ライフサイエンスコーパス: VLA

1 VLA disability was assessed using a 29-item scale, ratin

2 VLA disability was assessed using a scale rating the dif

3 VLA disability was common, with more disability noted in

4 VLA-4 (alpha(4)beta(1)) is a key integrin in the effecti

5 VLA-4 blockade in vivo significantly suppressed all uvei

6 VLA-4 conformational activation has been associated with

7 VLA-4 expression on Tc2 cells was down-regulated in an i

8 VLA-4 expression varied widely, with mean expression 60.

9 VLA-4 is a promising MM imaging and therapeutic biomarke

10 VLA-4 ligation retarded these flows, even in the absence

11 VLA-4 mean fluorescence intensity (MFI) varied 35-fold (

12 VLA-4 plays a critical role in T cell trafficking into i

13 VLA-4-negative MDA-MB-231/firefly luciferase (fluc) huma

14 VLA-5 recognized a 20-kDa protein, identified as cycloph

15 hibited subclinical disability in at least 1 VLA in year 1.

16 Almost all (91%) reported > or =1 VLA affected by SLE.

17 the subjects were unable to perform > or =1 VLA at baseline.

18 Although vascular cell adhesion molecule-1 (VLA-4 receptor) was expressed at all CNS barriers, P-sel

19 e we show that the integrin alpha(4)beta(1) (VLA-4) and its ligand VCAM-1 were required, whereas the

20 integrins, principally via alpha(4)beta(1) (VLA-4).

21 in turn activate multiple integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) and the ch

22 During T cell migration on VCAM-1, VLA-4 activation concurs with spatial redistribution of

23 CD20+ B cell depletion plus LFA-1/VLA-4 mAb treatment significantly prolonged Ag-specific

24 Here we show that interruption of the VCAM-1/VLA-4 axis with a small molecule inhibitor of VLA-4, BIO

25 Although it is well-established that VCAM-1/VLA-4 interactions can play important roles in mediating

26 e observed defective translocation of VLA-3, VLA-6, and neutrophil elastase from intracellular vesicl

27 mechanism of CD11c/CD18 and very late Ag-4 (VLA-4) activation and cooperation in shear-resistant cel

28 ty peptidomimetic ligand for very late Ag-4 (VLA-4; also called integrin alpha4beta1) binding cells i

29 uding CXCR4, very late activation antigen 4 (VLA-4), and lymphocyte function-associated antigen 1.

30 antigen 1 (LFA-1), and very late antigen 4 (VLA-4).

31 Anti-very late antigen 4 (VLA-4; on neutrophils) inhibited adhesion to TNF-alpha-a

32 Extremely potent very late antigen-4 (VLA-4) antagonists with picomolar, whole blood activity

33 igen (LFA-1) and VCAM-1/very late antigen-4 (VLA-4) at select time points compared with PBS-treated a

34 iently transfected with very late antigen-4 (VLA-4) binding to vascular cell adhesion molecule-1 (VCA

35 h factor receptor-1 and very late antigen-4 (VLA-4) have been shown to arrive at sites of metastasis

36 molecule 1 (VCAM-1) and very late antigen-4 (VLA-4) played an integral role in the activation of NF-k

37 atalizumab, which binds very late antigen-4 (VLA-4), is a potent therapy for multiple sclerosis (MS).

38 marrow is adhesion via very late antigen-4 (VLA-4), the alpha(4)beta(1) integrin heterodimer that bi

39 h integrin beta1, forms very late antigen-4 (VLA-4), which interacts with vascular cell adhesion mole

40 ts under long-term anti-very late antigen-4 (VLA-4)/natalizumab therapy (LTNT) and from CNS specimens

41 Very-late-antigen-4 (VLA-4, alpha4beta1 integrin, CD49d/CD29) is a transmembr

42 or leukocyte integrins, very late antigen-4 (VLA-4, CD49d/CD29).

43 Very late antigen-4 (VLA-4; also called integrin alpha4beta1) is a transmembr

44 , resulting in enhanced very late antigen-4 [VLA-4] directed adhesion and motility.

45 In contrast, HSPC mobilization by a VLA-4 antagonist was intact.

46 fic growth factors upregulate fibronectin--a VLA-4 ligand--in resident fibroblasts, providing a permi

47 In a VLA-4/VCAM-1-specific myeloid cell adhesion model system

48 afor, a CXCR4 antagonist, and natalizumab, a VLA-4 antibody.

