ライフサイエンスコーパス: JAM-C

1 JAM-C expressed on both murine B16 melanoma cells as wel

2 JAM-C expression was identified in human and murine mela

3 JAM-C has been implicated in leukocyte transendothelial

4 JAM-C inhibition significantly decreased the chemokine-i

5 JAM-C is an adhesion molecule that is expressed on cells

6 JAM-C knockdown caused a delay in the hfRPE cell polariz

7 JAM-C localized at the tight junctions of cultured hfRPE

8 JAM-C localizes specifically in the tight junctions of h

9 JAM-C may therefore provide a novel molecular target for

10 JAM-C surface expression in HUVEC was uniformly low, and

11 JAM-C thereby mediated both leukocyte adhesion and leuko

12 JAM-C was also expressed in human sural nerves with an e

13 JAM-C was also expressed on the surface of OA ST and RA

14 JAM-C was essential for the regulation of endothelial ac

15 JAM-C was highly expressed by RA ST lining cells, and it

16 JAM-C(-/-) mice as well as endothelial-specific JAM-C-de

17 d in the HT-lo/diss variant, whereas NCAM-1, JAM-C, and TF levels were increased in the HT-hi/diss va

18 ndidates, four targets (i.e. TIMP-2, NCAM-1, JAM-C, and tissue factor (TF)) were selected for further

19 ing in vivo differences in levels of TIMP-2, JAM-C, and TF were demonstrated in primary tumors grown

20 We have identified DHHC7 as a JAM-C palmitoylating enzyme by screening all known palmi

21 ractility and VE-cadherin-mediated adhesion, JAM-C helps to regulate vascular permeability and pathol

22 the primordial cell-cell contacts and after JAM-C knockdown, the organization of N-cadherin and ZO-1

23 presence of neutralizing antibodies against JAM-C.

24 increases are essential in angiogenesis, and JAM-C blockade reduced hyperpermeability and neovascular

25 turally related JAM family members JAM-B and JAM-C into Chinese hamster ovary cells, which are poorly

26 gnificant sub-functionalisation of JAM-B and JAM-C orthologues with respect to binding strength (but

27 the heterotypic adhesion molecules JAM-B and JAM-C.

28 where the closely-related JAM-A, JAM-B, and JAM-C are found.

29 ansepithelial migration, both JAM-C mAbs and JAM-C/Fc chimeras significantly inhibited the rate of PM

30 also formed a stable complex with Pals1 and JAM-C (a component of the apical ES) in normal testes.

31 Accordingly, anti-JAM-C antibodies blocked adhesion of JAM-C-expressing B

32 Neutralizing anti-JAM-C Abs inhibited RA synovial fluid-induced HMVEC chem

33 Long-term administration of anti-JAM-C antibodies prevented engraftment of JAM-Cpos lymph

34 Treatment with anti-JAM-C antibodies in short-term experiments reduced migra

35 followed by binding to desmosomal-associated JAM-C are key elements of the transmigration response.

36 o flow model showed that functional blocking JAM-C mAb alone had no inhibitory effect on polymorphonu

37 ssays of PMN transepithelial migration, both JAM-C mAbs and JAM-C/Fc chimeras significantly inhibited

38 xpression of junctional adhesion molecule C (JAM-C) at EC junctions, and they were enhanced by blocka

39 the role of junctional adhesion molecule C (JAM-C) in mediating leukocyte recruitment and retention

40 Junctional adhesion molecule C (JAM-C) is a transmembrane protein with significant roles

41 Junctional adhesion molecule C (JAM-C) is an immunoglobulin superfamily protein expresse

42 Junctional adhesion molecule C (JAM-C) is expressed by vascular endothelium and human bu

43 The junctional adhesion molecule C (JAM-C) was recently shown to undergo a heterophilic inte

44 s, including junctional adhesion molecule-C (JAM-C) and myelin-associated glycoprotein (MAG).

