ライフサイエンスコーパス: ICAM-3

1 mosome 19p13.2 that also contains ICAM-1 and ICAM-3.

2 uses on the 37-residue cytoplasmic region of ICAM-3.

3 rs containing purified full length ICAM-1 or ICAM-3.

4 CD4(+) T cells is independent of ICAM-2 and ICAM-3.

5 sulted in no increase in binding affinity to ICAM-3.

6 anner to gp120 when compared with ICAM-2 and ICAM-3.

7 f dendritic cells with T cells by binding to ICAM-3.

8 Orders of affinity were ICAM-1 > ICAM-2 > ICAM-3.

9 rine and macaque DC-SIGN molecules all bound ICAM-3.

10 s VCAM-1 with greater efficiency relative to ICAM-3.

11 Intercellular adhesion molecule-3 (ICAM-3), a ligand for beta2 integrins, elicits a variety

12 e all conserved between the bovine and human ICAM 3 aa sequences.

13 Another anti-ICAM-3 Ab (HP2/19), which activates T cells, did not act

14 with high affinity to the adhesion molecules ICAM-3 and -2 to promote important dendritic cell intera

15 integrins, alpha D beta 2, selectively binds ICAM-3 and does not appear to bind ICAM-1.

16 Coengagement of ICAM-3 and Fc receptors (FcgammaRI or FcgammaRII) was re

17 the deduced aa sequence with those of human ICAM-3 and ICAM-1 are 61% and 58%, respectively.

18 immunoglobulin superfamily (IgSF) domains of ICAM-3 and ICAM-3 IgSF domain chimeras with CD21 showed

19 e of other ICAM family members, particularly ICAM-3 and ICAM-5.

20 r a more extensive binding interface between ICAM-3 and LFA-1 than has previously been described.

21 ICAM-3 and moesin also coeluted from neutrophil lysates

22 s regulated substantially through binding of ICAM-3 and only minimally by ICAM-1.

23 t serve as adhesion receptors for ICAM-2 and ICAM-3 and participate in the transmission of human and

24 was substantially less effective at binding ICAM-3 and poorly transmitted HIV type 1 and SIV to targ

25 ct interaction of the cytoplasmic domains of ICAM-3 and PSGL-1 with the amino-terminal domain of reco

26 owed there is a single LFA-1 binding site in ICAM-3 and that IgSF domain 1 is necessary and sufficien

27 /CD18) to intercellular adhesion molecule 3 (ICAM-3) and Mac-1 (CD11b/CD18) to an unknown counter rec

28 Ig)-like domains similar to human ICAM-1 and ICAM-3, and belongs to the Ig gene superfamily.

29 ecules including integrin alpha, L-selectin, ICAM-3, and H-CAM.

30 cellular adhesion molecule (ICAM)-1, ICAM-2, ICAM-3, and ICAM-5 and may reflect a specialization of M

31 ICAM-3 appears to be unique among the ICAMs in utilizing

32 ercellular adhesion molecule 1 (ICAM-1), and ICAM-3 are enriched at the VS and that inhibition of the

33 We report that LFA-1 binds ICAM-3 as its primary ligand supporting homotypic adhesi

34 to endogenous adhesion molecules ICAM-2 and ICAM-3 as well as the viral envelope glycoprotein human

35 Blockade of ICAM-3, as well as ICAM-1, inhibited completely the augm

36 n 1 of ICAM-3, were able to block binding of ICAM-3 bearing cells to purified LFA-1, in agreement wit

37 bbing nonintegrin (DC-SIGN) as a DC-specific ICAM-3 binding receptor that enhances HIV-1 infection of

38 intercellular adhesion molecule (ICAM)-1 and ICAM-3 binding site, but the relationship of this site t

39 d the most complete blocking of HIVgp120 and ICAM-3 binding to L-SIGN also internalized most efficien

40 minate other cell surface glycoproteins from ICAM-3 binding.

41 ogated gp120 binding but enhanced ICAM-2 and ICAM-3 binding.

42 nced gp120 binding but diminished ICAM-2 and ICAM-3 binding.

43 ty to block ligand (HIV gp120, Ebola gp, and ICAM-3) binding.

44 Aggregation in response to ICAM-3, but not FMLP, was compromised at lower cell dens

45 (<4 h) in monocytes upon ligation of surface ICAM-3, but not P-selectin glycoprotein-1 even though bo

46 ization and kinase activity was required for ICAM-3-, but not FMLP-, induced aggregation.

47 We found that engagement of ICAM-3 by a mAb (CAL3.10), which binds in the region whe

48 In addition to an adhesive function, ICAM-3 can act as a signal-transducing molecule on T cel

49 LFA-1 and its ligands, ICAM-1, ICAM-2, and ICAM-3, can be expressed on the cells infected by HIV, a

50 o DC-SIGN in that it has a high affinity for ICAM-3, captures HIV-1 through gp120 binding, and enhanc

51 (PSGL-1), intercellular adhesion molecule 3 (ICAM-3), CD43, and CD44 are redistributed to a newly for

52 ICAM-3 (CD50), a member of the Ig superfamily, is a majo

53 Intercellular adhesion molecule 3 (ICAM-3; CD50) is the predominant counter-receptor on res

54 family members establish that the binding of ICAM-3 D1 onto the inserted domain represents a common d

55 Strikingly, anti-ICAM-3 did not induce degranulation or cause an increase

56 re expressed on the cell surface (ICAM-1 and ICAM-3) did not block aggregation.

