ライフサイエンスコーパス: plexin

1 cing formation of a specific active dimer of plexin.

2 s also explain the unique Rap-specificity of plexins.

3 evaluated gene expression of neuropilins and plexins.

4 cellular functions through their receptors, plexins.

5 These PKA-mediated Plexin-14-3-3epsilon interactions prevent PlexA from int

6 omain and Sema-1a mediates repulsion through Plexin A (PlexA) expressed in an adjacent region.

7 a) is a repulsive guidance cue that uses the Plexin A (PlexA) receptor during neural development.

8 Here we describe a role for Plexin A (PlexA), a protein with particularly well-chara

9 of other Drosophila circular RNAs, including Plexin A (PlexA), suggesting a common strategy for regul

10 sically associates with the Sema-1a receptor plexin A (PlexA).

11 ytoplasmic domain of the semaphorin receptor plexin A and mediates semaphorin-signaled collapse of th

12 embrane proteins semaphorin-1a (Sema-1a) and plexin A function together to regulate R axon lamination

13 Endogenous plexin A peptides and proteins, which share the core mot

14 We also show that the mRNA encoding plexin A remains highly polysome associated during stres

15 nteraction studies suggest that Highwire and Plexin A signals may interact to regulate normal morphog

16 ranscript expression was altered, decreasing plexin A1 and increasing plexin C1.

17 ent neurons failed to collapse and transport Plexin A1 to cell bodies.

18 We also demonstrate a role for Plexin A1, a zebrafish orthologue of Drosophila PlexA, i

19 Syb2 associated with Neuropilin 1 and Plexin A1, two essential components of the Sema3A recept

20 al glia and Plexin-A1 on chiasm neurons, and Plexin-A1 and Nr-CAM are also expressed on contralateral

21 laterally at the chiasm midline in vivo, and Plexin-A1 and Nr-CAM expression in RGCs is downregulated

22 Here, we show that neuropilin-2/plexin-A1 are also coexpressed on commissural axons prio

23 sm by which a complex of Sema6D, Nr-CAM, and Plexin-A1 at the chiasm midline alters the sign of Sema6

24 s, but Sema6D in combination with Nr-CAM and Plexin-A1 converts repulsion to growth promotion.

25 CAM are expressed on midline radial glia and Plexin-A1 on chiasm neurons, and Plexin-A1 and Nr-CAM ar

26 eted semaphorins signal through neuropilin-2/plexin-A1 receptor complexes on post-crossing commissura

27 alters the sign of Sema6D and signals Nr-CAM/Plexin-A1 receptors on RGCs to implement the contralater

28 nal cord, which can be rescued by inhibiting plexin-A1 signaling in vivo.

29 Sema6D, Plexin-A1, and Nr-CAM are all required for efficient RGC

30 ls (LEC) in a neuropilin-2-, plexin-D1-, and plexin-A1-dependent manner, while most other semaphorins

31 rate that Sema6B binds to floorplate-derived plexin A2 (PlxnA2) for navigation at the midline, wherea

32 Plexin A2 and A4, two Sema6A binding partners, are expre

33 brane protein semaphorin 6A and its receptor plexin A2 are critical for achieving radially symmetric

34 Plexin A2 is expressed in both On and Off SACs; however,

35 Furthermore, Sema6A/Plexin-A2/A4 signaling is required for the functional ou

36 Thus, plexin A3 dependent intrinsic and turnout dependent extr

37 d that null mutants of the guidance receptor plexin A3 display identical motor axon branching defects

38 t precocious branch formation in turnout and plexin A3 mutants is due to increased stability of other

39 ortantly, deletion of either neuropilin 1 or plexin A3 significantly reduces developmental cell death

40 c pathway and requires both neuropilin 1 and plexin A3.