45 e identified junctional adhesion molecule-C (JAM-C) as a novel player in melanoma metastasis to the l

46 Junctional adhesion molecule-C (JAM-C) is an adhesion molecule expressed at junctions be

47 Junctional adhesion molecule-C (JAM-C) is an adhesion molecule expressed by endothelial

48 The junctional adhesion molecule-C (JAM-C) was recently shown to be a counter receptor for t

49 superfamily, junctional adhesion molecule-C (JAM-C), is critically required for the differentiation o

50 ty of the EC junctional adhesion molecule-C (JAM-C).

51 n quiescent microvascular endothelial cells, JAM-C localized mainly intracellularly, and was recruite

52 Although under quiescent conditions, JAM-C predominantly localized to interendothelial cell-c

53 Compared to wild-type (WT) controls, JAM-C SC KO mice showed electrophysiological defects, mu

54 JAM-C-positive) and germinal center-derived (JAM-C-negative) B-cell lymphomas.

55 the classification of marginal zone-derived (JAM-C-positive) and germinal center-derived (JAM-C-negat

56 d vascular leakage, suggesting a role for EC JAM-C in the development of functional tumor vessels.

57 findings provide evidence for a role for EC JAM-C in tumor growth and aggressiveness as well as recr

58 However, tumor microvessels from EC JAM-C-deficient mice exhibited reduced pericyte coverage

59 , survival in this model was increased in EC JAM-C knockouts (KOs; 88 vs. 96 d, P=0.04) and reduced i

60 tumor growth was significantly reduced in EC JAM-C KOs (87% inhibition at 10 wk, P<0.0005), this was

61 (KOs; 88 vs. 96 d, P=0.04) and reduced in EC JAM-C transgenics (88 vs. 78.5 d, P=0.03), mice deficien

62 Local proteolytic cleavage of EC JAM-C by neutrophil elastase (NE) drove this cascade of

63 nt in promoting tumor growth, the role of EC JAM-C in tumor development was investigated using the ID

64 .03), mice deficient in or overexpressing EC JAM-C, respectively.

65 Thus, upon oxLDL stimulation endothelial JAM-C functions as both an adhesion, as well as a transm

66 , but not a DHHC7 catalytic mutant, enhances JAM-C S-palmitoylation.

67 h muscle cells (HASMC) were found to express JAM-C, and oxLDL, as well as enzymatically modified LDL

68 noma cell line NCI-H522 was found to express JAM-C.

69 othelial cells that constitutively expressed JAM-C in cell-cell contacts, in quiescent microvascular

70 Fibroblast JAM-C expression was also analyzed using Western blottin

71 Finally, JAM-C promotes the basal-to-apical transmigration of gra

72 ies identified JAM-B as the major ligand for JAM-C, whereas homotypic JAM-C interactions remained at

73 of transmigration of PMN or evoke a role for JAM-C in transendothelial migration.

74 During initial junction formation JAM-C was recruited to the primordial cell-cell contacts

75 iles and gene expression data generated from JAM-C-expressing leukemic cells, we defined a single cel

76 derlying cause of these defects, nerves from JAM-C SC KO mice were found to have morphological defect

77 Sciatic nerves from JAM-C-deficient [having the JAM-C gene knocked out (KO)]

78 he major ligand for JAM-C, whereas homotypic JAM-C interactions remained at background levels.

79 we used function-blocking mAbs against human JAM-C to determine its role in human leukocyte adhesion

80 Our results identify JAM-C as a key regulator of polarized neutrophil TEM in

81 le JAM-C in fluid phase bound to immobilized JAM-C as assessed in a purified system; moreover, JAM-C-

82 NCI-H522 cells adhered to immobilized JAM-C, as well as to JAM-C-transfected CHO cells, but no

83 ter ovary (CHO) cells adhered to immobilized JAM-C.

