ライフサイエンスコーパス: nectin

1 icular, viruses of different classes exploit nectins.

2 lex and pseudorabies viruses, use ubiquitous nectins 1 and 2.

3 third, membrane-proximal Ig module of mouse nectin-1 (nectin-1 Ig3) solved by means of nuclear magne

4 For primary murine keratinocytes, on which nectin-1 acts as a single receptor, electron microscopy

5 in nectin-1-deficient cells, suggesting that nectin-1 acts as the more efficient receptor.

6 Nectin-1 and -2 were expressed in all tissues during the

7 g agents disrupts the synaptically localized nectin-1 and afadin cluster at an early stage and elicit

8 Nectin-1 and afadin cluster at developing synapses betwe

9 In this work we studied the distribution of nectin-1 and afadin during hippocampal synapse formation

10 e found that SaHV-1 uses the entry receptors nectin-1 and CD155 but not HVEM or PILRalpha.

11 identified alphaherpesvirus entry receptors nectin-1 and CD155 but not with herpesvirus entry mediat

12 The cellular proteins nectin-1 and herpesvirus entry mediator (HVEM) act as ef

13 iously, we have explored the contribution of nectin-1 and herpesvirus entry mediator (HVEM) as recept

14 The cellular proteins nectin-1 and herpesvirus entry mediator (HVEM) can both

15 How HSV-1 enters skin and whether both nectin-1 and HVEM are involved are not known.

16 Nectin-1 and HVEM are the two major cellular receptors f

17 ing entry into cells grown in vitro revealed nectin-1 and HVEM as HSV receptors.

18 Our results demonstrate a role for both nectin-1 and HVEM as receptors and suggest a further rec

19 receptors by siRNAs interference implicates nectin-1 and HVEM as the major mediators of entry.

20 we demonstrated the distinct involvement of nectin-1 and HVEM for HSV-1 entry into epidermis and cha

21 outermost layer of skin, the contribution of nectin-1 and HVEM in the underlying dermis is still open

22 xpress all three major entry receptors, with nectin-1 and HVEM playing the predominant role in mediat

23 To explore the contributions of nectin-1 and HVEM to entry into a natural target tissue,

24 a indicate that the synaptic localization of nectin-1 and l-afadin are F-actin-dependent and that the

25 us clinical strains can effectively use both nectin-1 and nectin-2 as cellular receptors for entry in

26 The junctional recruitment of nectin-1 and nectin-3 and their protein levels are decre

27 PDZD11 forms a complex with nectin-1 and nectin-3, and its PDZ domain interacts dire

28 eptors herpesvirus entry mediator (HVEM) and nectin-1 are the primary entry receptors for HSV-2 in th

29 ted presence of HVEM can potentially replace nectin-1 as a receptor, illustrating the flexibility emp

30 a productive infection in RPE cells by using nectin-1 as an important entry receptor.

31 ificantly reduced viral entry and implicated nectin-1 as an important receptor, with HVEM and PILR-al

32 Ex vivo infection studies reveal nectin-1 as the primary receptor in epidermis, whereas H

33 ted an HSV-2 mutant, HSV2-gD27, in which the nectin-1 binding domain of gD2 is altered so that the vi

34 idues that likely play a role in shaping the nectin-1 binding site of gD.

35 t passage of a gD mutant virus defective for nectin-1 binding through cells that express a gD-binding

36 with recent findings that (i) either HVEM or nectin-1 can permit HSV infection of the vaginal epithel

37 ta28syn virus caused extensive fusion of CHO-nectin-1 cells but limited cell fusion of CHO-PILRalpha

38 tin-1 is regulated in neuronal cells and how nectin-1 cleavage affects synaptic adhesion is poorly un

39 al homology-based modeling of the B virus gD-nectin-1 complex revealed conformational differences bet

40 Thus, we concluded that nectin-1 directs internalization into keratinocytes via

41 Wild-type, HVEM KO, nectin-1 KO, and HVEM/nectin-1 double KO mice were inoculated with HSV into th

42 Wild-type, HVEM KO, nectin-1 KO, and HVEM/nectin-1 double-KO mice were infected via corneal scarif

43 We addressed the impact of nectin-1 during entry of HSV-1 into murine epidermis and

44 DAM10 is the major secretase responsible for nectin-1 ectodomain cleavage in neurons and the brain.

45 afadin cluster at an early stage and elicits nectin-1 ectodomain shedding.

