ライフサイエンスコーパス: PECAM-1

1 PECAM-1 (CD31) knockout (KO) mice exhibit excessive mega

2 PECAM-1 glycans account for approximately 30% of its mol

3 PECAM-1 had no effect on the phosphorylation of the NF-k

4 PECAM-1 is a 130-kDa member of the immunoglobulin (Ig) s

5 PECAM-1 is a cell adhesion and signaling receptor that i

6 PECAM-1 is a dual ITIM-containing receptor that inhibits

7 PECAM-1 is involved in sensing rapid changes in fluid sh

8 PECAM-1 knockout (KO) and wild-type littermates underwen

9 PECAM-1 polymorphism expressed in homozygous or heterozy

10 PECAM-1 transduces forces to activate src family kinases

11 PECAM-1 was the first ITIM-containing receptor identifie

12 PECAM-1 was therefore widely accepted as a major negativ

13 PECAM-1-containing nanodiscs retained not only their abi

14 PECAM-1-KO and chimeric mice revealed that its metastasi

15 PECAM-1-mediated homophilic interactions, known to be me

16 PECAM-1/CD31 is required for leukocyte transendothelial

17 atelet endothelial cell adhesion molecule 1 (PECAM-1) as a prototypical ITIM-bearing receptor, we dem

18 atelet/endothelial cell adhesion molecule 1 (PECAM-1) bind specifically to endothelium and inhibit ef

19 atelet endothelial cell adhesion molecule 1 (PECAM-1) but not other substrates is inhibited in the pr

20 atelet endothelial cell adhesion molecule 1 (PECAM-1) in Fgf-9(+/-) defects.

21 atelet Endothelial Cell Adhesion Molecule 1 (PECAM-1) is a major component of the endothelial cell in

22 atelet endothelial cell adhesion molecule 1 (PECAM-1) is involved in leukocyte migration and angiogen

23 Platelet EC adhesion molecule 1 (PECAM-1) is tyrosine phosphorylated when ECs are exposed

24 atelet/endothelial cell adhesion molecule 1 (PECAM-1) staining, as well as intra-vital fluorescein-co

25 atelet-endothelial cell adhesion molecule 1 (PECAM-1), a junctional protein that has been shown to be

26 atelet-endothelial cell adhesion molecule 1 (PECAM-1), CD99, and interleukin 8 (IL-8).

27 atelet endothelial cell adhesion molecule 1 (PECAM-1), drives advanced metastatic progression and is

28 atelet endothelial cell adhesion molecule 1 (PECAM-1), suggesting a role in neutrophil migration.

29 atelet/endothelial cell adhesion molecule 1 (PECAM-1)-mediated transendothelial migration.

30 atelet-Endothelial Cell Adhesion Molecule-1 (PECAM-1 or CD31) improves drug delivery and pharmacother

31 atelet endothelial cell adhesion molecule-1 (PECAM-1) and heterotrimeric G protein subunits Galphaq a

32 atelet-endothelial cell adhesion molecule-1 (PECAM-1) and the Src family kinase Lyn inhibit platelet

33 atelet endothelial cell adhesion molecule-1 (PECAM-1) at cell-cell junctions and integrins at cell-ma

34 atelet endothelial cell adhesion molecule-1 (PECAM-1) expression is pro-atherogenic.

35 atelet endothelial cell adhesion molecule-1 (PECAM-1) expression, which was surprisingly not associat

36 atelet endothelial cell adhesion molecule-1 (PECAM-1) is a 130-kDa member of the immunoglobulin gene

37 atelet-endothelial cell adhesion molecule-1 (PECAM-1), a transmembrane glycoprotein involved in leuko

38 atelet endothelial cell adhesion molecule-1 (PECAM-1), and participates in neutrophil transmigration.

39 atelet endothelial cell adhesion molecule-1 (PECAM-1), CD144/VE-cadherin, and CD106/Endoglin, from va

40 as platelet endothelial adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), va

41 atelet-endothelial-cell adhesion molecule-1 (PECAM-1), plays an important role in tight junction amon

42 atelet endothelial cell adhesion molecule-1 (PECAM-1), that convert mechanical force into biochemical

43 atelet endothelial cell adhesion molecule-1 (PECAM-1).