41 Using unbiased approaches, we identified Plexin A4 (PLXNA4) as a novel, high-affinity receptor fo

42 oxO6 binds to DAF-16-binding elements in the Plexin A4 (Plxna4) promoter region and affects Plxna4 ex

43 Be-loaded HLA-DP2-mimotope and HLA-DP2-plexin A4 tetramers detected high frequencies of CD4(+)

44 role of plexins to TLR signaling and suggest plexin-A4 and Sema3A as new intervention points for trea

45 Plexin-A4 is required for TLR-induced activation of the

46 , in this study we show a novel influence of plexin-A4 on TLR signaling.

47 Administration of a ligand of plexin-A4, Sema3A (semaphorin 3A), exacerbates the cytok

48 By studying plexin-A4-deficient (Plxna4(-/-)) innate immune cells, i

49 lyses support that these mechanisms underlie plexin activation and signaling.

50 degree of cross correlation, indicating that plexin activation does not lead to higher-order oligomer

51 imed for GAP activity and extend a model for plexin activation.

52 By reconstituting all possible plexin and neuropilin combinations, we found that SEMA3F

53 cone guidance molecules that signal through plexin and neuropilin coreceptors and since then have be

54 rganogenesis, and tumor progression, through Plexin and neuropilin receptors.

55 tributes to the specific interaction between plexin and PDZ-RhoGEF and to signaling by plexin in the

56 rands in extracellular cadherin and Ig-like, plexin and transcription factor domains.

57 n, O-Man glycosylation of IPT/TIG domains of plexins and hepatocyte growth factor receptor was not af

58 SEMA3F acts on its coreceptors, plexins and neuropilins, among which neuropilin-2 (NRP2)

59 ce through interaction with their receptors, plexins and neuropilins.

60 ules that are known primarily as ligands for plexins and neuropilins.

61 LARG), use their PDZ domains to bind class B plexins and play critical roles in signaling.

62 Plexins and semaphorins are ligand-receptor pairs that s

63 Plexins and semaphorins comprise a large family of recep

64 We believe that the plexins and semaphorins, which are strongly expressed in

65 The expression of Plexins and their ligands on DCs and T cells suggest fun

66 uch as ephrins and Ephs, and semaphorins and plexins, and through expression of clastokines.

67 Plexins are a family of genes (A,B,C, and D) that are ex

68 Plexins are a family of single-pass transmembrane protei

69 rin-Plexin recognition mode and suggest that Plexins are activated by dimerization.

70 However, semaphorins and plexins are also expressed in the adult brain.

71 Plexins are cell surface receptors that bind semaphorins

72 P domain-mediated developmental functions of plexins are not brought about via R-Ras and M-Ras inacti

73 Plexins are Ras/Rap family GTPase activating proteins (G

74 Plexins are similar to the Toll-like receptors (TLRs) in

75 Plexins are single-pass transmembrane receptors that bin

76 Plexins are transmembrane receptors that regulate proces

77 et-derived signal that acts upon presynaptic plexin B (PlexB) receptors to mediate the retrograde, ho

78 Sema-2b utilize the same neuronal receptor, plexin B (PlexB), but serve distinct guidance functions.

79 Mutations affecting the Sema-2a ligand, the plexin B receptor (plexB), the voltage-gated Ca(v)2.1 ca

80 d from the epidermis and signals through the Plexin B receptor in neighboring neurons.

81 ion in the skin, and suggest that Sema4D and Plexin B1 act cooperatively with HGF and c-Met to regula

82 However, because plexin B1 activates Akt, a multifunctional protein invol

83 Plexin B1 also activated Akt in melanoma.

84 These data demonstrate a role for Plexin B1 in maintenance of melanocyte survival and prol

85 Unexpectedly, introduction of plexin B1 into human melanoma cell lines suppressed, rat

86 A study by Argast et al. has shown that plexin B1 is a tumor-suppressor protein for melanoma met

87 In this report, we show that plexin B1 is lost in metastatic and deeply invasive mela

88 Plexin B1 is predicted to function as a classic tumor-su

89 Because our data show that Plexin B1 is profoundly downregulated by UVB in melanocy

90 downregulated by UVB in melanocytes, loss of Plexin B1 may accentuate HGF-dependent effects on melano