46 on of FGFR1c in the same manner as the whole nectin-1 ectodomain, and promoted survival of cerebellar

47 rrent study, we have shown that mice lacking nectin-1 exhibit defective enamel formation in their inc

48 essary but not sufficient for the removal of Nectin-1 from the cell surface.

49 erpes simplex virus 1 (HSV-1) entry receptor Nectin-1 from the surface of infected cells.

50 The removal of the HSV-1 entry receptor Nectin-1 from the surface of the infected cells may be p

51 urface plasmon resonance (SPR) analysis that nectin-1 Ig3 directly interacted with various isoforms o

52 Nectin-1 Ig3 induced phosphorylation of FGFR1c in the sa

53 Nectin-1 Ig3 was produced as a recombinant protein and i

54 mbrane-proximal Ig module of mouse nectin-1 (nectin-1 Ig3) solved by means of nuclear magnetic resona

55 Nectide mimicked all the effects of nectin-1 Ig3.

56 eptors herpesvirus entry mediator (HVEM) and nectin-1 in a manner dependent upon route of inoculation

57 obust alpha- and gamma-secretase cleavage of nectin-1 in mature cortical neurons.

58 a-and gamma-secretase-mediated processing of nectin-1 in primary cortical neurons and identified whic

59 Cbl-depleted cells, suggesting that the Cbl-Nectin-1 interaction is likely the key to the downregula

60 hat alpha- and gamma-secretase processing of nectin-1 is a Ca(2+)/calmodulin-regulated event that occ

61 l or intracranial inoculation of adult mice, nectin-1 is a major mediator of neurologic disease, whil

62 e F-actin-dependent and that the shedding of nectin-1 is a mechanism contributing to synaptic plastic

63 Nectin-1 is a member of a sub-family of immunoglobulin-l

64 The viral entry receptor Nectin-1 is also internalized during HSV-1 infection in

65 Nectin-1 is initially expressed at excitatory and inhibi

66 Nectin-1 is known to undergo ectodomain shedding by alph

67 Thus, expression of nectin-1 is necessary for HSV infection via the intracra

68 n of the vaginal epithelium in mice and (ii) nectin-1 is not the sole receptor capable of enabling sp

69 How secretase-mediated cleavage of nectin-1 is regulated in neuronal cells and how nectin-1

70 n infected cells; (ii) that during infection Nectin-1 is removed from the surface of the infected cel

71 Our results suggest that nectin-1 is the primary receptor in epidermis, while HVE

72 on of virus were significantly attenuated in nectin-1 knockout mice compared with HVEM knockout or wi

73 Nectin-1 knockout mice had delayed mortality after intra

74 Nectin-1 KO mice showed no signs of disease after intrac

75 icating that infection of these cells in the nectin-1 KO mice was dependent on the expression of HVEM

76 infection was attenuated in both HVEM KO and nectin-1 KO mice.

77 Wild-type, HVEM KO, nectin-1 KO, and HVEM/nectin-1 double KO mice were inocu

78 Wild-type, HVEM KO, nectin-1 KO, and HVEM/nectin-1 double-KO mice were infec

79 The usage of the HSV-1 gD receptor nectin-1 may explain interspecies transfer of the viruse

80 h nectin-1-expressing cells, indicating that nectin-1 mediated entry while HVEM and PILRalpha did not

81 ile it entered CHO cells expressing HVEM and nectin-1 more efficiently than the McKbac virus.