57 data indicate that DC-SIGN interactions with ICAM-3 do not promote DC-SIGN-mediated virus transmissio

58 a variety of carbohydrate ligands, including ICAM-3, Ebola, and HIV.

59 an Fc-mediated event as an appropriate anti-ICAM-3 F(ab')2 fragment still induced aggregation.

60 n 100- and 50-fold better than ICAM-2-Fc and ICAM-3-Fc, respectively.

61 eted with intercellular adhesion molecule 3 (ICAM-3) for adhesion to DC-SIGN and blocked HIV-1 transm

62 Phosphoamino acid analysis revealed that ICAM-3 from activated cells contained phosphoserine and

63 Notably, upon association, Gag excludes ICAM-3 from this subset of UDMs, revealing an active and

64 xpressing the lectin dendritic-cell-specific ICAM-3 grabbing non-integrin (DC-SIGN; also known as CD2

65 a specific C-type lectin, SIGN-R1, (specific ICAM-3 grabbing non-integrin-related 1) expressed on mac

66 V adhesion molecule, dendritic-cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN), its closely relat

67 infection after transfection of DC-specific ICAM-3 grabbing nonintegrin (DC-SIGN), or its homologue

68 study, we show that dendritic cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN; CD209) is a recept

69 ic cells (DCs) following binding to specific ICAM-3 grabbing nonintegrin receptor 1.

70 ated protein; liver- and lymph node-specific ICAM-3 grabbing nonintegrin) but not cells expressing CD

71 ls expressing CD209 (dendritic cell-specific ICAM-3 grabbing nonintegrin).

72 C-type lectin CD209L (dendritic cellspecific ICAM-3 grabbing nonintegrin-related protein; liver- and

73 , many of which express DC-SIGN (DC-specific ICAM-3 grabbing nonintegrin; CD209).

74 the immune modulatory receptors DC-specific ICAM-3 -: grabbing non integrin (DC-SIGN) and macrophage

75 specific intracellular adhesion molecule-3 (ICAM-3) grabbing nonintegrin (DC-SIGN), a C-type lectin

76 -specific intercellular adhesion molecule-3 (ICAM-3) -grabbing nonintegrin (DC-SIGN) and its related

77 -specific intercellular adhesion molecule-3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) with respect to r

78 -specific intercellular adhesion molecule 3 (ICAM-3)-grabbing nonintegrin binding receptor (DC-SIGN)

79 -specific intercellular adhesion molecule-3 (ICAM-3)-grabbing nonintegrin] and Langerin on immune cel

80 The C-type lectin dendritic cell-specific ICAM 3-grabbing nonintegrin (DC-SIGN)/CD209 efficiently

81 ype lectin DC-SIGNR (dendritic cell-specific ICAM-3-grabbing non-integrin-related; also known as L-SI

82 trast, coincubation with soluble DC-specific ICAM-3-grabbing nonintegrin (CD209) fusion protein as a

83 However, DC-specific ICAM-3-grabbing nonintegrin (CD209) up-regulation was no

84 e type II C-type lectin receptor DC-specific ICAM-3-grabbing nonintegrin (CD209) was determined to ha

85 he potential role of dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) binding in human i

86 by increasing dendritic cell-specific C type ICAM-3-grabbing nonintegrin (DC-SIGN) expression on dend

87 tify determinants in dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) necessary for huma

88 ved beta2 integrins, dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN), and TLR4 because

89 olve binding to the CD4 antigen, DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN), mannose binding C

90 g molecules, such as dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN), mannose-binding l

91 e lectin protein present on DCs, DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN), was shown to effi

92 eceptor (MR, CD206), dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN, CD209), Dectin-1,

93 e related molecule liver/lymph node-specific ICAM-3-grabbing nonintegrin (L-SIGN) do not.

94 consider targeting liver/lymph node-specific ICAM-3-grabbing nonintegrin (L-SIGN) for therapeutic pur

95 CD11b(-/low) and lacks CD1a and DC-specific ICAM-3-grabbing nonintegrin but expresses high levels of

96 dized-LDL receptor, Dectin-1, or DC-specific ICAM-3-grabbing nonintegrin favors the generation of ant

97 i and identified the dendritic cell-specific ICAM-3-grabbing nonintegrin homolog, SIGN-related 1 (SIG

98 through binding to cell surface DC-specific ICAM-3-grabbing nonintegrin molecules.

99 se receptor (MR) and dendritic cell-specific ICAM-3-grabbing nonintegrin on dendritic cells engage Ma

100 did not appear to be mediated by DC-specific ICAM-3-grabbing nonintegrin, but rather was regulated by

101 D209a, a murine homolog of human DC-specific ICAM-3-grabbing nonintegrin, compared with BL/6 DCs.

102 ted by CCR5-dependent as well as DC-specific ICAM-3-grabbing nonintegrin-dependent pathways.