44 atelet Endothelial Cell Adhesion Molecule-1 (PECAM-1, a highly expressed endothelial transmembrane pr

45 atelet-endothelial cell adhesion molecule-1 (PECAM-1/CD31) is expressed on the surface of endothelial

46 atelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) plays an important role in leukocyte-endot

47 atelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) regulates a variety of endothelial and imm

48 t-endothelial, and/or vascular CAMs (ICAM-1, PECAM-1, VCAM-1).

49 geting resulted in binding similar to ICAM-1/PECAM-1 combination and displayed the highest selectivit

50 In vivo, ICAM-1/PECAM-1-targeted nanocarriers outperformed PECAM-1/VCAM-

51 ICAM-1/PECAM-1-targeted nanocarriers surpassed PECAM-1/VCAM-1 i

52 its localization suggests the G alpha(q/11)-PECAM-1 complex is a critical mediator of vascular disea

53 to a rapid dissociation of the G alpha(q/11)-PECAM-1 complex within 30 s and a partial relocalization

54 temporal gradient flow-induced G alpha(q/11)-PECAM-1 dissociation.

55 ults allow us to conclude that G alpha(q/11)-PECAM-1 forms a mechanosensitive complex and its localiz

56 ulates endothelial endocytosis of Ab/NC in a PECAM-1 epitope specific manner.

57 ECAM-1 and Fyn are essential components of a PECAM-1-based mechanosensory complex in ECs.

58 Using a PECAM-1-independent transwell system, we found that CD17

59 ess triggers rapid increases in force across PECAM-1 but decreases the force across VE-cadherin, in c

60 In vitro, small interfering RNA against PECAM-1 blocked the induction of FN and the activation o

61 ansfection of small interference RNA against PECAM-1.

62 cyte transendothelial migration, in allowing PECAM-1 to serve as a mechanosensory complex in endothel

63 Associations among PECAM-1, Syk, and SHP-1 were found in wild-type BM monoc

64 erved a co-localization of G alpha(q/11) and PECAM-1 at the cell-cell junction in the atheroprotected

65 ET-based tension sensors for VE-cadherin and PECAM-1 using our previously developed FRET tension bios

66 nfluence of statins on platelet function and PECAM-1 signaling.

67 Disrupting the interaction between NB1 and PECAM-1 significantly inhibits neutrophil transendotheli

68 Our data suggest that inhibition of pIgR and PECAM-1 has the potential to prevent pneumococcal mening

69 ing surface concentrations of E-selectin and PECAM-1 under static and flow conditions.

70 transplants that involved both wild-type and PECAM-1-deficient mice revealed that the impaired angiog

71 genesis markers, VEGF, VEGFR1 and VEGFR2 and PECAM-1 were analyzed by RT-q PCR.

72 th, cell proliferation (Ki67), angiogenesis (PECAM-1), cell migration (MAP-Kinase), and keratinocyte

73 Anti-PECAM-1 mAb therapy suppresses both end-stage metastatic

74 dothelial cell migration; additionally, anti-PECAM-1 antibodies have been shown to inhibit in vivo an

75 asminogen activator (scuPA) fused to an anti-PECAM-1 antibody single-chain variable fragment (anti-PE

76 rfering RNA knockdown of PECAM-1 and by anti-PECAM-1 Ab blocking.

77 ding to VEC rather than to tumor cells, anti-PECAM-1 mAb appears to act independently of tumor type.

78 n endothelial cells treated with either anti-PECAM-1 antibody or PECAM-1 siRNA.

79 hosphorylation and increased EC surface anti-PECAM-1 mAb-binding activity.

80 modified 3D coculture assay showed that anti-PECAM-1 mAb inhibits the proliferation of PECAM-1-negati

81 l cells do not internalize PECAM antibodies, PECAM-1 engagement by multivalent anti-PECAM conjugates

82 1 complex, suggesting an interaction between PECAM-1 and BKRB2.

83 ontributes to PMN transmigration mediated by PECAM-1.

84 wound migration and single-cell motility by PECAM-1-null endothelial cells were also compromised.

