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1 e C-terminus of Sema3F with the b1 domain of neuropilin.
2 al domain of semaphorin and the b1 domain of neuropilin.
3 hat potently inhibits the binding of VEGF to neuropilin.
4 that acts through a mechanism distinct from neuropilins.
5 nteraction with their receptors, plexins and neuropilins.
6 However, invertebrates lack neuropilins.
7 ropose possible models for ligand binding to neuropilins.
8 tC signal independently of the Robos and the Neuropilins.
9 e known primarily as ligands for plexins and neuropilins.
10 L1) and the semaphorin 3A (Sema3A) receptor, neuropilin 1 (Npn1), important for establishment of area
13 BMA nucleus, owing to reduced expression of neuropilin 1 (Nrp1) and Nrp2, two semaphorin receptors t
15 mall molecule ligand for the VEGF-A receptor neuropilin 1 (NRP1) and the structural characterization
16 demonstrate that beta8 integrin (Itgb8) and neuropilin 1 (Nrp1) cooperatively promote CNS angiogenes
17 Moreover, high expression of PlGF receptor neuropilin 1 (Nrp1) correlates with poor overall surviva
19 tion, bevacizumab decreased Ang1 and induced neuropilin 1 (NRP1) expression in tumor-associated macro
20 semaphorin SEMA3C, and their shared receptor neuropilin 1 (NRP1) in OFT development, the precise mech
25 analyses with in vitro assays, we show that neuropilin 1 (NRP1) promotes contralateral RGC projectio
27 by endothelial cells where it partners with neuropilin 1 (Nrp1) to form a functional receptor for th
32 ssel growth, endothelial cells (ECs) express neuropilin 1 (NRP1), and NRP1 associates with the recept
33 f these targets is the guidance cue receptor Neuropilin 1 (Nrp1), which is sensitive to the repellent
36 r involved signaling through VEGF receptor 2-neuropilin 1 (VEGFR2-NP1) receptors on endometrial strom
39 aging, as well as suggest miR-208a, AT2R and neuropilin 1 as potential therapeutic targets and mechan
40 study highlights the proangiogenic receptor neuropilin 1 in macrophages and microglial cells in glio
44 betic female rats have reduced expression of neuropilin 1 that attenuates cardiomyopathy compared to
45 iple combination of selection markers--CD34, neuropilin 1, and human kinase insert domain-containing
46 ls of multiple genes and proteins (including Neuropilin 1, glucocorticoid-induced tumor necrosis fact
47 actor (VEGF), VEGF receptors, semaphorin 3F, neuropilin 1, neuropilin 2, podoplanin, and LYVE-1 by qu
48 evels of known A10 elevated genes, including neuropilin 1, neuropilin 2, slit2 and adenylyl cyclase-a
56 ssed in the lens epithelium and its receptor Neuropilin-1 (Npn1) is expressed in the trigeminal gangl
57 RPPR peptide, with affinity for the receptor neuropilin-1 (NRP), which is expressed on both endotheli
58 that must be C-terminally exposed to trigger neuropilin-1 (NRP-1) binding, cellular internalization a
60 eport that expression of the VEGF coreceptor neuropilin-1 (NRP-1) coincides with expression of Brachy
63 Heparin/heparan sulfate proteoglycans and neuropilin-1 (NRP-1) have been identified as co-receptor
64 gated the role of semaphorin 3A (Sema3A) and neuropilin-1 (Nrp-1) in lymphatic vessel maturation and
65 that trafficking of the angiogenic receptor neuropilin-1 (NRP-1) is abrogated by the liver kinase B1
67 essing a conditional deletion of endothelial neuropilin-1 (Nrp-1) or in wild-type mice systemically t
71 liver fibrosis, the axonal guidance molecule neuropilin-1 (NRP-1) was upregulated in activated HSCs,
72 , heparan sulfate proteoglycans (HSPGs), and neuropilin-1 (NRP-1) were demonstrated to facilitate HTL
73 and conditional knockout mice, we show that neuropilin-1 (NRP-1), a known receptor of VEGF, is neces
75 we demonstrate that a cell surface molecule, neuropilin-1 (Nrp-1), is expressed at high levels on nT
76 th heparan sulfate proteoglycans (HSPGs) and neuropilin-1 (NRP-1), two molecules important for HTLV-1
77 s mediated through a molecular cross-talk of neuropilin-1 (NRP-1), VEGFR1 (Flt-1), and phosphoinositi
89 ass spectrometry-based approach, we identify neuropilin-1 (NRP1) as a NE receptor that mediates uptak
95 Sema4a) and the Treg-cell-expressed receptor neuropilin-1 (Nrp1) interact both in vitro, to potentiat
100 tion of circulating monocytes expressing the neuropilin-1 (Nrp1) receptor (Nrp1-expressing monocytes;
101 onset of Sema3A sensitivity and concomitant neuropilin-1 (NRP1) receptor expression and caused cell-
105 ligo G) reduce endothelial levels of surface neuropilin-1 (NRP1), a receptor shared by semaphorin 3A
107 disrupts the developmental downregulation of Neuropilin-1 (Nrp1), the receptor for Sema3A, in sensory
109 Mice that lack the transmembrane receptor neuropilin-1 (Nrp1), which modulates GAM immune polariza
110 e show this is a key endothelial function of neuropilin-1 (Nrp1), which suppresses the stalk-cell phe
112 dritic cell (pDC) marker, BDCA4, identifying neuropilin-1 (NRP1); and the helper T cell marker, CD4.