82 We report that either HVEM or nectin-1 must be present for HSV-1 infection of the corn

83 olocalization of gD and its cognate receptor nectin-1 on infected neuronal surfaces.

84 otein D (gD) to a specific receptor, such as nectin-1 or herpesvirus entry mediator (HVEM), resulting

85 that were deficient in expression of either nectin-1 or HVEM or both receptors.

86 rophobicity of gD or on gD's ability to bind nectin-1 or HVEM receptors.

87 n was not prevented by the absence of either nectin-1 or HVEM, we conclude that they can act as alter

88 2N and gD-122D variants that affected the gD-nectin-1 protein-protein interface and binding affinity.

89 her, these results imply that HSV-1 uses the nectin-1 receptor to enter human keratinocyte cells via

90 cell surface heparan sulfate and binding to nectin-1 receptor.

91 ells infected with a DeltaICP0 mutant virus, Nectin-1 remained on the cell surface.

92 The function of the third Ig module of nectin-1 remains unknown.

93 Cleavage of nectin-1 required influx of Ca(2+) through the NMDA rece

94 -adhesion molecules comprising four members, nectin-1 through nectin-4.

95 Nectin-1 was most crucial for the neuronal spread of HSV

96 While strong immunostaining for nectin-1 was observed at the interface between the matur

97 Ralpha was overexpressed much more than when nectin-1 was overexpressed.

98 tion in these models, but when both HVEM and nectin-1 were absent, infection was completely prevented

99 ther of the host cell gD receptors (HVEM and nectin-1) is required in target primary fibroblasts for

100 Cell-cell fusion assays indicated that nectin-1, an HSV-1 gD receptor, mediated fusion of cells

101 c cell adhesion proteins such as N-Cadherin, Nectin-1, and APP may explain the postsynaptic defects a

102 We found the following: (i) that Cbl, Nectin-1, and the viral glycoprotein D (gD) form a compl

103 H1 cells bearing a single gD receptor, human nectin-1, but gained the ability to enter when phenotypi

104 shown to strongly depend on the presence of nectin-1, but the restricted presence of HVEM can potent

105 sed on epithelial cells and lymphocytes, and nectin-1, expressed on neurons and epithelial cells, are

106 titutively expressing HSV-1 human receptors, nectin-1, herpesvirus entry mediator (HVEM), or paired i

107 The common receptors for viral entry are nectin-1, HveA, and a specific O-linked sulfated proteog

108 ys confirm the expression of entry receptors nectin-1, HVEM, and 3-O-sulfated heparan sulfate (3-OS H

109 trated the expression of the entry receptors nectin-1, HVEM, and PILR-alpha and their localization pr

110 ptors, herpesvirus entry mediator (HVEM) and nectin-1, in infection of neurons in the CNS and the dev

111 the ability to infect cells expressing only nectin-1, including neuronal cell lines, and did not inf

112 aired HSV-1 infection, but not expression of nectin-1, indicating that galectin-3 is a herpesvirus en

113 ptors, herpesvirus entry mediator (HVEM) and nectin-1, mediate entry in murine models of HSV-1 and HS

114 ptors, herpesvirus entry mediator (HVEM) and nectin-1, mediate infection independently but are coexpr

115 alternative gD receptor HVEM, HSV-1 requires nectin-1, not HVEM, to enter these cells.

116 In nectin-1, the first and second Ig module in the extracel

117 Herpes Simplex Virus (HSV1) HSV-1 receptor, nectin-1, to allow for more efficient infection and repl

118 -1 entry to dermal fibroblasts isolated from nectin-1- or HVEM-deficient mice or from mice deficient

119 Using nectin-1- or HVEM-deficient mice, we demonstrated the di

120 Entry of the gB mutant virus into nectin-1-bearing cells was markedly accelerated compared

121 gV-core of the gD ectodomain was impaired on nectin-1-bearing cells.