85 of endothelial cells (including VE-cadherin, PECAM-1, and Flk-1) and committed B-lineage progenitors.

86 nosensory complex consisting of VE-cadherin, PECAM-1, and VEGFR2.

87 CD31/PECAM-1 influences multiple cell functions including adh

88 ng and neovascularization quantified by CD31/PECAM-1 immunofluorescence.

89 Expression of CD31/PECAM-1 by BPDCN adds new information about the antigeni

90 tochemical analysis demonstrated strong CD31/PECAM-1 (platelet endothelial cell adhesion molecule 1)

91 ared its effects to non-caveolar target CD31/PECAM-1.

92 er patient, 8 of 10 cases of BPDCN were CD31/PECAM-1 positive.

93 y scanning electron microscopy, whereas CD31/PECAM-1 was used to confirm endothelial maturity.

94 stochemical staining was performed with CD31/PECAM-1 and LYVE-1 to quantify the level of blood and ly

95 Because NB1 interacts with endothelial cell PECAM-1 at cell junctions where transmigration occurs, w

96 M-1, consistent with accumulation of cleaved PECAM-1.

97 ression and TGF-beta secretion, compensatory PECAM-1 modulation facilitates glomerular endothelial ce

98 ogy domains, are essential for concentrating PECAM-1 at endothelial cell intercellular junctions, whe

99 ation (TEM) depends on fractalkine (CX3CL1), PECAM-1 (CD31), and ICAM-1 (CD54) expression by the EC,

100 The decreased PECAM-1 levels were caused by caspase-mediated cytoplasm

101 This defect could be explained by defective PECAM-1(-/-) MK polarization of the SDF1 receptor CXCR4

102 c retinopathy (OIR) using PECAM-1-deficient (PECAM-1-/-) mice.

103 Capillary density (PECAM-1 staining) demonstrated fewer capillaries in both

104 f which has been shown previously to disrupt PECAM-1-mediated homophilic binding.

105 mity ligation assay, we show that endogenous PECAM-1.Galphaq/11 interactions in endothelial cells are

106 /TM and scFv/EPCR bound to mouse endothelial PECAM-1 with high affinity (EC50 1.5 and 3.8 nM, respect

107 nt transcriptional regulation of endothelial PECAM-1 expression.

108 her establish the involvement of endothelial PECAM-1 in angiogenesis and suggest that, in vivo, PECAM

109 ion factor GATA-2 that regulates endothelial PECAM-1 expression was blunted in LSP1-deficient or LSP1

110 However, the mechanism by which endothelial PECAM-1 functions as an anti-inflammatory protein is poo

111 ct of engaging, cross-linking, or expressing PECAM-1 on NF-kappaB activation in a variety of human ce

112 wth was detected by immunohistochemistry for PECAM-1 (CD31) following surgery.

113 e diseases, NB1 glycoprotein is a ligand for PECAM-1 and it may have a role in Wegener's granulomatos

114 Furthermore, tyrosine 663 is required for PECAM-1 to efficiently enter and exit the LBRC.

115 Lyn was required for PECAM-1 tyrosine phosphorylation and subsequent binding

116 Our findings suggest a novel role for PECAM-1 in arteriogenesis and collateral remodeling.

117 This study identifies a novel role for PECAM-1 in regulating MK migration and thrombopoiesis.

118 wild-type platelets, platelets derived from PECAM-1-deficient, Lyn-deficient, or PECAM-1/Lyn double-

119 study, we report a role for the glycoprotein PECAM-1 in thrombopoiesis.

120 confirmed the presence of two distinct human PECAM-1 alleles (L(98)S(536)R(643) and V(98)N(536)G(643)

121 the newly solved crystal structure of human PECAM-1 immunoglobulin homology domain 1 reveals that a

122 scFv) that binds with high affinity to human PECAM-1 and cross-reacts with its counterpart in rats an

123 nucleotide polymorphisms (SNPs) within human PECAM-1 mRNA, several of which have recently been associ

124 Furthermore, we identify PECAM-1 as the first molecule that determines preexistin

125 retinal neovascularization was attenuated in PECAM-1-/- mice during OIR despite an expression of VEGF

126 ffected, we identified a migration defect in PECAM-1-deficient MKs in response to a gradient of strom

127 tion in vitro and in vivo were diminished in PECAM-1(-/-) platelets.