84 This motif is conserved in JAM-C (Arg64-Ile65-Glu66), and a single amino acid mutat

85 Interestingly, JAM-C-blocking mAbs synergized with a combination of PEC

86 sion of JAM-C by infection with a lentivirus JAM-C GFP fusion protein did not increase adhesion or ex

87 ts reduced migration of normal and malignant JAM-C-expressing B cells to bone marrow, lymph nodes, an

88 RPE (hfRPE) with or without si-RNA mediated JAM-C knockdown and in adult native RPE wholemounts.

89 By immunofluorescence microscopy, JAM-C staining showed sparse localization to cell-cell j

90 mined the role of the cell adhesion molecule JAM-C, a protein known to mediate cellular polarity duri

91 Moreover, JAM-C was strongly up-regulated in the spontaneous early

92 as assessed in a purified system; moreover, JAM-C-transfected Chinese hamster ovary (CHO) cells adhe

93 We show that murine JAM-C is highly expressed on HSCs in the bone marrow (BM

94 y, anti-JAM-C antibodies blocked adhesion of JAM-C-expressing B cells to their ligand JAM-B, and immu

95 nal experiments revealed specific binding of JAM-C to CD11b/CD18 and provided evidence of other epith

96 vely, the generation and characterization of JAM-C SC KO mice has provided unequivocal evidence for t

97 enhanced by blockade or genetic deletion of JAM-C in ECs.

98 ns further, mice with a specific deletion of JAM-C in SCs (JAM-C SC KO) were generated.

99 oxLDL treatment induced a disorganization of JAM-C localization that was no more restricted to the in

100 Strikingly, disruption of JAM-C function decreased basal permeability and prevente

101 erotic vessels revealed a high expression of JAM-C in association with neointimal smooth muscle cells

102 n, we recently reported on the expression of JAM-C in Schwann cells (SCs) and its importance for the

103 identify the localization and expression of JAM-C, ZO-1, N-cadherin, and ezrin in cultures of human

104 orts on previously undetected expressions of JAM-C, namely on perineural cells, and in line with noci

105 We generated mice with inactivation of JAM-C.

106 Inclusion of JAM-C as a sole marker on lineage-negative BM cells yiel

107 The homophilic interaction of JAM-C can mediate tumor cell-endothelial cell interactio

108 Here, the homophilic interaction of JAM-C is presented and functionally characterized to med

109 The homophilic interaction of JAM-C was mediated by the isolated amino-terminal Ig dom

110 66R) abolished the homophilic interaction of JAM-C.

111 The level of JAM-C expression defines B-cell differentiation stages a

112 down decreases the S-palmitoylation level of JAM-C.

113 Desmosomal localization of JAM-C was further confirmed by experiments aimed at sele

114 Moreover, the loss of JAM-C expression resulted in stabilization of VE-cadheri

115 Overexpression of JAM-C by infection with a lentivirus JAM-C GFP fusion pr

116 ese results suggest that S-palmitoylation of JAM-C can be potentially targeted to control cancer meta

117 Palmitoylation of JAM-C promotes its localization to tight junctions and i

118 HUVEC revealed a large intracellular pool of JAM-C that showed little colocalization with von Willebr

119 e present study, we investigated the role of JAM-C in homing of human B cells, using a xenogeneic non

120 To determine the role of JAM-C in leukocyte retention in the RA synovium, in vitr

121 To investigate the role of JAM-C in neuronal functions further, mice with a specifi

122 Here, we investigated the role of JAM-C in oxidized low-density lipoprotein (LDL)-mediated

123 Our results highlight the novel role of JAM-C in recruiting and retaining leukocytes in the RA s

124 Here, the role of JAM-C in vascular permeability was investigated in vitro

125 f de novo AML patients at diagnosis based on JAM-C-expressing cells frequencies in the blood served a

126 ST fibroblasts and to RA ST was dependent on JAM-C.

127 AM-A but not those transfected with JAM-B or JAM-C.

128 hesion of NCI-H522 cells to JAM-C protein or JAM-C-transfected CHO cells was abolished in the presenc

129 Expression of related proteins JAM-C and CAR (Coxsackie and adenovirus receptor) was al

130 expression of JAM-A and the related proteins JAM-C, CAR, and AF-6 in the rabbit corneal endothelium.