49 igh-affinity CD11c, which directly activated VLA-4 adhesion via phosphorylated spleen tyrosine kinase

50 ta suggest that a subpopulation of activated VLA-4 is mainly localized to the leading edge of polariz

51 Selective inhibition of the activated VLA-4 at the leading edge with a small molecule inhibito

52 om a combination of visible light activated (VLA) photocatalysis and copper ion toxicity.

53 inical disability in valued life activities (VLAs) among individuals with rheumatoid arthritis (RA),

54 tionnaire (HAQ), the Valued Life Activities (VLAs), and the Short Physical Performance Battery (SPPB)

55 n the performance of valued life activities (VLAs), and to examine the impact of accounting for these

56 ment of a pre-existing pool of high-affinity VLA-4 as previously thought.

57 we evaluated 2 conjugates of a high-affinity VLA-4 peptidomimetic ligand, LLP2A, for PET/CT imaging i

58 64)Cu-CB-TE1A1P-PEG4-LLP2A), a high-affinity VLA-4 peptidomimetic-based radiopharmaceutical, was eval

59 CAM-1 depended on induction of high-affinity VLA-4 rather than recruitment of a pre-existing pool of

60 cule that preferentially binds high-affinity VLA-4 reduced PBL firm adhesion to VCAM-1 by 90%.

61 rm adhesion due to blockage of high-affinity VLA-4 was paralleled by a 4-fold increase in the fractio

62 onsistent with the half-life of low-affinity VLA-4-VCAM-1 bonds.

63 abrogated using blocking antibodies against VLA-4.

64 cific CXCR4 inhibitor and antibodies against VLA-4.

65 ch could be blocked using inhibitors against VLA-4 and CXCR4.

66 study, we report that integrin alpha3beta1 (VLA-3; CD49c/CD29) is dramatically upregulated on neutro

67 es adhesive functions of T-cell alpha4beta1 (VLA-4) and alphaLbeta2 (LFA-1) in in vivo and in vitro m

68 Here we show that integrin alpha4beta1 (VLA-4) and VCAM-1 promote close intercellular adhesion b

69 Here we show that integrin alpha4beta1 (VLA-4) promotes the homing of circulating progenitor cel

70 Alpha5beta1 (VLA-5) is one of two major FN receptors on T cells.

71 Coblockade of LFA-1 and VLA-4 adhesion molecules temporarily depleted long-lived

72 uce high-affinity conformations of LFA-1 and VLA-4 that recognize their endothelial cell ligands and

73 of the leukocyte adhesion markers LFA-1 and VLA-4, consistent with its ability to improve leukocyte

74 ymphocyte function-associated antigen-1) and VLA-4 (very late antigen-4) is essential for T-cell traf

75 P-1 (monocyte chemoattractant protein-1) and VLA-4 (very-late antigen-4).

76 reased renal expression of LLT-1, MCP-1, and VLA-4.

77 kinases control chemokine-induced LFA-1- and VLA-4-mediated adhesion as well as human T lymphocyte ho

78 confidence interval [95% CI] 1.01-1.18) and VLA disability (OR 1.14, 95% CI 1.06-1.23) over a prospe

79 ve intraperitoneal injections of VEGFR-3 and VLA-1-neutralizing antibodies or their controls twice a

80 ar endothelial growth factor receptor-3) and VLA-1 (very late antigen-1) promotes high-risk transplan

81 ce of cytokines, the engagement of VLA-4 and VLA-5 integrins to the fibronectin fragment CH-296 prese

82 n that engagement of the integrins VLA-4 and VLA-5 to the fibronectin fragment CH-296 in combination

83 re the result of LFA-1-mediated adhesion and VLA-3-mediated cell migration through the vascular basem

84 CD13 and VLA-4 blocking and activating Abs were used in flow-base

85 rating that two adhesion molecules, CD44 and VLA-4, must be physically associated with each other on

86 A-4-positive B16F10 mouse melanoma cells and VLA-4-negative MDA-MB-231/fluc human breast cancer tumor

87 cell cycle and more cells express CXCR4 and VLA-4 compared with G-CSF-mobilized CD34(+) cells.