128 ociation with beta-catenin was diminished in PECAM-1-null ECs, suggesting that lack of PECAM-1 inhibi

129 ng a role for an Asn-25-associated glycan in PECAM-1 homophilic interactions.

130 the peripheral platelet count is impaired in PECAM-1-deficient mice.

131 rosine residues that have been implicated in PECAM-1 signaling in other cells but never examined in t

132 a feature of motile cells, was inhibited in PECAM-1-null endothelial cells as well as in human endot

133 as tumor angiogenesis were both inhibited in PECAM-1-null mice.

134 ocalization of MKs within the bone marrow in PECAM-1-deficient mice, following immune-induced thrombo

135 in retinal vascular density was observed in PECAM-1-/- mice compared with PECAM-1+/+ mice.

136 eveloping retinal vasculature progression in PECAM-1-/- mice.

137 We observed that in PECAM-1-null endothelial cells (ECs), beta-catenin remai

138 d Src and eNOS signaling sequentially induce PECAM-1-mediated PMN transendothelial migration.

139 further show that stretch- and flow-induced PECAM-1 phosphorylation in intact ECs is abolished when

140 ho-ICAM-1 induction of Src signaling induced PECAM-1 Tyr686 phosphorylation and increased EC surface

141 vascular disease, but whether they influence PECAM-1 function is unknown.

142 ets that were treated with a PI3K inhibitor, PECAM-1 was phosphorylated but did not bind the tandem S

143 aneous increase in tension across junctional PECAM-1, while nonjunctional PECAM-1 was unaffected.

144 ation, capillarization, increased junctional PECAM-1 expression, protein nitration, and decreased liv

145 EM CD4+ T cells lack any known PECAM-1 counter receptor, but heterophilic engagement of

146 amine the adhesive properties of full-length PECAM-1 in a native lipid environment, we purified it fr

147 om a loss of endothelial, but not leukocyte, PECAM-1.

148 terfering RNA-knockdown of the mechanosensor PECAM-1 reverses frequency-dependent regulation of NF-ka

149 vated by PMN ligation of ICAM-1 in mediating PECAM-1-dependent PMN transmigration.

150 hermore, ICAM-2 appears capable of mediating PECAM-1-independent leukocyte transmigration.

151 In LSP1-deficient mice, PECAM-1 expression was reduced in endothelial cells, but

152 platelet endothelial cell adhesion molecule (PECAM-1).

153 platelet endothelial cell adhesion molecule (PECAM-1).

154 platelet-endothelial cell adhesion molecule (PECAM-1).

155 -chain fragments (scFv) of paired anti-mouse PECAM-1 antibodies to recombinant murine thrombomodulin

156 formed on P17 after staining with anti-mouse PECAM-1.

157 Cell adhesion assays on wildtype and mutant PECAM-1 further characterized the structural determinant

158 onfocal microscopy showed that although N25Q PECAM-1 concentrates normally at cell-cell junctions, th

159 ross junctional PECAM-1, while nonjunctional PECAM-1 was unaffected.

160 The absence of PECAM-1 and SHP-1 interactions in the KO cells leads to

161 rcumferential wall tension in the absence of PECAM-1, as evidenced by the upregulation of ephrin B2 a

162 culature were not affected in the absence of PECAM-1.

163 uggest that the anti-inflammatory actions of PECAM-1 in endothelial cells are not likely to involve i

164 Activation of PECAM-1 signaling results in its tyrosine phosphorylatio

165 In endothelial cells, binding of PECAM-1/VCAM-1-targeted nanocarriers was intermediate to

166 ur investigations of the bone marrow (BM) of PECAM-1 null (knockout, KO) mice, we observed that the t

167 ocking mAbs synergized with a combination of PECAM-1, ICAM-1, and CD99-blocking mAbs to inhibit PMN t

168 A complex consisting of PECAM-1, VE-cadherin, and vascular endothelial growth fa

169 Deletion of PECAM-1 blocks responses to flow in vitro and flow-depen

170 rol-rich plasmalemma domains and deletion of PECAM-1 cytosolic tail.