122 pressed on fibroblasts, entry was delayed in nectin-1-deficient cells, suggesting that nectin-1 acts

123 In nectin-1-deficient epidermis, entry was strongly reduced

124 Almost no entry was observed, however, in nectin-1-deficient keratinocytes grown in culture.

125 rmis and with the lack of HVEM expression in nectin-1-deficient primary keratinocytes.

126 Passaging of HVEM-restricted virus on nectin-1-expressing cells yielded a set of gD missense m

127 ive infection with BV was possible only with nectin-1-expressing cells, indicating that nectin-1 medi

128 ild-type gH and some gH mutants, fusion with nectin-1-expressing target cells occurred more rapidly t

129 the stratum intermedium (SI), its absence in nectin-1-null mice correlated with separation of the cel

130 Although the incisors of nectin-1-null mice were hypomineralized, the protein com

131 cinoma cells are susceptible to infection by nectin-1-restricted virus but are highly resistant to HV

132 not dependent on the presence or absence of nectin-1.

133 omodimerization, and heterodimerization with nectin-1.

134 ely the key to the downregulation of surface Nectin-1.

135 (PILRalpha) than with gD receptors HVEM and nectin-1.

136 ptors, herpesvirus entry mediator (HVEM) and nectin-1.

137 are critical for the interaction of gD with nectin-1.

138 at FGFR is a downstream signaling partner of nectin-1.

139 ls that express a gD-binding-impaired mutant nectin-1.

140 role for the herpesvirus entry mediator and nectin-1.

141 that each restored functional recognition of nectin-1.

142 function with PILRalpha and the gD receptor, nectin-1.

143 xible C terminus bound well to both HVEM and nectin-1.

144 ptors, herpesvirus entry mediator (HVEM) and nectin-1.

145 VEM, but not the other major virus receptor, nectin-1.

146 docytosis, requiring the gD-binding receptor nectin-1.

147 upon expression of either human nectin-2 or nectin-1.

148 , in addition to the reported receptor human nectin-1.

149 racts directly with the PDZ-binding motif of nectin-1.

150 H can interfere with the formation of stable nectin-1/nectin-4 heterodimers.

151 9 on EC as well as on PECAM-1 and depends on nectin-2 (CD112) and poliovirus receptor (CD155) as well

152 The DNAM-1 ligands Nectin-2 (CD112) and the poliovirus receptor (PVR; CD155

153 A-1 (CD11a/CD18) but not Mac-1 (CD11b/CD18); nectin-2 and poliovirus receptor are engaged by both DNA

154 trains can effectively use both nectin-1 and nectin-2 as cellular receptors for entry into human cell

155 The TIGIT/nectin-2 binding disrupted pre-assembled nectin-2 oligom

156 have determined the crystal structure of the nectin-2 homodimer at 1.3 A resolution.

157 bound to the first immunoglobulin domain of nectin-2 indicated that the receptor and ligand dock usi

158 dissected the energetic basis for the TIGIT/nectin-2 interaction and revealed that an "aromatic key"

159 Here we report that human nectin-2 is a target receptor for B virus entry, in addi

160 ction and revealed that an "aromatic key" of nectin-2 is critical for this interaction, whereas varia

161 GIT/nectin-2 binding disrupted pre-assembled nectin-2 oligomers, suggesting that receptor-ligand and

162 ical strains upon expression of either human nectin-2 or nectin-1.

163 TIGIT bound to the immunoglobulin domain of nectin-2 that is most distal from the membrane with an a

164 tient-derived myelomas expressing PVR and/or Nectin-2 was DNAM-1 dependent, revealing a functional ro

165 Furthermore, E-cadherin and nectin-2 were found between adjoining membranes, suggest

166 action is well understood, how TIGIT engages nectin-2, a receptor that is broadly over-expressed in b

167 6-binding proteins (ULBP)1-6 (NKG2D ligand), Nectin-2/CD112, and poliovirus receptor (PVR)/CD155 (DNA

168 ffects on the FAK signaling and retention of nectin-3 adhesion complex at the apical ES.