88 dependent adhesion, we showed that CXCR4 and VLA-4 directly interact in response to SDF-1, we further

89 Increased expression of CXCR4 and VLA-4 integrin resulted in concentration-dependent chemo

90 s, showing that cross-talk between CXCR4 and VLA-4 modulates marrow retention of these cells.

91 and adhesion receptors, including CXCR4 and VLA-4.

92 neously migrate beneath MSCs in a CXCR4- and VLA-4-dependent fashion (pseudoemperipolesis).

93 onal CXCR4 and CXCR5 chemokine receptors and VLA-4 adhesion molecules.

94 act as rapid effectors upon reinfection, and VLA-1 expression is integral to their accumulation in th

95 the presence of costimulatory blockade, anti-VLA-4 impaired T-cell trafficking to the graft but not m

96 latory blockade was coupled with either anti-VLA-4 or anti-LFA-1.

97 e observed a high level of mortality in anti-VLA-4 mAb (PS/2)-treated mice with actively induced EAE

98 y not appreciated deleterious effect of anti-VLA-4 Ab treatment in combination with exposure to pertu

99 ple sclerosis patients treated with the anti-VLA-4 mAb natalizumab, which selectively inhibits cell m

100 We wanted to determine whether anti-VLA-4 Ab treatment affected the function and persistence

101 tibody against very late activating antigen (VLA)-4, interferes with central nervous system immune su

102 Tc2 cells, we found that very late antigen (VLA)-4 (a heterodimer of CD49d and CD29), but none of ot

103 the alpha4beta1 integrin very late antigen (VLA)-4.

104 wth factor (VEGF)-induced very late antigen (VLA)-4.

105 Leaf vein length per unit leaf area (VLA; also known as vein density) is an important determi

106 luidic adhesion assay was used for assessing VLA-4 receptor-mediated cell docking in vitro.

107 signaling through neutrophil CXCR4 augments VLA-4 adhesion to VCAM-1 in vitro, an effect that is blo

108 istribution experiments in nude mice bearing VLA-4-positive B16F10 subcutaneous tumors in the flank w

109 Because VLA disability has been linked to psychological well-bei

110 However, the antibody used to block VLA-4 function in the mouse (hybridoma clone PS/2) is no

111 blocking alone, but was abrogated when both VLA-4 and MCAM were inhibited.

112 on of MCAM(+)/TH17 cells was not affected by VLA-4 blocking alone, but was abrogated when both VLA-4

113 the blood to sites of infection mediated by VLA-4.

114 ase in the percentage of nonapoptotic CD11b+ VLA-4-negative macrophages/monocytes in blood.

115 alpha(1)beta(1) and alpha(2)beta(1) (CD49a, VLA-1 and CD49b, VLA-2, respectively), on CD4 and CD8 T

116 and alpha(2)beta(1) (CD49a, VLA-1 and CD49b, VLA-2, respectively), on CD4 and CD8 T cells during the

117 results underscore the importance of B-cell VLA-4 expression in the pathogenesis of CNS autoimmunity

118 Costimulatory VLA-4 ligands also prevented the centralization of SLP-7

119 nctional BM niche with hematopoietic CXCR4(+)VLA-4(+)LFA-1(+) nursery cells, which provide PC surviva

120 d these cells' relative expression of CXCR4, VLA-4, and LFA-1, the homing and adhesion molecules that

121 onstrate that CypA serves as a ligand for DC VLA-5, that binding of CypA to VLA-5 is at a site differ

122 o identify ligand(s) on Hc recognized by DC, VLA-5 was used to probe a Far Western blot of a yeast fr

123 perimental clinical agent, AS101, to degrade VLA-4-mediated chemoresistance and improve clinical resp

124 mokine receptor CXCR4 and the integrin dimer VLA-4, but lack expression of E-selectin ligands that pr

125 coating, relative to a purely fluorine-doped VLA photocatalyst.

126 etimes expressing CD69 but not CD25, HLA-DR, VLA-1, or effector cytokines.

127 Subclinical disability was defined for each VLA as no reported difficulty with use of any modificati

128 Enhanced VLA-4 expression has been observed in multiple myeloma (

129 We also show that VEGFR1+ cells express VLA-4 (also known as integrin alpha4beta1), and that tum

130 utant form Stat6 (Stat6VT) failed to express VLA-4 even in the absence of IL-4-stimulation.

