmembrane lectin DC-SIGN and act as inhibitors to prevent the binding of
139 G-I and Mda5 by activating the C-type lectin DC-SIGN and inducing signaling that prevents RLR dephosp
140                            The C-type lectin DC-SIGN expressed on dendritic cells (DCs) facilitates c
141 en a human dendritic cell associated lectin (DC-SIGN) and the viral envelope glycoprotein gp120.
142  blocked viral binding to the C-type lectin, DC-SIGN.
143 eceptors CD81, SR-BI, and the C-type lectins DC-SIGN and L-SIGN.
144 rmore, CV-N competed with the C-type lectins DC-SIGN and mannose receptor for ligand binding and inhi
145 ween two closely related tetrameric lectins, DC-SIGN (simultaneous binding to one GNP) and DC-SIGNR (
146 cell lines transduced to express full-length DC-SIGN but not in B-cell lines transduced to express DC
147 ld be involved in targeting or cross-linking DC-SIGN.
148 studies using Fc chimeras revealed that LRP, DC-SIGN, and mannose receptor can bind to FVIII; however
149 s in the healthy human brain through the MOG-DC-SIGN homeostatic regulatory axis, which is comprised
150 ular adhesion molecule-grabbing nonintegrin (DC-SIGN) (CD209) receptor, expressed by APCs, to be capt
151 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN) and heparan sulfate proteoglycan were implicate
152 ar adhesion molecule 3-grabbing nonintegrin (DC-SIGN) and the macrophage galactose lectin, to glycopr
153 ion molecule 3 (ICAM3) grabbing nonintegrin (DC-SIGN) leads to a reduction in the expression of Toll-
154 hesion molecule type-3-grabbing nonintegrin (DC-SIGN) level in aged DCs.
155 c cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) necessary for human immunodeficiency virus, typ
156 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN) on microglia and DCs.
157 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN) or DC-SIGN-related (DC-SIGNR), suggesting that
158 on molecule-3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) with respect to retrovirus binding.
159 c cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN), and TLR4 because ActApo-induced up-regulation
160 c cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN), mannose-binding lectin, and heparan sulfate, e
161 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN), so that the blockade of this receptor through
162 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN), which could in turn trigger delayed but long-l
163 ar adhesion molecule 3-grabbing nonintegrin (DC-SIGN).
164 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN).
165 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN).
166 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN)/CD23, are increased.
167 c cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN, CD209), Dectin-1, Toll-like receptors (TLRs), c
168 ar adhesion molecule-3-grabbing nonintegrin (DC-SIGN; CD209).
169 hat ES targets DC-specific ICAM nonintegrin (DC-SIGN) to survive in myeloid DCs for which outer membr
170                                   This novel DC-SIGN-T(H)2 pathway initiated by an endogenous ligand,
171 stimulatory blockade favored accumulation of DC-SIGN-expressing macrophages that inhibited CD8(+) T c
172 urther confirmed by its specific blocking of DC-SIGN engagement with the Ebola virus glycoprotein.
173 prehensive report on the characterization of DC-SIGN-binding proteins in common allergenic foods such
174                                  Deletion of DC-SIGN-expressing macrophages in vivo, interfering with
175 ther investigate the lateral distribution of DC-SIGN.
176 ayers displaying the extracellular domain of DC-SIGN and a neoglycolipid bearing an oligosaccharide l
177   In the work reported here, neck domains of DC-SIGN and DC-SIGNR expressed in isolation are shown to
178    ET treatment results in downregulation of DC-SIGN, a marker of immature DCs, and upregulation of D
179 ersely correlated with surface expression of DC-SIGN (DC-specific intercellular adhesion molecule-3-g
180 th HHV-8 resulted in increased expression of DC-SIGN and a decrease in the expression of CD20 and maj
181 rate that cocaine induces over expression of DC-SIGN and significantly enhances virus transfer from D
182                      Thus, the expression of DC-SIGN is essential for productive HHV-8 infection of a
183 in on LC but downregulated the expression of DC-SIGN on iDDC, as we previously reported for MDDC.
184    This profile is enhanced by expression of DC-SIGN on MoDCs and minor mfa-1 fimbriae on P. gingival
185                   The relative expression of DC-SIGN, GLUT-1, HSPGs, and NRP-1 first was examined on
186                    Indeed, the generation of DC-SIGN(+) MoDCs in response to LPS was severely impaire
187 s of CD209e (DC-SIGNR4), a murine homolog of DC-SIGN, were increased in the lungs of HDM-challenged V
188   In addition, differences in the lengths of DC-SIGN and DC-SIGNR extracellular domains with equivale
189 eas immature DC, expressing higher levels of DC-SIGN and similar FcgammaRIIa levels, did not undergo
190                                  Location of DC-SIGN in FL tissue revealed high levels in sinusoidlik
191 luence the nanoscale lateral organization of DC-SIGN but restrict the mobility of the receptor to dis
192 he absence of Ca(2+) and by preincubation of DC-SIGN with mannan, suggesting that C1q binds to DC-SIG
193 thrin, thereby increasing the probability of DC-SIGN-clathrin interactions beyond random encountering
194                    Consequently, the role of DC-SIGN and other HTLV-1 attachment factors was analyzed
195                 However, the precise role of DC-SIGN in food allergy pathogenesis is not yet understo
196 lycosylation on the folding and stability of DC-SIGN have not been reported.