169 esion kinase (FAK)-Tyr(397) and retention of nectin-3 adhesion protein at the apical ES.

170 are necessary for the trans-interaction with nectin-3 and formation of cis-dimers, respectively.

171 The junctional recruitment of nectin-1 and nectin-3 and their protein levels are decreased via prot

172 PDZD11 forms a complex with nectin-1 and nectin-3, and its PDZ domain interacts directly with the

173 yers II/III and V-VI), whereas others (e.g., Nectin-3, Plexin-D1, and Dkk3) discriminate between CPN

174 p between p-FAK-Tyr(397) and localization of nectin-3, we overexpressed sFRP1 using lentiviral vector

175 or expression, HLFs expressed both CADM1 and nectin-3, whereas HASMCs expressed only nectin-3.

176 and nectin-3, whereas HASMCs expressed only nectin-3.

177 , leading to a decline in phosphorylation of nectin-3.

178 um-based assays in Vero, Vero-SLAM, and Vero-Nectin 4 cell lines.

179 AM; CD150) and the adherens junction protein nectin-4 (poliovirus receptor-like 4 [PVRL4]) as recepto

180 ion subtractive hybridization and identified nectin-4 (PVRL4), a type I transmembrane protein and mem

181 d ADAM10 cleave Nectin-4 and release soluble Nectin-4 (sN4).

182 A soluble form of nectin-4 abolished vaccine MV entry in nectin-4- and CD4

183 n the beta4-beta5 groove drastically reduced nectin-4 and CD46 binding while minimally altering SLAM

184 overlap between the functional footprints of nectin-4 and CD46 but not those of SLAM.

185 drophobic pocket affected entry through both nectin-4 and CD46 but not through SLAM.

186 Thus, while nectin-4 and CD46 interact functionally with the H prote

187 y, the C'C" loop governs dissociation of the nectin-4 and H ectodomains.

188 We report that ADAM17 and ADAM10 cleave Nectin-4 and release soluble Nectin-4 (sN4).

189 enfortumab vedotin comprising the human anti-nectin-4 antibody conjugated to the highly potent microt

190 rug conjugate enfortumab vedotin, human anti-nectin-4 antibody is linked to the cytotoxic microtubule

191 Overall, these findings validate nectin-4 as an attractive therapeutic target in multiple

192 irus (MV) uses the adherens junction protein nectin-4 as its epithelial receptor provides a new vanta

193 tant was less effective than wild-type human nectin-4 at promoting MV infection in primary cultures o

194 Nectin-4 binds a hydrophobic groove located between blad

195 Further, by using a nectin-4 blocking antibody or recombinant MeV unable to

196 However, the mechanism of Nectin-4 cleavage in ovarian cancer has not yet been det

197 MV receptor CD46 and nectin-4 expression was confirmed by immunohistochemistr

198 ates the importance of MeV interactions with nectin-4 for clinical disease in the new and better-perf

199 n the C'C" loop modulate the dissociation of nectin-4 from the viral hemagglutinin.

200 gle amino acid variant in the BC loop of pig nectin-4 fully accounts for restricted MeV entry.

201 same key residues in the BC and FG loops of nectin-4 govern binding to the MeV attachment protein he

202 hree loops forming the adhesive interface of nectin-4 have different roles in supporting MeV H associ

203 erfere with the formation of stable nectin-1/nectin-4 heterodimers.

204 nt protein hemagglutinin (H) and cell entry, nectin-4 homodimerization, and heterodimerization with n

205 rane proteins, and ADAM17 is known to cleave Nectin-4 in breast cancer.

206 t tumor specimens, whereas the expression of nectin-4 in normal tissue was more limited.