131 n-specific respiratory CD8 T cells expressed VLA-1, a marker that is associated with heterologous inf

132 tudy argued against the existence of a fixed VLA value for a given leaf, proposing instead that VLA i

133 utant activated PC, with a high affinity for VLA-3, shows significantly improved binding to neutrophi

134 sts; 2) decrease ligand binding affinity for VLA-4 approximately 2 orders of magnitude; 3) exhibit an

135 determined the affinity of the compounds for VLA-4.

136 ion molecules (such as VCAM-1 the ligand for VLA-4), and leukocyte adhesion to vascular endothelium.

137 ate that the first step is rate limiting for VLA-4-VCAM-1 interactions.

138 ens a range of therapeutic possibilities for VLA-4-related pathologies.

139 s indicate [(64)Cu]-LLP2A is a PET probe for VLA-4, which when used in conjunction with [(18)F]-FDG,

140 s (P<0.05), suggesting an important role for VLA-4 in EIU.

141 P2A-Cy5 demonstrated binding specificity for VLA-4 in an immune-competent murine MM model.

142 LLP2A-Cy5 demonstrated high specificity for VLA-4-positive mouse 5TGM1-GFP myeloma and nonmalignant

143 High VLA-4 expression (> median MFI), compared with low expre

144 High VLA-4 expression is associated with better clinical outc

145 erived from patient leukemic cells with high VLA-4 expression and activity, we demonstrated that AS10

146 ivated protein C (PC) to Gr1(high)CD11b(high)VLA-3(high) cells isolated from the bone marrow of septi

147 was found to bind directly to purified human VLA-5.

148 tion between alpha2beta1 integrin (GPIa/IIa, VLA-2) and vascular collagen is one of the initiating ev

149 Changes in VLA disability from baseline to 1-year followup were ass

150 ere examined as predictors of and changes in VLA disability using multiple regression analyses.

151 ke of (64)Cu-CB-TE2A-LLP2A was determined in VLA-4-positive B16F10 mouse melanoma cells and VLA-4-neg

152 suggesting that CD49d is solely expressed in VLA-4 complexes.

153 Uptake of (64)Cu-CB-TE2A-LLP2A was higher in VLA-4-positive human melanoma B16F10 cells than in VLA-4

154 isease status was predictive of increases in VLA difficulty; few predictors of improvements were iden

155 positive human melanoma B16F10 cells than in VLA-4-negative MDA-MB-231 cells (P < 0.05).

156 res accounted for 62-72% of the variation in VLA difficulty.

157 Respondents rated difficulty in VLAs and then reported whether they used any of 4 behavi

158 rted a direct effect of myeloma on increased VLA-4 expression in host hematopoietic microenvironmenta

159 agement of CD44 or of HCELL directly induces VLA-4 activation via G-protein-dependent signaling, trig

160 he collagen-binding alpha(1)beta(1) integrin VLA-1 is essential for the development of memory CD8(+)

161 ted PC have a stronger affinity for integrin VLA-3, which reveals novel therapeutic possibilities.

162 zation and the signaling pathway of integrin VLA-4.

163 d severe polymicrobial peritonitis, integrin VLA-3 (CD49c/CD29) is specifically upregulated on hyperi

164 The integrin VLA-4 (alpha(4)beta(1)) mediates tethering and rolling e

165 We report that costimulation by the integrin VLA-4 (alpha4beta1) required SLP-76 domains implicated i

166 Interaction between the integrin VLA-4 on acute myelogenous leukemia (AML) cells with str

167 ing P-selectin, interactions of the integrin VLA-4 with its ligand VCAM-1, and pertussis toxin-sensit

168 1 with its ligand ICAM-1 and of the integrin VLA-4 with its ligand VCAM-1, of polarized T cells at th

169 hAPC binds to human neutrophils via integrin VLA-3 (CD49c/CD29) with a higher affinity compared with

170 Because alpha(4)beta(1) integrin (VLA-4) and its ligand VCAM-1 play a central role in the

171 f adhesion between the alpha4beta1 integrin, VLA-4, and VCAM-1.