113 microenvironment by increasing the levels of neuropilin-1 (NRP1, a co-receptor of vascular endothelia
114 ration of siRNAs against the Sema3A receptor neuropilin-1 also resulted in polarization defects in vi
115 Patients with low baseline expression of neuropilin-1 also showed a trend toward improved overall
117 First, aged Tregs had high expression of neuropilin-1 and Helios, and had a broad Vbeta repertoir
118 pecific genes including VEGFR-3, FGFR-3, and neuropilin-1 and is required along with Prox1 to maintai
120 1 involves heparan sulfate proteoglycans and neuropilin-1 and results in long-term productive infecti
122 ng of VEGF to low-affinity binding sites and neuropilin-1 and stimulates further growth factor recept
123 also upregulated VEGFR2 and its co-receptor neuropilin-1 and suppressed the expression of semaphorin
124 th factor A (VEGF-A) isoforms, expression of neuropilin-1 and VEGF receptor 1 in tumors or plasma, an
130 CI, 0.59 to 0.97) versus patients with high neuropilin-1 expression (HR, 1.07; 95% CI, 0.81 to 1.40;
133 Baseline plasma VEGF-A levels and tumor neuropilin-1 expression were identified as potential pre
135 the translation of the guidance cue receptor Neuropilin-1 in RGCs, with Hermes knock-down resulting i
136 hosphorylation status and down-regulation of neuropilin-1 in the HemSCs demonstrate that VEGFR-2 and
137 e transfer experiments and the expression of neuropilin-1 indicate that these cells are predominantly
138 s a critical role for heparin-binding domain/Neuropilin-1 interaction and its regulation by plasmin p
141 surprise, we found that membrane-associated neuropilin-1 is polysialylated at approximately 50% of t
145 ar tumor areas is regulated by Semaphorin 3A/Neuropilin-1 signaling; interference with this pathway e
148 implicate Sema3A as an autocrine signal for neuropilin-1 to promote GBM dispersal by modulating subs
149 stemmed from a failure to expand functional neuropilin-1(+) regulatory T (T reg) cells in the absenc
150 th, portal vessels undergo a transition from Neuropilin-1(+)Ephrin-B2(+) artery to EphB4(+) vein phen
152 ound was driven by the CD4(+)CD25(+)Foxp3(+) neuropilin-1(low) peripheral Treg (pTreg), resulting in
154 owed slightly decreased binding to the NRP1 (neuropilin-1) receptor, and analyses suggested the hepar
155 of domain swap chimeras with sequences from neuropilin-1, a protein for which polysialylation had no
156 r to those of others following inhibition of neuropilin-1, a receptor previously implicated in TGFbet
157 finity for its primary receptor and binds to neuropilin-1, activating a tissue penetration pathway th
158 ication of sialoglycoproteins such as CD105, neuropilin-1, and CLEC14A, which have already been descr
159 (VEGF) and three of its receptors, VEGFR-2, neuropilin-1, and neuropilin-2, in paraffin-embedded sam
160 ate the role of a potential guidance factor, neuropilin-1, and use functional knockdown assays, tissu
161 wth factor-A (VEGF-A), protein expression of neuropilin-1, and VEGF receptors-1 and -2 (VEGFR-1 and V
162 express similar levels of Sema3A receptors (neuropilin-1, cell adhesion molecule L1, and plexinA4),
163 rent iNKT subsets defined by CD4, NK1.1, and neuropilin-1, indicating that distinct functional subpop
164 that VEGF immobilization, interactions with Neuropilin-1, perturbations of VEGFR2 trafficking, and c
165 dipocytes, probably through up-regulation of neuropilin-1, the OB-mediated enhanced hematopoiesis fun
166 rnalized into cultured tumor cells through a neuropilin-1-activated pathway and triggered cell death.
167 nd tLyP-1 internalize into cells through the neuropilin-1-dependent CendR internalization pathway.
168 tissue permeability in a tumor-specific and neuropilin-1-dependent manner, allowing coadministered d
170 istic insights into the regulation of PlGF-2/Neuropilin-1-mediated tissue vascularization and growth.
172 pment and is not required for maintenance of neuropilin-1-positive natural Tregs in the periphery, it
173 h 2 (ba2), is due to chemoattraction through neuropilin-1-vascular endothelial growth factor (VEGF) i
183 esults support that Farp1 interacts with the Neuropilin-1/PlexinA1 complex and colocalizes with Plexi
185 screen identified the transmembrane protein neuropilin 2 (NRP2) and tetraspanin CD63 as factors for
186 a3f, but not Sema3b, phenocopies the loss of neuropilin 2 (Nrp2) for axonal wiring of GC-D+ neurons.