91 ved in tumor progression in several cancers, plexin B1 may function as a tumor promoter in melanomas

92 Plexin B1 significantly abrogated cell migration in resp

93 Interestingly, the inhibitory response to plexin B1 was reduced or absent in cells from a matched

94 We recently reported that Plexin B1, the Semaphorin 4D (Sema4D) receptor, is a tum

95 Plexin B1, the semaphorin 4D receptor, activates oncogen

96 nded on residues in the C-terminal domain of plexin B1, which mediate receptor GTPase activating prot

97 mplexes of the semaphorin-binding regions of plexins B1 and A2 with semaphorin ectodomains (human PLX

98 ame system of proteins, suggesting that both plexin-B1 and semaphorin 4D are important in the promoti

99 Our data unravel a role for Plexin-B1 as a ligand and Sema4A as a receptor and chara

100 ly, we show that the monomeric intracellular plexin-B1 binds R-Ras but not H-Ras.

101 igration, we develop an optogenetic tool for Plexin-B1 designated optoPlexin.

102 -overexpressing breast cancer, low levels of Plexin-B1 expression correlated with good prognosis.

103 Thus, our data demonstrate a causal role of Plexin-B1 for CIL in osteoblasts and reveals a previousl

104 -activated signalling pathways downstream of plexin-B1 function in prostate cancer progression.

105 We show here that Sema4D/plexin-B1 increases the expression of androgen-responsiv

106 In this study, we show that plexin-B1 is overexpressed in tissues and cell lines fro

107 Plexin-B1 is therefore a promising target for cancer the

108 Our data suggest that Plexin-B1 represents a new candidate therapeutic target

109 Activation of plexin-B1 results in phosphorylation of AR at Serine 81,

110 These results show that Sema4D/plexin-B1 signalling promotes the translocation of AR to

111 xamine causality and elucidate how localized Plexin-B1 stimulation may spatiotemporally coordinate it

112 breast cancer, ablation of the gene encoding Plexin-B1 strongly reduced the occurrence of metastases.

113 ransduce signals triggered by the binding of Plexin-B1 through reverse signaling.

114 We further show that binding of Plexin-B1 to Sema4A promotes the interaction of Sema4A w

115 Plexin-B1, the receptor for semaphorin4D (Sema4D), has b

116 a ubiquitin-like RhoGTPase binding domain of plexin-B1, we removed either internal or global motions.

117 on and activation of the semaphorin receptor Plexin-B1.

118 on (CIL) in osteoblasts through its receptor Plexin-B1.

119 The discovery of immune functions for plexin B2 and CD100 provides insight into the complex ce

120 Plexin B2 competes with p190RhoGAP for binding to Rnd3,

121 In vitro blocking of plexin B2 or CD100 inhibited gammadelta T cell activatio

122 Here we show that the Plexin B2 receptor interacts physically and functionally

123 Here, we identify a role for interaction of plexin B2 with the CD100 receptor in epithelial repair.

124 Here, we show that plexin-B2 (PLXNB2) is the functional receptor for ANG in

125 Plexin-B2 and Plexin-D1 are reciprocally expressed in my

126 In this study, the expression pattern of Plexin-B2 and Plexin-D1 in dendritic cells (DCs), which

127 Expression of Plexin-B2 and Plexin-D1 is modulated upon activation of

128 Absence of Plexin-B2 and Plexin-D1 on DCs did not affect the abilit

129 This work also shows the presence of Plexin-B2 and Plexin-D1 on mouse DC subpopulations, and

130 Additionally, Plexin-B2 and Plexin-D1 were dispensable for chemokine-d

131 first report to show an association between Plexin-B2 and Plexin-D1 with the negative regulation of