172 mediated in part by the leukocyte integrin, VLA-4, which binds to endothelial vascular cell adhesion

173 ously shown that engagement of the integrins VLA-4 and VLA-5 to the fibronectin fragment CH-296 in co

174 Here, we investigate VLA-4's role in endotoxin-induced uveitis (EIU).

175 ariety of membrane proteins, one of which is VLA-4.

176 Multivariate analyses showed that low VLA-4 expression was an independent adverse prognostic f

177 patients with standard-risk AML, in whom low VLA-4 expression was associated with inferior DFS (34% +

178 Patients with low VLA-4 expression, compared with high expression, had a h

179 b-mediated blockade of the adhesion molecule VLA-4 has been shown to ameliorate disease in human mult

180 dies that target the cell adhesion molecules VLA-4 (natalizumab; Tysabri for multiple sclerosis and C

181 through downregulation of adhesion molecules VLA-4 and LFA-1, which are necessary for macrophage migr

182 okine receptors (CXCR4), adhesion molecules (VLA-4 and CD44), and hypoxia-related proteins.

183 CD62L(-)) and expressing adhesion molecules (VLA-4(+)LFA-1(+)) complementary to activated brain endot

184 Moreover, VLA-1 gene depletion led to a marked inhibition of lymph

185 -mediated adhesion of BMDM to ICAM-1 but not VLA-4-mediated adhesion to VCAM-1 was enhanced by Cbl-b

186 esonance energy transfer analysis of a novel VLA-4 FRET sensor under total internal reflection fluore

187 a greater proportion of affected obligatory VLAs.

188 cal disability, and estimated the ability of VLA subclinical disability to predict later decrements i

189 Functional activation of VLA-4 in vivo was investigated in our previously introdu

190 est the effect of systemic administration of VLA-1-neutralizing antibody on lymphatic formation and m

191 uption of CXCR4 signaling and attenuation of VLA-4 function are independent mechanisms of mobilizatio

192 edly did not significantly affect binding of VLA-4 to its ligand VCAM-1 (vascular cell adhesion molec

193 mber of the T(EM) express the alpha-chain of VLA-2, CD49b.

194 acokinetic profiles typical of this class of VLA-4 antagonists, and sustained activity as measured by

195 f adjacent thiols in the exofacial domain of VLA-4 after its ligation to stromal fibronectin.

196 ure system was used to examine the effect of VLA-1 gene depletion on lymphatic endothelial cell funct

197 the presence of cytokines, the engagement of VLA-4 and VLA-5 integrins to the fibronectin fragment CH

198 However, engagement of VLA-4 integrins on UCB-derived CD34(+) cells reduced cel

199 unity, Nguyen et al. show that engagement of VLA-4 promotes sustained signaling by altering the dynam

200 mma chain and Syk, leading to enhancement of VLA-4-mediated adhesion to VCAM-1.

201 icient to restrict CD8+ T cell expression of VLA-4 (by IL-4), thereby serving as a regulator for CD8+

202 Increased expression of VLA-4 also resulted in increased transendothelial migrat

203 rofoundly reduced cell surface expression of VLA-4 before and after stimulation.

204 cordance with the differential expression of VLA-4 on Tc1 versus Tc2 cells, Tc1 cells alone were comp

205 the relationship of functional expression of VLA-4 to prognosis in AML, we studied marrow samples fro

206 l of potency against the unactivated form of VLA-4 was shown to be sufficient to overcome the poor ph

207 be developed by promoting the generation of VLA-4(+) antitumor Tc1 cells.

208 argeted intraarterial delivery and homing of VLA-4-expressing hGPs to inflamed endothelium is feasibl

209 re we describe experiments toward imaging of VLA-4-positive BMD cells using a high-affinity PET probe

210 We found that the apparent increase of VLA with magnification was an artifact of (1) using low-

211 an breast tumor cells suggested an influx of VLA-4-positive BMD cells that corresponded to metastasis

212 , we report that the selective inhibition of VLA-4 expression on B cells impedes CNS accumulation of

213 LA-4 axis with a small molecule inhibitor of VLA-4, BIO5192, results in a 30-fold increase in mobiliz

214 the utility of small molecule inhibitors of VLA-4 either alone or in combination with G-CSF or AMD31

215 gest that beta1, but not alpha4, integrin of VLA-4 is the sex-specific molecule on T cell surface, an

216 g to infection expressed increased levels of VLA-4, with consequent improved entry into inflamed tiss

217 n MS pathogenesis and express high levels of VLA-4.