187 and protein expression analysis showed that neuropilin 2 (NRP2), a key factor for vascular developme
192 VEGF receptors, semaphorin 3F, neuropilin 1, neuropilin 2, podoplanin, and LYVE-1 by quantitative (re
193 A10 elevated genes, including neuropilin 1, neuropilin 2, slit2 and adenylyl cyclase-activating pept
194 d in neural and vascular patterning, such as neuropilin-2 (NETO2), a plexin domain containing recepto
195 mplex in brain with Sema3F receptor subunits Neuropilin-2 (Npn-2) and PlexinA3 (PlexA3) through an Np
196 Here we show that NrCAM interaction with neuropilin-2 (Npn-2) is critical for semaphorin 3F (Sema
197 guidance cue semaphorin 3F (Sema3F) and its neuropilin-2 (Npn-2)/plexinA3 (PlexA3) holoreceptor medi
198 ding Sema3F, and its holoreceptor components neuropilin-2 (Npn-2, also known as Nrp2) and plexin A3 (
201 ared the PBR sequence requirements for NCAM, neuropilin-2 (NRP-2), and synaptic cell adhesion molecul
205 eptors, plexins and neuropilins, among which neuropilin-2 (NRP2) is highly expressed in lymphatic end
209 the ability of ST8SiaIV/PST to polysialylate neuropilin-2 and SynCAM 1, suggesting that Arg(82) plays
210 and the O-glycan-containing linker region of neuropilin-2 are necessary and sufficient for its polysi
211 lylated at approximately 50% of the level of neuropilin-2 but not polysialylated when it lacks its cy
212 Our results show that floor plate-derived neuropilin-2 is developmentally regulated, functioning a
213 f floor plate-derived, but not axon-derived, neuropilin-2 is required for precrossing axon pathfindin
214 gnizes and docks on an acidic surface of the neuropilin-2 MAM domain to polysialylate O-glycans on th
221 he transmembrane nontyrosine kinase receptor neuropilin-2 was found to be essential for the VEGF-C-me
224 of its receptors, VEGFR-2, neuropilin-1, and neuropilin-2, in paraffin-embedded samples from 21 vesti
227 on of lymphatic endothelial cells (LEC) in a neuropilin-2-, plexin-D1-, and plexin-A1-dependent manne
232 SEMA3F acts on its coreceptors, plexins and neuropilins, among which neuropilin-2 (NRP2) is highly e
239 y, we found that the intracellular region of neuropilin and tolloid-like proteins (Neto) 1 and Neto2,
240 ified and characterized the Drosophila neto (neuropilin and tolloid-like) as an essential gene requir
243 KARs associate with the auxiliary proteins neuropilin- and tolloid-like 1 and 2 (Neto1 and Neto2),
247 class 3 semaphorin family, but VEGF164, the neuropilin-binding isoform of the classical vascular gro
248 circulation-independent, and mediated by the neuropilin-binding RXXK tissue-penetration peptide motif
249 By reconstituting all possible plexin and neuropilin combinations, we found that SEMA3F acts throu
252 nce molecules that signal through plexin and neuropilin coreceptors and since then have been establis
255 ted that all known ligands and inhibitors of neuropilin interact with the b1 domain of neuropilin via
258 ro models, we show here that the alternative neuropilin ligand VEGF164 promotes the survival of migra
259 of retinal axons to Sema3D, Sema3E, or other neuropilin ligands at the midline, and consequently faci
262 Here, we determined that the discoidina neuropilin-like membrane protein DCBLD2 is upregulated i
263 Endothelial and smooth muscle cell-derived neuropilin-like protein (ESDN) is a neuropilin-related t
264 Endothelial and smooth muscle cell-derived neuropilin-like protein (ESDN) is up-regulated in the ne
266 ndantly through both its classical receptors neuropilin (NRP) 1 and, unconventionally, NRP2, while th
268 in the class 3 semaphorin (SEMA3) receptors neuropilin (NRP) 1 or 2 raised the possibility that each
269 composed of a ligand binding subunit termed neuropilin (NRP) and a signal transduction subunit of th
274 transcription of VEGF receptor (VEGFR)-2 and neuropilin (NRP)-1, the primary receptors regulating end
276 ost & Microbe, Raaben et al. (2017) identify neuropilin (NRP)-2 as cell surface receptor and the tetr
286 al growth factor (VEGF) receptors, including neuropilins (NRPs), which regulate interstitial fluid fl
291 ibodies for VEGF receptor (VEGFR) 1 and 2 or neuropilin receptor 1 or by VEGFR2 inhibitors (SU 1498 a
292 lass 3 semaphorin SEMA3A signals through its neuropilin receptors, NRP1 and NRP2, to organise the axo
294 he developing cerebellum, genetic removal of Neuropilins reduces Hh signaling activity and suppresses
295 -derived neuropilin-like protein (ESDN) is a neuropilin-related transmembrane protein expressed in EC
296 o examine which A-type plexin conveyed SEMA3/neuropilin signals during facial nerve development, we c
297 sphodiesterase 4D (PDE4D) acts downstream of Neuropilins to control Hh transduction and medulloblasto
300 Here we demonstrate that select plexins and neuropilins, which serve as coreceptors for semaphorins,
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