ライフサイエンスコーパス: Con A

1 Con A affinity chromatography of the Df extract revealed

2 Con A caused a dose-dependent increase in [Ca2+]i in Jur

3 Con A concentrations can be determined by measuring the

4 Con A hepatitis is regarded as a T cell-mediated model o

5 Con A in TFE provides an example of an intermediate with

6 Con A induced the recruitment of CD49d(+) monocytic myel

7 Con A injection induces expression of eotaxins in the li

8 Con A injection is a widely accepted mouse model to stud

9 Con A pretreatment primed LHPC and LEPC for a rapid and

10 Con A treatment leads to induction of p73 and several ot

11 Con A was immobilized on Cu(II)-charged iminodiacetic ac

12 Con A-activated splenocytes of IL-12R beta 2(-/-) mice f

13 Con A/PMA-stimulated supernatants were assayed by ELISA

14 Thus, Alexa 488-Con A appears in the void space outside of the beads and

15 hamber and competitively displaces Alexa 488-Con A molecules from the glucose residues of the Sephade

16 inear range spanning 6 (SNA), 7 (RCA), or 8 (Con A) orders of magnitude.

17 e release on pathology we used two models: a Con A-triggered activation of T cells to mimic sterile i

18 ion indicated that MPD flippase (i) is not a Con A-binding glycoprotein and (ii) can be resolved from

19 ncentrations of polysaccharides are run on a Con A-immobilized gold crystal surface, and the frequenc

20 soform of the coding agent were applied to a Con A lectin column alone to select glycopeptides contai

21 by pretreating cultures with concanamycin A (Con A) prevents cleavage of SNAP-25 with IC50 values of

22 gammaGTases were resolved by concanavalin A (Con A) affinity chromatography, indicating that they are

23 sing Alexa Fluor 647-labeled concanavalin A (Con A) and a fourth-generation PAMAM Alexa Fluor 594-lab

24 erivatized with two lectins, Concanavalin A (Con A) and Aleuria aurantia lectin (AAL), and binding pr

25 specific interaction between Concanavalin A (Con A) and D-(+)-mannose.

26 rical synapse was blocked by concanavalin A (Con A) and dynamin inhibitory peptide (DIP), both of whi

27 on the binding constants of Concanavalin A (Con A) and glycogen and Con A-mannan using quartz crysta

28 rm for the immobilization of Concanavalin A (Con A) and is capable of LPS binding measurements via or

29 g probes for lectins such as concanavalin A (Con A) based on the molecular recognitions between the g

30 uctures of the legume lectin concanavalin A (Con A) bound to closely related carbohydrate ligands sho

31 ctin columns consisting of a concanavalin A (Con A) column coupled to an SNA column for selecting sia

32 he adhesive strength between concanavalin A (Con A) coupled to an AFM tip and Con A receptors on the

33 the mannose-specific lectin concanavalin A (Con A) even though homogeneous beta-Lact clusters are no

34 aces was probed using lectin concanavalin A (Con A) from Canavalia ensiformis.

35 Hepatitis induced by concanavalin A (Con A) in mice is well known to be a T-lymphocyte-mediat

36 Injection of concanavalin A (Con A) into mice recapitulates the histological and path

37 Concanavalin A (Con A) kills procyclic (insect) forms of Trypanosoma bru

38 sion were studied by using a concanavalin A (Con A) liver injury model followed by partial hepatectom

39 i-mannose binding as well as Concanavalin A (Con A) mediated lipopolysaccharides (LPS)-mannose bindin

40 eloped a nanoscale chelating Concanavalin A (Con A) monolithic capillary prepared using GMA-EDMA (gly

41 that had been incubated with concanavalin A (Con A) or a lectin from Lens culinaris (LC), both of whi

42 These sensors utilize Concanavalin A (Con A) protein hydrogels with a 2D PC embedded on the Co

43 e asymmetric accumulation of concanavalin A (Con A) receptors toward one side of the cells within 10

44 tonic crystal sensor detects Concanavalin A (Con A) through shifts in the 2-D diffraction wavelength.

45 a mobile fluorophore-labeled Concanavalin A (Con A) to immobile pendant glucose moites inside of inte

46 escein isothiocyanate (FITC)-concanavalin A (Con A) was determined using a fluorescence competition a

47 r in combination with lectin concanavalin A (Con A) was used as molecular recognition elements for th

48 ational structure changes in concanavalin A (Con A), a legume lectin protein which is composed of 18

49 -dextran), was conjugated to concanavalin A (Con A), an enzyme with specific affinity to glucose.