218 VCAM-1 is one of the main ligands of VLA-4, an integrin that is highly expressed on the surfa

219 vel evidence for functional up-regulation of VLA-4 during EIU and suggest VLA-4 blockade as a promisi

220 e show that IL-4-mediated down-regulation of VLA-4 expression is completely abrogated in Stat6-defici

221 mechanisms are involved in the regulation of VLA-4.

222 We investigated the role of VLA-1 on virus-specific CD4(+) T cells during and after

223 alyses indicated that the prognostic role of VLA-4 expression was most prominent in patients with sta

224 ely, these data support the critical role of VLA-4 in the effective intracranial tumor homing of adop

225 Both alpha4 and beta1, subunits of VLA-4 integrin, were found to be necessary for T cell co

226 lank were conducted to validate targeting of VLA-4-positive cells in vivo.

227 ally, we observed defective translocation of VLA-3, VLA-6, and neutrophil elastase from intracellular

228 d flow cytometry also showed upregulation of VLA-4-positive cell clusters and BMD cells at the metast

229 l cell-derived factor-1alpha (SDF-1alpha) on VLA-4-mediated lymphocyte adhesion, human PBL were flowe

230 ct of accounting for these accommodations on VLA disability scores.

231 neal cavity after CLP, which is dependent on VLA-4, is impaired in above mutant and FcRgamma chain-de

232 4beta1 (also known as very late antigen-4 or VLA-4).

233 Similarly, CXCR4 or VLA-4 inhibition led to significant inhibition of adhesi

234 ransformed cells, and targeting NF-kappaB or VLA-4/VCAM-1 signaling could be a clinically relevant me

235 ng agents for melanoma and potentially other VLA-4-positive tumors.

236 otential imaging candidate for overexpressed VLA-4.

237 4-naive hGPs and LPS, and rats that received VLA-4-expressing hGPs and LPS.

238 but did not receive LPS, rats that received VLA-4-expressing hGPs but not LPS, rats that received VL

239 ressing hGPs but not LPS, rats that received VLA-4-naive hGPs and LPS, and rats that received VLA-4-e

240 ting of three rats each): rats that received VLA-4-naive hGPs but did not receive LPS, rats that rece

241 alpha-chain of the type IV collagen receptor VLA-1, and these cells were highly activated, producing

242 ell motility in monocytes, alongside reduced VLA-4 expression, an integrin predominantly involved in

243 Dl-1, and BTLA expression; and (iv) reducing VLA-4 expression in both the T- and B-cell populations.

244 suggesting that IL-4 uniquely down-regulates VLA-4 expression on these cells.

245 Secondly, VLA-4 synergizes with the B-cell receptor (BCR), providi

246 Unlike selectins, VLA-4 integrin-mediated lymphocyte adhesiveness can be m

247 c are early and critical events in signaling VLA-4 adhesive function on foamy monocytes competent to

248 p-regulation of VLA-4 during EIU and suggest VLA-4 blockade as a promising therapeutic strategy for t

249 These data suggest VLA-1 expression defines a population of tissue memory C

250 d of the ipsilateral carotid artery and that VLA-4-expressing cells exhibited significantly enhanced

251 These novel findings together indicate that VLA-1 is critically involved in the processes of lymphan

252 lue for a given leaf, proposing instead that VLA increases with the magnification of the image due to

253 In accord with reports that VLA-4 antagonists in vivo induce mobilization of hematop

254 ative in vivo MR cell tracking revealed that VLA-4-expressing cells docked exclusively within the vas

255 ection fluorescence microscopy, we show that VLA-4 activation localizes to the lamellipodium in livin

256 In this study, we show that VLA-4 is expressed on murine marrow neutrophils and decr

257 Our data suggest that VLA-4 integrin hybrid domain movement does not depend on

258 Our recent studies have suggested that VLA-4 expression on CD8+ T cells is negatively controlle

259 data demonstrated, for the first time, that VLA-1 blockade significantly suppressed corneal lymphang

260 We propose that TNFR-II and the VLA-1 synergize to protect effector CD8 T cells in the i

261 (64)Cu-CB-TE2A-LLP2A had high uptake in the VLA-4-rich organs marrow, spleen, and tumor (11.26% +/-

262 model system, changes in the affinity of the VLA-4-binding pocket were reflected in rapid cell aggreg

263 , and analysis with error-free software, the VLA can be measured precisely and accurately.