103 ng positive for CD11b, CD1a, and DC-specific ICAM-3-grabbing nonintegrin.

104 olecule is L-SIGN, liver/lymph node-specific ICAM-3-grabbing nonintegrin.

105 -specific intracellular adhesion molecule 3 [ICAM-3]-grabbing nonintegrin)in the dendritic-cell-T-cel

106 This putative bovine ICAM-3 has five immunoglobulin (Ig)-like domains similar

107 s) and certain macrophages in vivo, binds to ICAM-3, ICAM-2, and human and simian immunodeficiency vi

108 f a panel of 45 point mutants of domain 1 of ICAM-3 identified five residues that may contact LFA-1 a

109 lin superfamily (IgSF) domains of ICAM-3 and ICAM-3 IgSF domain chimeras with CD21 showed there is a

110 oeluted from neutrophil lysates with an anti-ICAM-3 immunoaffinity assay.

111 In addition, disrupting DC-SIGN/ICAM-3 interactions between cells with MAbs did not impa

112 Previous mutagenesis of ICAM-1 and ICAM-3, interpreted in light of the recently determined

113 ICAM-3 is a preferred counterreceptor for the leukocyte

114 rresponding integrin binding site residue in ICAM-3 is also essential to alpha D beta 2 binding.

115 dramatic spreading of monocytes when surface ICAM-3 is engaged by immobilized Abs.

116 ICAM-3 is expressed at high levels on myeloid leukocytes

117 ICAM-3 is highly expressed on resting leukocytes and on

118 r LFA-1 and demonstrate that ICAM-2, but not ICAM-3, is expressed on the bronchial epithelium.

119 c adhesion that is mediated predominantly by ICAM-3 ligation and that this binding causes augmented e

120 Assuming that the Mac-1 counter receptor is ICAM-3-like in strength and number, rate processes were

121 Fab and F(ab')2 fragments of triggering anti-ICAM-3 mAb, demonstrating direct outside-in signaling, b

122 These experiments indicate that ICAM-3 may transmit outside-in signals when it is engage

123 nd functional studies performed with 17 anti-ICAM-3 monoclonal antibodies demonstrated that only some

124 a 1.65-A-resolution crystal structure of the ICAM-3 N-terminal domain (D1) in complex with the insert

125 The dendritic cell-specific ICAM-3 non-integrin (DC-SIGN) and its close relative DC-

126 ory signals using immobilized mAbs to engage ICAM-3 on freshly isolated human monocytes and neutrophi

127 Finally, forced expression of ICAM-3 on target cells did not increase their susceptibi

128 ter in two distinct locations on domain 1 of ICAM-3 on the BED face (Asn23 and Ser25) and on the C st

129 The constitutive high expression of CD50 (ICAM-3) on resting leukocytes, coupled with the observat

130 ining PSGL-1, CD43, and CD44 but not ICAM-1, ICAM-3, or CD59.

131 These functional changes were due to ICAM-3 outside-in signaling because aggregation and adhe

132 ICAM-3 outside-in signaling reorganizes the cytoskeleton

133 tercellular adhesion molecule 2 (ICAM-2) and ICAM-3 promoted LFA-1-directed perforin release, whereas

134 pture and transmission of HIV-1 with soluble ICAM-3 prophylaxis were limited in success, with a maxim

135 ties of soluble ICAM-1 (sICAM-1) and soluble ICAM-3 (sICAM-3) for LFA-1.

136 We conclude that engagement of ICAM-3 stimulates PMN as well as T cells, but that the a

137 cytes (PMN) are reported to be refractory to ICAM-3 stimulation.

138 d residues within the cytoplasmic portion of ICAM-3 that are important for T cell function.

139 relative contributions of LFA-1, Mac-1, and ICAM-3 to homotypic neutrophil adhesion over the time co

140 elative contributions of beta2 integrins and ICAM-3 to neutrophil adhesion is regulated by the magnit

141 ide, a protein kinase C inhibitor, prevented ICAM-3-triggered spreading.

142 ICAM-1 and ICAM-3, uropod-directed proteins that do not copatch wit

143 erently to its endogenous ligands ICAM-2 and ICAM-3 versus HIV-1 gp120.

144 A panel of blocking Abs to LFA-1, Mac-1, and ICAM-3 was added to assess the relative contributions of

145 ontrast, the interaction of I-GPI cells with ICAM-3 was blocked by MEM-83.

146 The adhesion molecules PSGL-1 and ICAM-3 were found to colocalize with the cytoskeletal pr

147 Eighteen point mutations in ICAM-3 were generated, and residues important for bindin

148 racellular adhesion molecule 1 (ICAM-1), and ICAM-3 were upregulated following HCMV infection and tha

149 ies, with epitopes wholly within domain 1 of ICAM-3, were able to block binding of ICAM-3 bearing cel

150 ze epitopes in the extracellular domain 1 of ICAM-3, which is critical for recognition by the alphaL/

151 ular adhesion molecules-1 and -3 (ICAM-1 and ICAM-3) with lymphocyte function-associated antigen-1 (L