207 Nectin-4 is a tumour-associated antigen found on the sur

208 ously showed that the cell adhesion molecule Nectin-4 is overexpressed in ovarian cancer tumors, and

209 We also generated a nectin-4 mutant without the afadin-binding site in its c

210 cells and spread without the need to engage nectin-4 or CD150, known receptors for MeV that are not

211 We have confirmed that the ovine Nectin-4 protein, when overexpressed in epithelial cells

212 t F-mediated fusion when H is engaged to its nectin-4 receptor than when H is engaged to its CD150 re

213 We quantified Nectin-4 shedding from the surface of ovarian cancer cel

214 Understanding the function of Nectin-4 shedding in ovarian cancer progression is criti

215 Ms and DCs rely on cell-to-cell contacts and nectin-4 to efficiently deliver MeV to the basolateral s

216 evance of the protein afadin, which connects nectin-4 to the actin cytoskeleton, we knocked down its

217 were able to bind to cell surface-expressed nectin-4 with high affinity and induced cell death in vi

218 idues in all three loops, the association of nectin-4 with the measles virus hemagglutinin requires o

219 Furthermore, we detected RNA for Nectin-4, ADAM10, and ADAM17 in primary ovarian carcinom

220 oarray data showed that higher expression of Nectin-4, ADAM10, and ADAM17 is associated with signific

221 he infection spreads to epithelia expressing nectin-4, an adherens junction protein expressed prefere

222 rus measles virus (MeV) uses tissue-specific nectin-4, and the positive-strand RNA virus poliovirus u

223 so to infect epithelia of tissues expressing nectin-4, including the trachea.

224 ecombinant MeV unable to enter cells through nectin-4, we demonstrated formally that transfer from im

225 n is an antibody-drug conjugate that targets Nectin-4, which is highly expressed in urothelial carcin

226 ble to interact with the epithelial receptor nectin-4, while causing immunosuppression, resulted in o

227 rm of nectin-4 abolished vaccine MV entry in nectin-4- and CD46-expressing cells but only reduced ent

228 Similar titers of the wild-type and nectin-4-blind MeV were detected in peripheral blood mon

229 ransfer from immune cells to HAE occurs in a nectin-4-dependent manner.

230 -blind" derivative, which is unable to enter nectin-4-expressing cells because of the targeted mutati

231 /expansion study that enrolled patients with Nectin-4-expressing solid tumors (eg, metastatic urothel

232 velopment, investigation, and application of nectin-4-targeting ADCs.

233 molecule (SLAM), and the epithelial receptor nectin-4.

234 (poliovirus-receptor-like 4), also known as Nectin-4.

235 es comprising four members, nectin-1 through nectin-4.

236 at 69% of all specimens stained positive for nectin-4.

237 way epithelial cells, MV spread requires the nectin-4/afadin complex and is based on cytoplasm transf

238 V-2 infection by siRNA-mediated knockdown of nectin, a host cell protein.

239 n formation and elongation require afadin, a nectin adaptor protein implicated in adherens junction f

240 o provide the first direct evidence that the nectin-afadin axis is essential for proper palate shelf

241 These nectin-afadin clusters uniformly colocalize with N-cadhe

242 The nectin-afadin complex also localizes to AJs and links to

243 Furthermore, the nectin-afadin system is required for the deposition of t

244 Several nectin and cadherin clusters that constitute an individu

245 Nectin and nectin-like (Necl) adhesion molecules are bro

246 TIGIT recognizes nectin and nectin-like adhesion molecules and thus plays

247 rging family of receptors that interact with nectin and nectin-like proteins.

248 Our findings identify nectins and afadin as components of the reelin signaling

249 al. show that the differential expression of nectins and cadherins establishes this pattern.

250 ditional loss of afadin (Afdn) - an obligate nectin- and actin-binding protein - induces a high penet

251 Cadherin and nectin are distinct transmembrane proteins of adherens j

252 Nectins are cell adhesion molecules that are widely expr

253 Nectins are cell adhesion molecules that, together with

254 Nectins are immunoglobulin superfamily glycoproteins tha

255 Nectins are involved in formation of the mechanical adhe

256 Nectins are members of the Ig superfamily that mediate c

257 Different viruses utilize nectins as receptors.

258 pe virus background enabled the use of other nectins as virus entry receptors.