132 Plasmacytoid DCs have high Plexin-B2 but low Plexin-D1, while the opposite is true

133 f transgenic and knockout mice indicate that Plexin-B2 controls the cell division axis by signaling t

134 Plexin-B2 expression is downregulated in the olfactory b

135 Plexin-B2 is a semaphorin receptor previously known to a

136 w here that, in the postnatal and adult CNS, Plexin-B2 is expressed in the subventricular zone lining

137 opy, revealed that neuroblasts deficient for Plexin-B2 migrate faster than control ones and leave the

138 ial cells lacking the transmembrane receptor Plexin-B2 or its semaphorin ligands fail to correctly or

139 Mice in which endogenous Plexin-B2 or Plexin-D1 is replaced by transgenic version

140 However, the absence of either Plexin-B2 or Plexin-D1 on DCs leads to constitutive expr

141 Overall, these results show that Plexin-B2 plays a role in postnatal neurogenesis and in

142 In contrast to the GAP domain mutants, Plexin-B2 transgenic mice defective in Rho guanine nucle

143 Semaphorin3E, a ligand for Plexin-D1 and Plexin-B2, is expressed by T cells, and interestingly, i

144 mode of interaction triggers all semaphorin-plexin based signalling, while distinct insertions withi

145 to achieve Sema7A mimicry by preserving key Plexin-binding determinants seen in the mammalian Sema7A

146 lent 2:2 complex (monomeric semaphorin binds plexin but fails to trigger signalling).

147 aphorins are dimeric molecules that activate plexin by binding two copies of plexin simultaneously an

148 he results suggest that semaphorin activates plexin by disrupting an inhibitory plexin dimer and indu

149 he contributions of the semaphorin receptor, plexin C1 (PLXNC1), and the exocytic calcium sensor, syn

150 in C1 in wild-type mice treated with an anti-Plexin C1 antibody and a Semaphorin 7A peptide reduced h

151 Plexin C1 deficiency permits synaptotagmin 7-mediated ma

152 In mouse xenografts, Plexin C1 delayed tumor growth of melanoma at early time

153 These results describe a role for Plexin C1 during ischemia-reperfusion injury, highlight

154 ence, we investigated the functional role of Plexin C1 in a mouse model of early hepatic ischemia-rep

155 These data suggest that loss of Plexin C1 in melanoma may promote early steps in melanom

156 injury, highlight the role of hematopoietic Plexin C1 in the development of hepatic ischemia-reperfu

157 We found that the functional inhibition of Plexin C1 in wild-type mice treated with an anti-Plexin

158 in melanoma, whereas in melanocytes, loss of Plexin C1 increased migration and proliferation.

159 tumor suppressor for melanoma, we introduced Plexin C1 into a primary human melanoma cell line, and p

160 schemia-reperfusion injury, and suggest that Plexin C1 is a potential drug target.

161 To determine if Plexin C1 is a tumor suppressor for melanoma, we introdu

162 Plexin C1 is a type I transmembrane receptor with intrin

163 indicate that the neuronal guidance receptor Plexin C1 is involved in the control of the acute inflam

164 himeric mice revealed that the hematopoietic Plexin C1 knockout is crucial for reducing the extent of

165 Plexin C1 lowered R-Ras activity in melanoma and melanoc

166 In primary melanoma, loss of Plexin C1 may function in early steps of melanoma progre

167 In primary melanoma, loss of Plexin C1 may function in early steps of melanoma progre

168 cytes, consistent with inhibitory effects of Plexin C1 on migration of melanocytes and melanoma.

169 Experiments using Plexin C1 receptor-deficient (PLXNC1) mice also demonstr

170 r inhibitory ways with its beta1 integrin or Plexin C1 receptors, respectively.