171 The cytoplasmic domain of PECAM-1 contains two tyrosine residues that have been im

172 es evidence that the extracellular domain of PECAM-1 is critical for this interaction.

173 lls, we found that the cytoplasmic domain of PECAM-1 is not required for its association with Galphaq

174 targeting the heterophilic binding domain of PECAM-1 significantly inhibited transmigration of NB1-po

175 acellular, but not the cytoplasmic domain of PECAM-1, consistent with accumulation of cleaved PECAM-1

176 residues within the extracellular domain of PECAM-1.

177 atidylinositol 3-kinase (PI3K) downstream of PECAM-1 promotes cell-wide activation of integrins and t

178 This study investigated the effect of PECAM-1 deficiency on thrombus resolution in FVB/n mice

179 ter receptor, but heterophilic engagement of PECAM-1 can involve glycosaminoglycans.

180 ll-Angle X-ray Scattering (SAXS) envelope of PECAM-1 IgL1-6 supported such a dimer formation in solut

181 We found that expression of PECAM-1 imparts on cells the ability to support TEM and

182 Furthermore, the expression of PECAM-1 promoted filopodia formation and increased the p

183 lls mitigated mRNA and protein expression of PECAM-1, but not ICAM-1 or VCAM-1.

184 The expression of PECAM-1-sensitive alpha6beta1 integrins on the surface o

185 hese and other unique structural features of PECAM-1 allow for the development of an atomic-level mod

186 unction, we generated an N25Q mutant form of PECAM-1 that is not glycosylated at this position and ex

187 unctions, the ability of this mutant form of PECAM-1 to support re-establishment of a permeability ba

188 By expressing truncated forms of PECAM-1 in human embryonic kidney (HEK293) cells, we fou

189 sion between the two homozygous genotypes of PECAM-1 but when monocytes expressed both alleles in het

190 Since the identification of PECAM-1, several other ITIM-containing platelet receptor

191 Given the importance of PECAM-1-mediated homophilic interactions in mediating ea

192 mechanism of trans-homophilic interaction of PECAM-1 remains unclear.

193 r results provide evidence of interaction of PECAM-1 with BKRB2 and of its possible role in regulatin

194 ll mice to further define the involvement of PECAM-1 in blood vessel formation.

195 ng phosphorylation of the N-terminal ITIM of PECAM-1 by other Src homology 2 domain-containing nonrec

196 tyrosine-based inhibitory motifs (ITIMs) of PECAM-1.

197 copied by small interfering RNA knockdown of PECAM-1 and by anti-PECAM-1 Ab blocking.

198 in PECAM-1-null ECs, suggesting that lack of PECAM-1 inhibits the ability of this adherens junction c

199 ich were associated with increased levels of PECAM-1 and MCP-1 in lal(-/-) ECs.

200 On surfaces with high levels of PECAM-1, there is a near doubling in random motility at

201 ductants cotransduced to express a mutant of PECAM-1 not subject to K3-induced ubiquitylation.

202 elial NO synthase (eNOS), phosphorylation of PECAM-1 and VEGFR-2, as well as activation of SRC and AK

203 Single nucleotide polymorphisms of PECAM-1 encoding amino acid substitutions at positions 9

204 A critical pool of PECAM-1 resides in the lateral border recycling compartm

205 ti-PECAM-1 mAb inhibits the proliferation of PECAM-1-negative tumor cells by altering the concentrati

206 The finding that the adhesive properties of PECAM-1 are regulatable suggests novel approaches for co

207 mplex, we determined the critical regions of PECAM-1 involved in this interaction.

208 vascular barrier integrity via regulation of PECAM-1 (CD31) expression.

209 o a decreased number of EC in the retinas of PECAM-1-/- mice.

210 a provide evidence for a fundamental role of PECAM-1 in the inhibitory effects of statins on platelet

211 Here we determined the role of PECAM-1 in the postnatal development of retinal vasculat

212 To understand the role of PECAM-1 in this complex, we determined the critical regi

213 Our data suggest a regulatory role of PECAM-1 in venous thrombus resolution and suggest a pred

214 areas as well as in all arterial sections of PECAM-1 knockout mice.