197 glycoprotein modifications, the stability of DC-SIGN is better correlated with the number of glycosyl
198                  The surprising stability of DC-SIGN microdomains may reflect structural features tha
199 the effects of O-glycans on the stability of DC-SIGN.
200 ains to Raji cells and MoDCs is dependent on DC-SIGN, whereas the double fimbriae mutant strain does
201 , antigen structure has a dramatic effect on DC-SIGN-mediated uptake and trafficking.
202                         Blocking of MMR-1 or DC-SIGN with neutralizing Abs partially inhibits this ef
203 derived inflammatory DCs such as CD14 and/or DC-SIGN, E-Cadherin, and/or CX3CR1.
204 pressing the interleukin-3 receptor CD123 or DC-SIGN.
205  versatility in entry routes (FcgammaRIIa or DC-SIGN) in mature DC broadens target options and sugges
206 s on the C-type lectin receptor, langerin or DC-SIGN, involved in gp120 interaction.
207 ctin domains of the mannose receptor (MR) or DC-SIGN bind mannosylated Igs in vitro and bind to FL ce
208 iated knockdown of LRP, mannose receptor, or DC-SIGN expression in monocyte-derived dendritic cells d
209 molecule-3-grabbing nonintegrin (DC-SIGN) or DC-SIGN-related (DC-SIGNR), suggesting that inefficient
210                 The immune scavenger protein DC-SIGN interacts with glycosylated proteins and has a p
211 k regions, and receptor diffusion to provide DC-SIGN with the exquisite ability to dock pathogens at
212               A human orthologue of SIGN-R1, DC-SIGN, displays a similar binding specificity to SIGN-
213 f the dendritic cell glycan-binding receptor DC-SIGN and the closely related endothelial cell recepto
214 Targeting of myeloid-dendritic cell receptor DC-SIGN by numerous chronic infectious agents, including
215                  The dendritic cell receptor DC-SIGN mediates pathogen recognition by binding to glyc
216 cell contact and the dendritic cell receptor DC-SIGN.
217  fimbria, targets the C-type lectin receptor DC-SIGN for invasion and persistence within human monocy
218  cells expressing the C-type lectin receptor DC-SIGN, persisted at sites of HSV-2 reactivation for mo
219 12 and PGT123, or the C-type lectin receptor DC-SIGN.
220 port that SAP but not CRP binds the receptor DC-SIGN (SIGN-R1) to affect the innate immune system, an
221 mains (CRDs) in the glycan-binding receptors DC-SIGN (dendritic-cell-specific intercellular adhesion
222 tivalent interactions of HIV/Ebola receptors DC-SIGN and DC-SIGNR (collectively termed as DC-SIGN/R)
223 gens and on mammalian cells by the receptors DC-SIGN (CD209) and DC-SIGNR (L-SIGN, CD299) is dependen
224                 However, soluble recombinant DC-SIGN was shown to inhibit the binding between SP-D an
225  Indeed, removal of fucose on myelin reduced DC-SIGN-dependent homeostatic control, and resulted in i
226           Finally, we show that, by reducing DC-SIGN in the cellular membrane, miR-155 is involved in
227 through a similar pathway to IVIG, requiring DC-SIGN, STAT6 signaling, and FcgammaRIIB.
228 y stimulation of IL-33 production that seems DC-SIGN independent.
229 an H. pylori carriers exhibited a semimature DC-SIGN(+)HLA-DR(hi)CD80(lo)CD86(lo) phenotype.
230                                      Several DC-SIGN-binding proteins show reactivity in serum IgE im
231 1-grabbing nonintegrin; CD209) and DC-SIGNR (DC-SIGN-related receptor, also known as L-SIGN and vario
232 Intriguingly, our data showed that silencing DC-SIGN on DCs promotes a Th2 phenotype in DC/T cell co-
233           Mechanistically, that simultaneous DC-SIGN engagement by fucosylated ligands and TLR4 signa
234                               In this study, DC-SIGN dynamics in microdomains were explored with seve
235 uced interleukin-4 production and subsequent DC-SIGN expression in this cell population.
236                            Thus, MV subverts DC-SIGN to control RLR activation and escape antiviral r
237                            Infection of T1H6-DC-SIGN cells with HHV-8 induces expression of beta-gala
238 infective dose (TCID50) assay using the T1H6-DC-SIGN cell line.
239  mutant molecule with K270W and a C-terminal DC-SIGN CRD subdomain transmitted HIV-1.
240 immune system differently from CRP, and that DC-SIGN is a target for antifibrotics.