171 Plexin C1 significantly inhibited migration and prolifer

172 d proliferation, but pro-survival effects of Plexin C1 ultimately abrogate the tumor suppressive effe

173 Complimentary studies in which Plexin C1 was silenced in human melanocytes were perform

174 ventually escaped the suppressive effects of Plexin C1, due to Plexin C1-dependent activation of the

175 ors for melanoma, and express high levels of Plexin C1, which is lost in melanoma in vitro and in viv

176 the suppressive effects of Plexin C1, due to Plexin C1-dependent activation of the pro-survival prote

177 ly abrogate the tumor suppressive effects of Plexin C1.

178 altered, decreasing plexin A1 and increasing plexin C1.

179 ignalling through members of the two largest plexin classes, B and A, respectively.

180 The semaphorins and their receptors, the plexins, compose a family of proteins originally shown t

181 Mammalian plexins constitute a family of transmembrane receptors f

182 nsgenic mice, we show that the GAP domain of plexins constitutes their key signaling module during de

183 ome-wide association studies have implicated PLEXIN D1 (PLXND1) in body fat distribution and type 2 d

184 Sema3e signals through plexin D1 (Plxnd1) to regulate vascular patterning by mo

185 Activation of plexin D1 by Sema3E causes the rapid disassembly of inte

186 This metastatic potential was dependent on Plexin D1 expression but was independent of NRP expressi

187 Sema3E acts on plexin D1 to initiate a two-pronged mechanism involving

188 Plexin D1 was identified for the first time in the corne

189 Of clinical importance, Sema3E and Plexin D1 were found to be upregulated in human colon ca

190 hrough a single-pass transmembrane receptor, plexin D1, to provide a repulsive cue for plexin D1-expr

191 GnRH neurons from cell death by triggering a plexin D1-dependent (PLXND1-dependent) activation of PI3

192 r, plexin D1, to provide a repulsive cue for plexin D1-expressing endothelial cells, thus providing a

193 er, the molecular mechanisms by which Sema3E-Plexin-D1 activates Arf6 remained to be identified.

194 in, semaphorin 3E (Sema3E), and its receptor Plexin-D1 also control the vascular patterning during de

195 athway whereby Sema3E activates Arf6 through Plexin-D1 and consequently controls integrin-mediated en

196 Dll4-Notch signaling is regulated by Sema3E-Plexin-D1 and is required for its function in vivo.

197 Semaphorin3E, a ligand for Plexin-D1 and Plexin-B2, is expressed by T cells, and in

198 Plexin-B2 and Plexin-D1 are reciprocally expressed in myeloid and plas

199 Here, we show that the receptor Plexin-D1 contains a sorting motif that interacts with t

200 that gain and loss of function of Sema3E and Plexin-D1 disrupts normal Dll4 expression, Notch activit

201 , we have recently shown that Sema3E acts on Plexin-D1 expressed in endothelial cells, thus initiatin

202 Plexin-D1 expression was increased following B cell acti

203 er, these data reveal a novel role of Sema3E-Plexin-D1 function in modulating angiogenesis via a VEGF

204 etinal vasculature of mice lacking sema3E or plexin-D1 has an uneven growing front, a less-branched v

205 udy, the expression pattern of Plexin-B2 and Plexin-D1 in dendritic cells (DCs), which are central in

206 eted semaphorin 3E (Sema3E) and its receptor Plexin-D1 is a critical determinant of synaptic specific

207 Expression of Plexin-B2 and Plexin-D1 is modulated upon activation of DCs by TLR lig

208 Mice in which endogenous Plexin-B2 or Plexin-D1 is replaced by transgenic versions harboring m

209 mouse retina as a model system, we show that Plexin-D1 is selectively expressed in endothelial cells

210 Absence of Plexin-B2 and Plexin-D1 on DCs did not affect the ability of these cel

211 However, the absence of either Plexin-B2 or Plexin-D1 on DCs leads to constitutive expression of IL-

212 ork also shows the presence of Plexin-B2 and Plexin-D1 on mouse DC subpopulations, and indicates that

213 ide evidence that upon activation by Sema3E, Plexin-D1 recruits phosphatidylinositol-4-phosphate 5-ki

214 nce of interaction with GIPC1, missorting of Plexin-D1 results in loss of signalling activity.