259 Lens fiber cell N-cadherin/beta-catenin/Rap1/Nectin-based cell-cell junction formation and WAVE-2/Abi

260 against glycoprotein D (gD) protected these nectin-bearing cells from B virus infection, and a gD-ne

261 Nectins belong to a family of immunoglobulin (Ig)-like c

262 ewly defined canonical adhesive interface of nectins, but how viruses utilize this interface has rema

263 proteins match the boundaries of cadherin or nectin clusters.

264 led to delayed and diminished integration of nectin complexes and failure to recruit R-cadherin.

265 is for recognition and selectivity among the nectin family members.

266 th naturally occurring ligand binding in the nectin family suggest which specific structural rearrang

267 irus and its receptor are reminiscent of the nectin family, by involving the burying of otherwise-exp

268 lic and heterophilic interactions within the nectin family.

269 Nectins have been shown to regulate tight junction forma

270 We showed that cadherin and nectin in the junctions of A431 cells and human keratino

271 Previous in vitro studies demonstrated that Nectin like 4 (Necl-4, also known as cell adhesion molec

272 Nectin and nectin-like (Necl) adhesion molecules are broadly overex

273 s and Schwann cells express distinct sets of nectin-like (Necl) proteins: axons highly express Necl-1

274 Nectins (nectin1-4) and Necls [nectin-like (Necl1-5)] are Ig superfamily cell adhesion

275 Nectin-like 1 (Necl-1) is a neural-specific cell adhesio

276 tic Cell Adhesion Molecule 1 (SynCAM 1/CADM1/nectin-like 2 protein).

277 molecular level, 4.1G is associated with the nectin-like 4 (NECL4) adhesion molecule.

278 Nectin-like 4 (NECL4, CADM4) is a Schwann cell-specific

279 he positive-strand RNA virus poliovirus uses nectin-like 5 (necl-5), also known as poliovirus recepto

280 TIGIT recognizes nectin and nectin-like adhesion molecules and thus plays a critical

281 show that the intercellular adhesion protein nectin-like molecule 2 (Necl2) is highly expressed in bu

282 esion molecule (SynCAM) proteins (also named nectin-like molecules) are immunoglobulin adhesion prote

283 tin in the Schwann cell cytoskeleton and the Nectin-like protein, Necl4, at the contact site between

284 he structure of human DNAM-1 in complex with nectin-like protein-5 (Necl-5) at 2.8 angstrom resolutio

285 Although the TIGIT nectin-like protein-5 (necl-5) interaction is well under

286 y of receptors that interact with nectin and nectin-like proteins.

287 ystal structure of poliovirus receptor (PVR)/Nectin-like-5/CD155) in complex with its cognate immunor

288 tation, cellular organization and junctional nectin localization.

289 ed to enter these cells, indicating that the nectin-mediated B virus entry depends on gD.

290 family members and also offer insights into nectin-mediated transinteractions between engaging cells

291 , we highlight the "guiding" role of JAM/CAR/nectin molecules for germ cell passage.

292 Interestingly, JAM/CAR/nectin molecules mediate virus uptake and leukocyte tran

293 We demonstrate that while nectin-nectin interactions require residues in all three

294 inding motifs previously observed to mediate nectin/nectin homotypic interactions as well as TIGIT/ne

295 these findings broaden our understanding of nectin/nectin receptor interactions and have implication

296 Nectins (nectin1-4) and Necls [nectin-like (Necl1-5)] ar

297 ort cell entry of other viruses that utilize nectins or other cell adhesion molecules of the immunogl

298 he immunoglobulin superfamily (e.g., JAM/CAR/nectin) participate in germ cell migration by conferring

299 Nectins share the same overall structural topology with

300 w that the PLEKHA7-PDZD11 complex stabilizes nectins to promote efficient early junction assembly and