50 ckia amurensis lectin (MAL), concanavalin A (Con A), and wheat germ agglutinin (WGA).

51 n the absence or presence of concanavalin A (Con A), phorbol myristate acetate (PMA)/ionomycin, or an

52 ction of biosensors based on Concanavalin A (Con A), Sambucus nigra agglutinin type I (SNA), and Rici

53 tivity to its target lectin, concanavalin A (Con A), surpassing the formerly used linear glycopolymer

54 fy a plant-derived compound, Concanavalin A (Con A), which differentially kills p53-null cells.

55 articles are aggregated with concanavalin A (Con A), which results in a significant shift and broaden

56 Concanavalin A (Con A), which selectively blocks KAR desensitization, ma

57 epatitis, and of mice during concanavalin A (Con A)-induced hepatitis (CIH).

58 Concanavalin A (Con A)-induced injury is an established natural killer T

59 We used concanavalin A (Con A)-induced liver injury to study the role of galecti

60 The effect of AT-III on concanavalin A (Con A)-stimulated rat spleen cell proliferation was also

61 lpha-mannose-specific lectin concanavalin A (Con A).

62 Cer), anti-CD3 antibody, and concanavalin A (Con A).

63 stering of a model receptor, concanavalin A (Con A).

64 a model protein, the lectin concanavalin A (Con A).

65 ls (TIB 155) stimulated with concanavalin A (Con A).

66 P), transthyretin (TTR), and concanavalin A (Con A).

67 mption) in mice treated with concanavalin A (Con A).

68 copy during its binding with concanavalin A (Con A).

69 istic mimetic also prevented Concanavilin A (Con A) induced hepatitis, a CD4(+) T cell-mediated anima

70 ect of rhIL-11 in a model of Concanavalin A (Con-A)-induced T-cell-mediated hepatotoxicity was examin

71 ors, two unrelated proteins, concanavalin-A (Con-A) and postsynaptic density protein 95 (PSD-95), bin

72 -known lectin macromolecule (concanavalin A, Con A) monolayer was functionalized on 3D graphene (3D-G

73 T6 gene by way of genetic knockout abolishes Con A-mediated liver injury without affecting IFN-gamma/

74 nificantly decreased in CD39 null mice after Con A administration.

75 enous IL-6 given immediately before PH after Con A, augmented both LHPC and LEPC expansion in the IL-

76 incle deletion or blockade protected against Con A hepatitis, whereas Mincle ligation exacerbated dis

77 lent model lectin: the leguminous agglutinin Con A, which is structurally related to endogenous cargo

78 nsor consists of the dyed beads and Alexa488-Con A confined inside a sealed, small segment of a hollo

79 absence of glucose, the majority of Alexa488-Con A resides inside the colored beads bound to fixed gl

80 escence emission at 520 nm from the Alexa488-Con A residing within the beads.

81 igh loading degree of Sephadex with Alexa488-Con A (10 mg mL(-1) bead suspension), the absolute fluor

82 MC) allografts in vivo and lysing allogeneic Con A lymphoblasts in vitro.

83 Although Con A-activated splenocytes from IL-12R beta 2(-/-) mice

84 xpressing SRA, which effectively ameliorates Con A-induced hepatic injury.

85 ve been activated by treatment with IL-2 and Con A.

86 esser degree purified protein derivative and Con A, but had no inhibitory effect on serum Ab levels t

87 issociation constants for Con A-glycogen and Con A-mannan interactions are KA=3.93+/-0.7x10(6) M(-1)/

88 s of Concanavalin A (Con A) and glycogen and Con A-mannan using quartz crystal microbalance (QCM), co

89 inear relationship between the impedance and Con A concentration was obtained, and the detection limi

90 ion of IL-2 to T cells treated with 4-MU and Con A reversed the block in cell proliferation, showing

91 We found that mouse peritoneal resident and Con A-elicited macrophages collected on day 3 or day 5 e

92 anavalin A (Con A) coupled to an AFM tip and Con A receptors on the surface of NIH3T3 fibroblast cell

93 d an overlapping staining of cathepsin W and Con A, an ER-specific lectin.