215 ly distributed throughout the retina, Sema3E-Plexin-D1 signaling is spatially controlled by VEGF thro

216 Sema3E-Plexin-D1 signaling then negatively regulates the activi

217 as well as vascular structures, that rely on Plexin-D1 signalling for their development.

218 hus, our results demonstrate that Sema3E and Plexin-D1 specify the degree of glutamatergic connectivi

219 Plexin-D1 was not required for B cell maturation, margin

220 Additionally, Plexin-B2 and Plexin-D1 were dispensable for chemokine-directed in-vit

221 to show an association between Plexin-B2 and Plexin-D1 with the negative regulation of IL-12/IL-23p40

222 s sorting process promotes colocalization of Plexin-D1 with vesicular pools of active R-ras, leading

223 ns, whereas in the striatum Plxnd1 (encoding Plexin-D1) is selectively expressed in direct-pathway me

224 f a host tissue-derived signal (Semaphorin3E-Plexin-D1) that accelerates tip cell selection rate, yie

225 ew member of the plexin family of molecules, plexin-D1, controls the GC reaction and is required for

226 hat VEGF directly controls the expression of Plexin-D1, the receptor for the traditional repulsive ax

227 Plasmacytoid DCs have high Plexin-B2 but low Plexin-D1, while the opposite is true of myeloid DCs.

228 endothelial cells (LEC) in a neuropilin-2-, plexin-D1-, and plexin-A1-dependent manner, while most o

229 controlled by VEGF through its regulation of Plexin-D1.

230 activates plexin by disrupting an inhibitory plexin dimer and inducing the active dimer.

231 ng mechanism involving semaphorin-stabilized plexin dimerization, possibly followed by clustering, wh

232 en question is whether there are preexisting plexin dimers that could act as autoinhibitory complexes

233 absence of any structural information on the plexin ectodomain or its interaction with semaphorins th

234 In vitro studies have shown that plexins exert their effects via an intracellular R-Ras/M

235 Plexins expressed in the immune system have been implica

236 factor that directly responds to Semaphorin/Plexin extracellular repulsive cues.

237 Members of the plexin family are unique transmembrane receptors in that

238 We report that a new member of the plexin family of molecules, plexin-D1, controls the GC r

239 Thus, plexins function in epithelial wound healing in diverse

240 of these signaling pathways are relevant for plexin functions in vivo is largely unknown.

241 The plexin GAP is activated by semaphorin-induced dimerizati

242 cues semaphorins (Semas) and their receptors plexins have been shown to regulate both physiological a

243 Semaphorins and their receptors plexins have diverse roles in many cancers affecting tum

244 en plexin and PDZ-RhoGEF and to signaling by plexin in the cell.

245 These data show a new role for immune plexins in the GC reaction and generation of immunologic

246 Furthermore, plexin inhibits presynapse formation by suppressing syna

247 The regulation of the guidance receptor plexin is incompletely understood.

248 Repulsive signaling by Semaphorins and Plexins is crucial for the development and homeostasis o

249 The intracellular region of plexins is essential for signaling and contains a R-Ras/

250 signal, interaction of Sema3s and NRPs with plexins is obligatory.

251 both necessary and sufficient for semaphorin-plexin-mediated F-actin reorganization in vivo.

252 (GAP) domain for R-Ras, which is crucial for plexin-mediated regulation of cell motility.

253 nce and functional specificity of individual plexin-mediated signaling pathways during development.