264 lammatory neutrophils and that targeting the VLA-3(high) neutrophil subpopulation improved survival i

265 en together, these results indicate that the VLA-4/VCAM adhesion pathway is critical in the retention

266 These results show that the VLA-4/VCAM-1 interaction during membrane antigen recogni

267 e of HUTS-21 binding was also related to the VLA-4 activation state even at saturating ligand concent

268 DC recognize Hc yeasts via the VLA-5 receptor, whereas Mphi recognize yeasts via CD18.

269 This VLA-4 activation is mediated via a Rac1/Rap1 GTPase sign

270 nd NODAGA-PEG4-LLP2A showed high affinity to VLA-4, with a comparable dissociation constant (0.28 vs.

271 LFA-1 conformation in a manner analogous to VLA-4.

272 Antibody to VLA-4 blocked the accumulation of peripheral tissue-deri

273 Virus binds to VLA-2 on the apical cell surface and moves rapidly to ea

274 ligand for DC VLA-5, that binding of CypA to VLA-5 is at a site different from FN, and that there is

275 Similar to VLA-4 integrin, modulation of the ligand dissociation ra

276 se (hybridoma clone PS/2) is not specific to VLA-4 but inhibits both alpha4beta1 and alpha4beta7 inte

277 s in disability scores (e.g., the mean total VLA difficulty score increased by 84% after adjustment f

278 ement of hMSC HCELL with E-selectin triggers VLA-4 adhesiveness, resulting in shear-resistant adhesio

279 nd therapeutic potential comprised of TYRP2, VLA-4, HSP70, an HSP90 isoform and the MET oncoprotein.

280 at lymphocyte trafficking into the CNS under VLA-4 blockade can occur by using the alternative adhesi

281 ed rolling and residual adhesion, even under VLA-4 blockade.

282 and without the IL-18 receptor (IL-18R)/VEGF/VLA-4-expressing phenotype were identified, and their me

283 anoma cells with and without the IL-18R/VEGF/VLA-4 phenotype had distinct transcript patterns.

284 m melanomas with and without the IL-18R/VEGF/VLA-4 phenotype may serve as diagnostic biomarkers of me

285 anoma cells with and without the IL-18R/VEGF/VLA-4 phenotype.

286 cells with, but not without, the IL-18R/VEGF/VLA-4 phenotype.

287 IL-18R/VEGF/VLA-4-expressing A375 and 1182 melanoma cells produced a

288 xpression patterns of fibronectin and VEGFR1+VLA-4+ clusters dictate organ-specific tumour spread.

289 ver, increased binding of soluble VCAM-1 via VLA-4 was significantly associated with longer OS, corre

290 Marrow neutrophils adhere via VLA-4 to VCAM-1, which is expressed on marrow endotheliu

291 ic binding of rhAPC to human neutrophils via VLA-3 was inhibited by an antagonistic peptide (LXY2).

292 ient transfection of SPIO-labeled cells with VLA-4 in combination with their arterial injection and t

293 gnificantly enhanced homing as compared with VLA-4-naive cells (1448 significant pixels+/-366.5 vs 11

294 helium significantly increased compared with VLA-4-naive control cells (71.5 cells per field of view+

295 Thus, PIM interacts directly with VLA-5 on CD4+ T lymphocytes, inducing activation of the

296 = 7 and 8 mice) on nude mice implanted with VLA-4-negative MDA-MB-231/fluc human breast tumor cells

297 entified characteristics of individuals with VLA subclinical disability, and estimated the ability of

298 ate that the CXCR4/SDF-1 axis interacts with VLA-4 in regulating migration and adhesion of WM cells i

299 study demonstrated the potential of PET with VLA-4-targeted (64)Cu-CB-TE2A-LLP2A to visualize BMD cel

300 precursor cells (hGPs) were transfected with VLA-4 and labeled with superparamagnetic iron oxide that

301 Chinese hamster ovary cells transfected with VLA-5.