131 itis (OA), and normal ST samples to quantify JAM-C expression.

132 dified LDL (eLDL) significantly up-regulated JAM-C on both HASMC and endothelial cells in a time- and

133 equivocal evidence for the involvement of SC JAM-C in the fine organization of peripheral nerves and

134 ce with a specific deletion of JAM-C in SCs (JAM-C SC KO) were generated.

135 l cells was significantly blocked by soluble JAM-C or the isolated D1.

136 lls was abolished in the presence of soluble JAM-C or the isolated D1.

137 Recombinant soluble JAM-C in fluid phase bound to immobilized JAM-C as asses

138 is found in soluble form and whether soluble JAM-C (sJAM-C) mediates angiogenesis.

139 lung, whereas treatment of mice with soluble JAM-C prevented melanoma lung metastasis.

140 -C(-/-) mice as well as endothelial-specific JAM-C-deficient mice displayed significantly decreased B

141 Targeting JAM-C could thus constitute a new therapeutic strategy t

142 n the RA synovium and suggest that targeting JAM-C may be important in combating inflammatory disease

143 Recently, a JAM protein family member termed JAM-C was implicated in leukocyte adhesive interactions;

144 e that JAM-C defines HSCs in the BM and that JAM-C plays a role in controlling myeloid progenitor gen

145 These results demonstrate that JAM-C is a component of the autotypic junctional attachm

146 Here, we demonstrate that JAM-C is abundantly expressed basolaterally in intestina

147 Finally, we demonstrated that JAM-C controls Src family kinase (SFK) activation in LSC

148 These results provide evidence that JAM-C defines HSCs in the BM and that JAM-C plays a role

149 We found that JAM-C is present in soluble form in normal serum and ele

150 l and electron microscopy, we show here that JAM-C is also expressed in peripheral nerves and that th

151 Our results show that JAM-C exists in soluble form and suggest that modulation

152 Here, we show that JAM-C expression defines a subset of leukemic cells endo

153 Here, we show that JAM-C undergoes S-palmitoylation on two juxtamembrane cy

154 These data suggest that JAM-C has a minimal role, if any, in PMN transmigration

155 nsepithelial migration and also suggest that JAM-C may play a role in desmosomal structure/function.

156 atic nerves from JAM-C-deficient [having the JAM-C gene knocked out (KO)] mice exhibited loss of inte

157 and in line with nociception defects of the JAM-C SC KO animals, on finely myelinated sensory nerve

158 The underlying mechanisms of the JAM-C-mediated increase in endothelial permeability were

159 O cells or to CHO cells transfected with the JAM-C mutant (E66R).

160 SFK activation was uniquely found within the JAM-C-expressing LSC compartment.

161 Thus, JAM-C undergoes a homophilic interaction via the Arg64-I

162 adhered to immobilized JAM-C, as well as to JAM-C-transfected CHO cells, but not to mock-transfected

163 Adhesion of NCI-H522 cells to JAM-C protein or JAM-C-transfected CHO cells was abolish

164 core gene expression signature correlated to JAM-C expression that reveals LSC heterogeneity.

165 ion, and actin stress fiber formation due to JAM-C knockdown.

166 events as supported by presentation of NE to JAM-C via the neutrophil adhesion molecule Mac-1.

167 Together, JAM-C represents a novel therapeutic target for melanoma

168 Taken together, JAM-C is up-regulated by oxLDL and may thereby contribut

169 ) was efficacious at causing loss of venular JAM-C and promoting neutrophil reverse transendothelial

170 xLDL treatment of endothelial cells, whereas JAM-C on quiescent endothelial cells only mediates leuko

171 n the current study, we investigated whether JAM-C is found in soluble form and whether soluble JAM-C

172 f association of the Par6/Pals1 complex with JAM-C, thereby destabilizing apical ES to facilitate spe