94 ensitization was similar in both control and Con-A conditions, whereas PSD-95 accelerated recovery al

95 Finally, eotaxin blockade attenuates Con A-induced liver injury and leukocyte infiltration.

96 intravenously administered 30 minutes before Con A administration.

97 of hepatic ILC2s, 3-d IL-33 treatment before Con A challenge potently suppressed development of immun

98 istration of a single dose of rhIL-11 before Con-A administration reduced centrilobular liver necrosi

99 o quantify the specific interactions between Con A and mannose by measuring the impedance change of m

100 ogether to PBMC cultures, completely blocked Con A- and partially blocked anti-CD3- and PMA/ionomycin

101 eliminated in VAP-1-deficient mice and both Con A-induced liver injury and CD4 T-cell infiltration w

102 FN-gamma, IL-10, and IL-4 production by both Con A- and myelin basic protein Ac(1-11) peptide-stimula

103 tory effects on T cell proliferation to both Con A as well as the central nervous system Ag myelin ba

104 Specifically, surface-bound Con A binds certain Man7, Man8, and Man9 RNase B glycofo

105 mediated inhibition was partially blocked by Con A, DIP and SVKI.

106 ed T cell proliferative responses induced by Con A and alloantigen stimulation in a dose-dependent ma

107 he mouse ameliorates liver injury induced by Con A and impinges on hallmarks of NKT cell activation i

108 , intracellular calcium elevation induced by Con A or TCR cross-linking, proliferation, or TNF produc

109 ression because delta OR mRNA was induced by Con A stimulation of splenocytes from CD28-deficient mic

110 rved after Th1-mediated hepatitis induced by Con A.

111 h as adenosine triphosphate, are released by Con A-stimulated cells and bind to specific purinergic t

112 dergo Th1 differentiation when stimulated by Con A and APCs.

113 A(-/-) mice are hyperresponsive to anti-CD3, Con A, and alpha-galactosylceramide stimulation and secr

114 o various mitogens, including PHA, anti-CD3, Con A, and LPS.

115 eated or anti-delta-dextran-treated B cells, Con A-stimulated spleen cells, liver cells, or a number

116 ort and less ramified while in A375-P cells, Con A binds to long, branched mannose and glucose types

117 ein (cCNBP) cDNA was isolated from a chicken Con-A-stimulated immune cell library by differential scr

118 pression profiling was carried out comparing Con A elicited peritoneal macrophages from C57BL6 and FV

119 hat, upon addition of TFE, low-concentration Con A transforms to a highly alpha-helical conformation

120 In contrast, Con A inhibited, but did not prevent, translocation of B

121 When compared with conventional Con A lectin chromatography, the monolithic capillary en

122 eletion of CD39 is protective in [corrected] Con A-induced hepatitis.

123 udies, BI-78D3 not only blocks JNK dependent Con A-induced liver damage but also restores insulin sen

124 iation and dissociation constants describing Con A-polysaccharides interaction are determined in a sa

125 KR:(-/-) mice were hyperproliferative during Con A-mediated stimulation.

126 F-alpha reduced induction of IL-18 by either Con A (70% reduction) or PEA (40% reduction).

127 -gamma secretion when stimulated with either Con A or anti-CD3 mAb in vitro.

128 adults when stimulated in vitro with either Con A or anti-CD3 mAB: However, TNF-alpha and IFN-gamma

129 nd CD8+ T cells after activation with either Con A or anti-CD3 without a requirement for either de no

130 ing capacities for microaffinity enrichment: Con A was able to bind 75 mug of a standard glycoprotein

131 nst chicken CD25 was confirmed by evaluating Con A-induced CD25 upregulation in thymocytes and by qua

132 min, as visualized by postfield fluorescent Con A labeling.

133 were able to detect glycoproteins from 1 fM (Con A), 10 fM (Ricinus communis agglutinin (RCA), or 100

134 e., 3-7 for pili-mannose binding and 2-8 for Con A mediated binding), high specificity and selectivit

135 strate the selective affinity of RNase B for Con A.

136 m association and dissociation constants for Con A-glycogen and Con A-mannan interactions are KA=3.93

137 T-1 and NF-kappaB signaling is essential for Con A-induced inducible NO synthase (iNOS) and NO in mur

138 Our observed detection limit for Con A is 0.02 mg/mL (0.7 muM).

139 Transfer of spleen cells from Con A-injected CD44 KO mice into CD44 WT mice induced hi

140 m is restored by displacing the dextran from Con A.