241 ingle particle tracking, we demonstrate that DC-SIGN intrinsic nanoclustering strictly depends on its
242          Fluorescence imaging indicated that DC-SIGN microdomains may contain other C-type lectins an
243                         Blink indicates that DC-SIGN, another CTL (CD206), and influenza hemagglutini
244                    Although it is known that DC-SIGN organizes in nanoclusters at the surface of DCs,
245          We estimate, as a lower limit, that DC-SIGN and HA nanodomains contain on average two tetram
246  the QD surface mannose valency reveals that DC-SIGN binds more efficiently to densely packed mannosi
247           In the present study, we show that DC-SIGN, a C-type lectin expressed on DCs, binds directl
248                  We have recently shown that DC-SIGN, a C-type lectin first identified on dendritic c
249                      These data suggest that DC-SIGN structural elements distinct from the oligosacch
250  receptors on DCs and strongly suggests that DC-SIGN plays a critical role in HTLV-1 binding, transmi
251  conferred to L-SIGN chimeras containing the DC-SIGN CRD.
252 onfirmed that the minor fimbria contains the DC-SIGN-targeting carbohydrates fucose (1.35 nmol/mg), m
253                 We identified Trp-258 in the DC-SIGN CRD to be essential for HIV-1 transmission.
254 himeras demonstrated that replacement of the DC-SIGN carbohydrate-recognition domain (CRD) with that
255  no competition against known ligands of the DC-SIGN CRD.
256 s section and the gas-phase stability of the DC-SIGN isoforms.
257  and reduced transcriptional activity of the DC-SIGN promoter, which is likely to be the basis for it
258 for the complete extracellular region of the DC-SIGN tetramer was similar for all antibody glycoforms
259 SF1-dependent development, or preventing the DC-SIGN signaling pathway abrogated tolerance.
260 y reduce neutrophil influx via targeting the DC-SIGN murine homolog SIGN-related 1.
261 ay contain other C-type lectins and that the DC-SIGN cytoplasmic region is not required for microdoma
262  DC differentiation and function through the DC-SIGN-mediated induction of cell-signaling pathways.
263 rotein capable of selectively binding to the DC-SIGN protein.
264 ocyte-derived dendritic cells (MDDC) through DC-SIGN, resulting in nonproductive infection.
265 nner leaflet lipids are able to move through DC-SIGN microdomains.
266                                Antibodies to DC-SIGN, a c-type lectin selectively expressed by macrop
267 ctivation of human DCs by LPS via binding to DC-SIGN and MMR-1, leading to attenuated TLR signaling.
268                                MV binding to DC-SIGN leads to activation of the kinase Raf-1, which i
269                                   Binding to DC-SIGN on MoDCs is followed by the internalization of P
270 id (aa) 196 and E1 aa 139 mediate binding to DC-SIGN, which supports the results of a previous report
271 action, were not required for C1q binding to DC-SIGN.
272 ts, chickpea, and corn, showed no binding to DC-SIGN.
273 GN with mannan, suggesting that C1q binds to DC-SIGN at its principal Ca(2+)-binding pocket, which ha
274              Mannosylated scFv also bound to DC-SIGN on the surface of dendritic cells.
275 m as neither recombinant Fc nor sFc bound to DC-SIGN.
276 C1q and the globular portion of C1q bound to DC-SIGN.
277 tion confers broader binding capabilities to DC-SIGN.
278  stability of DC-SIGNR tetramers compared to DC-SIGN.
279 herapy does not involve binding of IgG Fc to DC-SIGN and that alternative cell-surface lectins are re
280 d the binding of highly sialylated IgG Fc to DC-SIGN-expressing myeloid cells.
281 ferentially deliver the PSCA antigen gene to DC-SIGN-expressing 293T cells and bone marrow-derived DC
282 the binding of HIV envelope protein gp120 to DC-SIGN at nanomolar concentrations.
283 he entry of HHV-8 into B cells is related to DC-SIGN-mediated endocytosis.
284 er full-length nor cytoplasmically truncated DC-SIGN in microdomains appreciably exchanged with like
285  complex to high mannose, these vectors used DC-SIGN as their receptor.
286 control monoclonal antibody or delivered via DC-SIGN, another lectin receptor.
287 ficant mobility within microdomains, whereas DC-SIGN does not.
288 y revealed that C1q and gC1qR associate with DC-SIGN on blood DC precursors and immature DCs.
289  and was significantly reduced in cells with DC-SIGN knockdown.
290 est that allergens are able to interact with DC-SIGN and induce tumor necrosis factor-alpha expressio
291  whether our targeting vectors interact with DC-SIGN, which traps many types of viruses and gene ther
292 ound that these vectors do not interact with DC-SIGN.
293  non-IgE-binding proteins that interact with DC-SIGN; these proteins may be important for regulating
294 her fucosylation and better interaction with DC-SIGN [DC-specific intercellular adhesion molecule-3 (
295                        The interactions with DC-SIGN demonstrated the significance of alpha(1-6)manna
296 study that Y. pestis directly interacts with DC-SIGN and invades both DCs and alveolar macrophages.
297           We conclude that ES interacts with DC-SIGN to subvert the host immune responses by disarmin
298                  The interaction of MOG with DC-SIGN in the context of simultaneous TLR4 activation r
299  that, rather than being densely packed with DC-SIGN proteins, an elemental substructure exists.
300 ell in response to select microbes, yielding DC-SIGN(+) cells with critical functions of DCs.

 
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