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-4-targeted PET/CT was performed 24 h after intraveno

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 ) (alpha(L)beta(2)) and very late antigen 4 (VLA-4) (alpha(4)beta(1)).

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

32 (CCR2) and the integrin Very Late Antigen 4 (VLA-4).

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

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

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

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

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

38 ther, B cell-restricted very late antigen-4 (VLA-4) deficiency abrogated EAE dependent on B cell anti

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

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

41 of targeted imaging of very late antigen-4 (VLA-4), as a key integrin mediating the adhesion and rec

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

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

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

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

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

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

48 n-1 receptor (MC1R) and very late antigen-4 (VLA-4, integrin alpha(4)beta(1)) are 2 attractive molecu

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

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

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

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

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

54 These parameters were analyzed using a VLA-4-targeted liposome system in a multiple myeloma mou

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 abrogated using blocking antibodies against VLA-4.

70 cific CXCR4 inhibitor and antibodies against VLA-4.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ression of multiple inflammatory markers and VLA-4.

94 review highlights the advances of MC1R- and VLA-4-targeted radiolabeled peptides and peptide-conjuga

95 MC1R- and VLA-4-targeting peptides and peptide-conjugated Cornell

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

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

98 echanism between LFA-1-mediated upstream and VLA-4-mediated downstream phenotypes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 ings demonstrate that neutrophils coordinate VLA-4-dependent B cell accumulation within the meninges

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 (CD11c/CD18) that activates beta1-integrin (VLA-4) to bind endothelial VCAM-1.

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

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

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

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

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

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

179 increased the abundance of adhesion molecule VLA-4 on Th17 cells, knockout of HuR impaired splenic Th

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 relevant target in ALI, and the accuracy of VLA-4-targeted PET in quantification of ongoing lung inf

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

191 1c correlated with concomitant activation of VLA-4 within focal adhesive contacts was required for ar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 ates the feasibility of molecular imaging of VLA-4, as a mechanistically relevant target in ALI, and

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

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

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

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

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

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

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

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

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

220 de synthase-2, highlighting the potential of VLA-4 as a surrogate marker of acute lung inflammation.

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

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

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

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

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

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

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

228 Expression levels of both subunits of VLA-4, that is, integrins alpha(4) and beta(1), signific

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

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

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

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

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

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

235 4beta1 (also known as very late antigen-4 or VLA-4).

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

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

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

239 otential imaging candidate for overexpressed VLA-4.

240 liposomes by cancerous cells overexpressing VLA-4 to 15-fold over that of non-targeted liposomes in

241 4-naive hGPs and LPS, and rats that received VLA-4-expressing hGPs and LPS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 ith an inhibiting cross talk of LFA-1 toward VLA-4.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.