215 Using model REN cells expressing a series of PECAM-1 deletion and point mutants, we found that the PE

216 Silencing of PECAM-1 or key ER stress genes abrogated SS regulation o

217 r response is normalized on stabilization of PECAM-1, which reverses intimal remodeling in vivo.

218 Here, we present the crystal structure of PECAM-1 IgL1-2 trans-homo dimer.

219 Domain swapping of PECAM-1 with intracellular cell adhesion molecule 1 (ICA

220 mAb-based targeting of PECAM-1 represents a TME-targeted therapeutic approach t

221 ite an expression of VEGF similar to that of PECAM-1+/+ mice.

222 nd dilated vessels in retinal vasculature of PECAM-1-/- mice.

223 n eNOS, expression in retinal vasculature of PECAM-1-/- mice.

224 apoptosis was observed in retinal vessels of PECAM-1-/- mice, which was compensated, in part, by an i

225 g in response to direct force application on PECAM-1.

226 ated TEM depends on CD99 on EC as well as on PECAM-1 and depends on nectin-2 (CD112) and poliovirus r

227 work suggested that flow increases force on PECAM-1, which initiates signaling.

228 the prediction that shear increases force on PECAM-1.

229 monstrate that localized tensional forces on PECAM-1 result in, surprisingly, global signaling respon

230 Tension on PECAM-1 was mediated by flow-stimulated association with

231 the ECM influences EC response to tension on PECAM-1.

232 treated with either anti-PECAM-1 antibody or PECAM-1 siRNA.

233 ed from PECAM-1-deficient, Lyn-deficient, or PECAM-1/Lyn double-deficient mice were equally hyperresp

234 1/PECAM-1-targeted nanocarriers outperformed PECAM-1/VCAM-1 in control and disease-like conditions, a

235 1), based on side population (SP) phenotype, PECAM-1 (CD31) and platelet-derived growth factor recept

236 Csk bound to and phosphorylated PECAM-1 more efficiently than did Btk and required its S

237 endothelial, and not leukocyte or platelet, PECAM-1 conferred protection against inflammatory insult

238 AM-1 cytoplasmic domain and, more precisely, PECAM-1 tyrosine 686, is critical in mediating RhoA acti

239 for the endothelial cell junctional protein, PECAM-1.

240 by the inhibitory platelet adhesion receptor PECAM-1 (platelet endothelial cell adhesion molecule-1),

241 ut not K5 transduction significantly reduces PECAM-1 expression, and the effect on TCR-induced TEM is

242 These results reveal PECAM-1 signaling and interactions with the cytoskeleton

243 However, the physiological role PECAM-1 plays during vascular development and angiogenes

244 cence analysis revealed increased sinusoidal PECAM-1 and laminin-1 protein expression, suggesting gai

245 Soluble PECAM-1 levels were negatively associated with repetitiv

246 ce and the extent to which levels of soluble PECAM-1 (sPECAM-1) correlate with delayed thrombus resol

247 Caspase blockade stabilized PECAM-1 levels, restored endothelial shear responsivenes

248 AM-1/PECAM-1-targeted nanocarriers surpassed PECAM-1/VCAM-1 in control, but showed lower selectivity

249 our knowledge, the first demonstration that PECAM-1 genotype can alter the level of monocyte binding

250 We hypothesized that PECAM-1 plays an important role in arteriogenesis and co

251 ith a GPVI-specific agonist, indicating that PECAM-1 and Lyn participate in the same inhibitory pathw

252 atomic-level model of the interactions that PECAM-1 forms during assembly of endothelial cell interc

253 We show that PECAM-1 phosphorylation occurs when detergent-extracted

254 nd loss of function strategies, we show that PECAM-1 provides endothelial cytoprotection against mesa

255 Co-immunoprecipitation studies show that PECAM-1.Galphaq/11 binding is dramatically decreased by

256 /-) and ApoE(-/-)PECAM(-/-) mice showed that PECAM-1 was essential for FN accumulation in atheroprone

257 Previous studies have shown that PECAM-1 homophilic interactions, mediated by amino-termi

258 Previous studies have shown that PECAM-1/PECAM-1 homophilic interactions play a key role

259 We suggest that PECAM-1 and Fyn are essential components of a PECAM-1-ba

260 These results suggest that PECAM-1 expression and its potential interactions with E

261 It was recently suggested that PECAM-1 exerts its anti-inflammatory effects in endothel

262 This result also suggests that PECAM-1 does not directly interact with Galphaq/11.

263 itro and in vivo model systems suggests that PECAM-1 suppresses cytokine production and vascular perm

264 all interfering RNAs, we identify Fyn as the PECAM-1 kinase associated with the model.

