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 brane is likely facilitated by clustering of nectin-1 (or HVEM) in phagosomes, which was observed in

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

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

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

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

9 Nectin-1 and afadin cluster at developing synapses betwe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 These studies indicate that access to nectin-1 contributes to preferential apical infection of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Nectin-1 is initially expressed at excitatory and inhibi

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

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

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

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

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

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

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

75 Nectin-1 knockout mice had delayed mortality after intra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 yme 3-O sulfotransferase 3 (3-OST-3) but not nectin-1 or nectin-2.

91 2N and gD-122D variants that affected the gD-nectin-1 protein-protein interface and binding affinity.

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

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

94 It does not infect cells expressing HveA or nectin-1 receptors or cells expressing IL-13Ralpha2 that

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

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

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

98 tion with small interfering RNA specific for nectin-1 resulted in a significant reduction in suscepti

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

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

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

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

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

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

105 Transfection with siRNA targeting nectin-1, a glycoprotein D receptor, also prevented both

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 -1 entry to dermal fibroblasts isolated from nectin-1- or HVEM-deficient mice or from mice deficient

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 omodimerization, and heterodimerization with nectin-1.

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

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

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

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

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

144 that each restored functional recognition of nectin-1.

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

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

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

148 pressing the natural viral receptors HveA or nectin-1.

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

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

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

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

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

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

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

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

157 odomain of one of three gD receptors (HVEMt, nectin-1t, or nectin-2t) and incubated under different p

158 9 on EC as well as on PECAM-1 and depends on nectin-2 (CD112) and poliovirus receptor (CD155) as well

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 otransferase 3 (3-OST-3) but not nectin-1 or nectin-2.

174 6-binding proteins (ULBP)1-6 (NKG2D ligand), Nectin-2/CD112, and poliovirus receptor (PVR)/CD155 (DNA

175 of three gD receptors (HVEMt, nectin-1t, or nectin-2t) and incubated under different pH and temperat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 Nectin-4 binds a hydrophobic groove located between blad

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 Several nectin and cadherin clusters that constitute an individu

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

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

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

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

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 Two recent studies report that the nectin-like (Necl) proteins Necl-1 and -4 are internodal

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

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

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

287 tation, cellular organization and junctional nectin localization.

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

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

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

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

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

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

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

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

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

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

298 Nectins share the same overall structural topology with

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

300 r junction genes including occludin, testin, nectin, zyxin, vinculin, laminingamma3, gelsolin, connec