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

12 ss protrusions in neighboring cells and that Plexin A is the receptor that transduces this signal.

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 mechanism that appears to be independent of Plexin A.

17 rotrusion collapse, induced by Semaphorin-5C-Plexin-A interactions at the cell-cell contact, promotes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 Thus, plexin A3 dependent intrinsic and turnout dependent extr

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

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

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

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

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

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

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

45 Our results unravel a novel Semaphorin3A-Plexin-A4 downstream signaling pathway and shed light on

46 ecific amino acids, the KRK motif within the Plexin-A4 receptor cytoplasmic domain, are required to c

47 The Semaphorin3A-Neuropilin1/Plexin-A4 signaling pathway has been shown to have multi

48 induces expression of the repulsive receptor Plexin-A4, via induction of the transcription factor MEF

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

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

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

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

55 alyses to gain insight into the evolution of plexin and semaphorin families.

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

57 l mechanism for cross-talk between different plexins and co-receptors to allow fine-tuning of cell si

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

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

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

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

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

63 Plexins and semaphorins comprise a large family of recep

64 s are consistent with an ancient function of plexins and semaphorins in regulating cytoskeletal dynam

65 Remarkably, we detected plexins and semaphorins in unicellular choanoflagellates

66 The receptor and ligand pairing of plexins and semaphorins regulates cellular interactions

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

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

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

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

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

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

73 Plexins are cell surface receptors that bind semaphorins

74 Plexins are key cell-surface receptors of the semaphorin

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

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

77 Plexins are receptors for semaphorins that transduce sig

78 Plexins are single-pass transmembrane proteins with mult

79 Plexins are single-pass transmembrane receptors that bin

80 Plexins are transmembrane receptors that regulate proces

81 d mouse cochleae with Sema5B-Fc (to activate Plexin-As) led to type I SGNs with less numerous, but lo

82 We previously reported that Plexin B (PlexB) controls multiple steps during the asse

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

84 -2b) acts through its transmembrane receptor Plexin B (PlexB) to locally attract neural processes to

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

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

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

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

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 Plexin B1 significantly abrogated cell migration in resp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 Plexin B2 competes with p190RhoGAP for binding to Rnd3,

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

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

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

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

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

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

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

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

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

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

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

126 Our data therefore establish Plexin-B2 as an important link that integrates biochemic

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

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

129 Plexin-B2 deletion in myeloid cells impairs corralling,

130 Plexin-B2 expression is downregulated in the olfactory b

131 Corralling begins early and requires Plexin-B2 in both microglia and macrophages.

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

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

134 Plexin-B2 is upregulated in IAMs and is required for mot

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

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

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

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

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

140 Mechanistically, Plexin-B2 promotes microglia motility, steers IAMs away

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

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

143 moted IEC survival and proliferation through plexin-B2-mediated production of tRNA-derived stress-ind

144 omeric semaphorins can mediate a distinctive plexin binding mode.

145 Binding of semaphorin homodimer to plexin brings two plexins in close proximity which is a

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

147 Semaphorin activates plexin by binding to its extracellular N-terminal Sema d

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

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

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

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

152 Plexin C1 deficiency permits synaptotagmin 7-mediated ma

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

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

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

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

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

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

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

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

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

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

163 Plexin C1 is a type I transmembrane receptor with intrin

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

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

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

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

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

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

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

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

172 Plexin C1 significantly inhibited migration and prolifer

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

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

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

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

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

178 ly abrogate the tumor suppressive effects of Plexin C1.

179 ated in axon growth inhibition by Semaphorin/Plexin complexes.

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 Here we show that plexin D1 (PLXND1) has a role in mechanosensation and me

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

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

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

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

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

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

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

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

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

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

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

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

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

197 Plexin-D1 expression was increased following B cell acti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Of these, Plexin domain containing 2 (Plxdc2) was selected as the

229 The plexin domain structure is conserved throughout all clad

230 How Plexins employ their diverse structural motifs in vivo t

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

232 Plexins exhibit multitudinous, evolutionarily conserved

233 Plexins expressed in the immune system have been implica

234 a novel type of Met-like RTK with a complete plexin extracellular domain was detected in Lophotrochoz

235 sine kinases (RTKs), which carry a truncated plexin extracellular domain, in several bilaterian clade

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

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

238 Thus, plexins function in epithelial wound healing in diverse

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

240 The plexin GAP is activated by semaphorin-induced dimerizati

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

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

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

244 of semaphorin homodimer to plexin brings two plexins in close proximity which is a prerequisite for p

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 ema domain, inducing the active dimer of the plexin intracellular region.

248 hanism underlying this activation process of plexin is incompletely understood.

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

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

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

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

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

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

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

256 -attached semaphorins interact in trans with plexins on opposing cells, but also in cis on the same c

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

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

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

260 Semaphorins (SEMAs) and their Plexin (PLXN) receptors are central regulators of metazo

261 neurites expressing Neuropilin (Nrp) and/or Plexin (Plxn) receptors.

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

263 However, a role for plexin proteins in mechanotransduction has not been exam

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

265 The Semaphorin ligands and their Plexin receptors are known to induce cell-cell repulsion

266 Semaphorin ligands and their plexin receptors are one of the major cell guidance fact

267 Semaphorin ligands interact with plexin receptors to contribute to functions in the devel

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

269 n family of guidance cues, signaling through Plexin receptors, influences the development of both axo

270 and binding to their cognate neuropilin and plexin receptors.

271 ma6A mediate binding in cis to their cognate plexin receptors.

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

273 How plexin regulation of neurite outgrowth, lymphoid traffic

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

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

276 biochemical switch that controls Semaphorin/Plexin repulsive guidance.

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

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

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

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

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

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

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

284 Plexin signaling depends on their cytoplasmic GTPase act

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

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

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

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

289 In the absence of endothelin or plexin signaling, sympathetic neurons misproject to inco

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

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

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

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

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

295 close proximity which is a prerequisite for plexin signalling.

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

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

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