265 -type animals, but to a lesser extent in the PECAM-1-null mice.

266 at determining the crystal structure of the PECAM-1 homophilic-binding domain, which is composed of

267 omozygous and heterozygous expression of the PECAM-1 LSR and VNG genotypes on the adhesive interactio

268 ptor, with PECAM-1 enhances formation of the PECAM-1-Galphaq/11 complex, suggesting an interaction be

269 to reveal the nature and orientation of the PECAM-1-PECAM-1 homophilic-binding interface, we underto

270 The nature of the PECAM-1.Galphaq/11 interaction is still unclear although

271 al cell-cell interactions by stabilizing the PECAM-1 homophilic binding interface.

272 eletion and point mutants, we found that the PECAM-1 cytoplasmic domain and, more precisely, PECAM-1

273 We found that the PECAM-1 cytoplasmic domain is unstructured in an aqueous

274 aken together, our results indicate that the PECAM-1.Galphaq/11 mechanosensitive complex contains an

275 moieties bind tightly to a groove within the PECAM-1 homophilic interface in an orientation that favo

276 These PECAM-1 polymorphisms are associated with graft-versus-h

277 Thus, PECAM-1 may have a critical role in the endothelium's ex

278 Thus, PECAM-1 modulates megakaryocytopoiesis in a hierarchic m

279 by thrombin instead of plasmin; (2) binds to PECAM-1; (3) does not consume plasma fibrinogen; (4) acc

280 only their ability to bind homophilically to PECAM-1-expressing cells, but exhibited regulatable adhe

281 te endothelial endocytosis of NC targeted to PECAM-1, but the specificity and mechanism of effects of

282 ion of LSP1 in endothelial cells upregulated PECAM-1 expression.

283 Using PECAM-1 gain and loss of function strategies, we show th

284 gen-induced ischemic retinopathy (OIR) using PECAM-1-deficient (PECAM-1-/-) mice.

285 ally through vascular endothelial cell (VEC) PECAM-1.

286 1 in angiogenesis and suggest that, in vivo, PECAM-1 may stimulate endothelial cell motility by promo

287 e (VEGF, VEGFR2, BFGF, PGF, HGF, Ang-1, VWF, PECAM-1 and ENOS) expression analysis after 2 weeks of c

288 K1/2 by bradykinin in HUVEC is enhanced when PECAM-1 expression is inhibited by transfection of small

289 rylated when ECs are exposed to flow or when PECAM-1 is directly pulled, suggesting that it is a mech

290 Here, we investigated whether PECAM-1 and G alpha(q/11) could act in unison to rapidly

291 n receptor; however, it is not known whether PECAM-1 and Lyn function in the same or different inhibi

292 is attenuated in endothelial cells in which PECAM-1 was knocked down and reconstituted with a bindin

293 These results support a model in which PECAM-1/SHP-2 complexes, formed in a Lyn-dependent manne

294 dherin as an essential component, along with PECAM-1 and VEGFR2, of a complex that mediates flow sign

295 ges infiltrating the kidney, associated with PECAM-1 and chemokine upregulation.

296 lent anti-PECAM complexes is associated with PECAM-1 phosphorylation.

297 as observed in PECAM-1-/- mice compared with PECAM-1+/+ mice.

298 te proteoglycan syndecan-1 in complexes with PECAM-1 that are rapidly decreased in response to flow.

299 Studies were therefore performed with PECAM-1-null mice to further define the involvement of P

300 (BKRB2), a Galphaq/11-coupled receptor, with PECAM-1 enhances formation of the PECAM-1-Galphaq/11 com