254 The gene family plexins, members of which are mutated in several monogen

255 hat semaphorin dimers independently bind two plexin molecules and that signalling is critically depen

256 full-length PlexinA4 to control proteins and plexin mutants, we show that dimerization of inactive Pl

257 sylation is primarily found on cadherins and plexins on beta-strands in extracellular cadherin and Ig

258 In the plexin or semaphorin mutants, synaptic domains from both

259 t families of axon guidance cues and utilize Plexin (Plex) receptors to exert repulsive effects on ax

260 identified roles for Semaphorins (Sema) and Plexins (Plex) in walking behavior.

261 Class A plexins (PlxnAs) act as semaphorin receptors and control

262 , the sole member of the vertebrate-specific PlexinD (PlxnD1) subfamily.

263 horin known to be capable of signaling via a plexin receptor without a neuropilin coreceptor.

264 semaphorin ligands through interaction with plexin receptors is important for the homeostasis and mo

265 t Mical directly links semaphorins and their plexin receptors to the precise control of actin filamen

266 and binding to their cognate neuropilin and plexin receptors.

267 ex structures support a conserved Semaphorin-Plexin recognition mode and suggest that Plexins are act

268 How plexin regulation of neurite outgrowth, lymphoid traffic

269 hat Abl allows growth factors and Semaphorin/Plexin repellents to combinatorially increase Mical-medi

270 Focusing on Semaphorin/Plexin repulsion, we identified an interaction between t

271 biochemical switch that controls Semaphorin/Plexin repulsive guidance.

272 full-length extracellular region of class A plexins, revealing its dual role in both autoinhibition

273 Robo-Slit and Plexin-Semaphorin signaling participate in various devel

274 iews of the hybrid domain interface with the plexin-semaphorin-integrin (PSI) domain in different ori

275 Pathogenic hantaviruses bind to the plexin-semaphorin-integrin (PSI) domain of inactive, bet

276 (SH2)- and SH3-containing domains], and the plexin-semaphorin-integrin domain of beta(1) integrin in

277 mediated by the combined action of different Plexin/Semaphorin signaling systems, are required for th

278 of the MET Sema domain fused to the adjacent Plexins, Semaphorins, Integrins domain (MET Sema-PSI), a

279 Our data uncover semaphorin-plexin signaling as a central regulatory mechanism of mi

280 Plexin signaling depends on their cytoplasmic GTPase act

281 Semaphorin-Plexin signaling is critical for many cellular aspects o

282 colocalization with PlexinA4 is reduced and Plexin signaling is not initiated.

283 The importance of these interactions in plexin signaling is shown by both cell-based and in vivo

284 (CRMP2/DPYSL2), a mediator of the semaphorin-plexin signaling pathway, as redox-regulated target of G

285 Hence, contact-dependent, intra-axonal plexin signaling specifies synaptic circuits by inhibiti

286 ating dendrite differentiation is Semaphorin/Plexin signaling, specifically through binding of solubl

287 elial cell-cell communication via semaphorin-plexin signaling.

288 screen to obtain a more complete picture of plexin signaling.

289 llular specificity and mechanism controlling plexin signalling has remained unresolved.

290 During neural development, semaphorin-plexin signalling instructs axon guidance and neuronal m

291 We propose that semaphorin-plexin signalling is an essential platform for the stabi

292 s, an interaction between the cell-extrinsic Plexin signalling pathway and the cell-intrinsic Ascl1-R

293 hat activate plexin by binding two copies of plexin simultaneously and inducing formation of a specif

294 Plexin stabilizes the switch II region of Rap in an unpr

295 peller (sema) domains of both semaphorin and plexin, suggests that a common mode of interaction trigg

296 These findings expand the role of plexins to TLR signaling and suggest plexin-A4 and Sema3

297 In addition, plexin transcript expression was altered, decreasing ple

298 lacks the first extracellular immunoglobulin-plexin-transcription domain.

299 Our results demonstrate plexin-tunable molecular features of integrin adhesion w

300 duces a large-scale conformational change in plexin, which opens the GAP active site to allow Rap bin

301 to associate with the cytoplasmic portion of plexins, which are large cell-surface semaphorin recepto