141 However, HCs from Con A-pretreated IFN regulatory factor 1(-/-) mice, whic

142 HCs from Con A-pretreated mice showed enhanced expression of the

143 vivo, mice null for CD39 are protected from Con A-induced liver injury and show substantively lower

144 type I NKT cells and affords protection from Con A-induced hepatitis.

145 of NKT cells in the liver and protects from Con A- and alpha-galactosylceramide-induced hepatitis, b

146 Furthermore, Con A-induced hepatitis is caspase-1 dependent.

147 regenerable sorbents by forming a IDA:Cu(II):Con A sandwich affinity structure that has high column c

148 hat the affinity of polydopamine-immobilized Con A for the glycoforms of RNase B is significantly aff

149 The biosensor is prepared by immobilizing Con A on a 5MHz gold crystal by carbodiimide crosslinkin

150 d FasL, as well as the role of caspase-1, in Con A-induced hepatitis.

151 and a role for monocyte-derived TNF-alpha in Con A-, TCR complex-, and PMA/ionomycin-induced HA bindi

152 pendent manner anti-CD3-induced apoptosis in Con A/IL-2-preactivated peripheral T cells and the murin

153 t study, we investigated the role of CD44 in Con A-induced hepatitis.

154 and alpha4 integrin have opposing effects in Con A-induced hepatic injury, which is associated with b

155 filtration of neutrophils and eosinophils in Con A-induced hepatitis is markedly suppressed in IL-4 (

156 n-2, and interferon-gamma mRNA expression in Con A-stimulated spleen cells was not inhibited by CMX-1

157 ntrahepatic inflammation and liver injury in Con A hepatitis.

158 diates were increased in the murine liver in Con A hepatitis.

159 e deletion lowered production of nitrites in Con A hepatitis and inhibition of both C/EBPbeta and HIF

160 3 plays an important proinflammatory role in Con A-induced hepatitis by promoting the activation of T

161 est that IL-4/STAT6 plays a critical role in Con A-induced hepatitis, via enhancing expression of eot

162 s suggest that STAT1 plays a harmful role in Con A-mediated hepatitis by activation of CD4(+) and NK

163 e cultured with different stimuli, including Con A, PMA/ionomycin, and allogeneic spleen cells.

164 of either IL-18 or TNF-alpha did not inhibit Con A-induced production of IFN-gamma.

165 Ebselen at 5-20 micro M inhibited Con A-induced proliferation and cytokine production by t

166 In contrast, when NAD is injected into Con A- or alpha-galactosylceramide-primed mice, liver in

167 ets as effectors and a panel of 51Cr-labeled Con A lymphoblasts as targets in the presence or the abs

168 uction in the binding of LPS with the lectin Con A sensor upon exposure to various antibiotics has a

169 re recognized by the mannose-binding lectin, Con A, and the biotin-binding protein avidin-peroxidase.

170 of polysaccharides to an immobilized lectin, Con A.

171 e tested for their effects on anti-CD3 mAb-, Con A-, and PMA/ionomycin-mediated monocyte HA binding i

172 Weak interactions with MAL, Con A, and WGA were also quantified.

173 ohydrate-protein interactions (i.e., mannose-Con A; ECL-lactose, alpha-Gal-anti-Gal).

174 In control mice Con A markedly increased the serum alanine aminotransfer

175 In NKT cell-depleted mice, Con A-induced liver injury is diminished; this can be re

176 hibitory effect and is capable of mitigating Con A-induced liver pathology.

177 nal B cell activator LPS, the T cell mitogen Con A, and staphylococcal enterotoxin A superantigen.

178 o T cell proliferation to the potent mitogen Con A, suggesting that protease inhibition may inhibit T

179 ld-type mice when presented with the mitogen Con A.

180 rs are completely reversible and can monitor Con A solution concentration changes.

181 milar in control (taufast = 5.5 +/- 0.4 ms), Con-A-treated patches (taufast = 6.1 +/- 0.5 ms) and pat

182 cute liver injury was assessed in the murine Con A hepatitis model using C57BL/6, Mincle(-/-), and De

183 nylated Con A was without effect and neither Con A nor LC increased binding to solubilized AMPA recep

184 ion to excised patches revealed that neither Con-A nor PSD-95 affect the onset of desensitization.

185 , and the detection limit reaches to 0.12 nM Con A in a buffer solution (pH=7.4), whereas the additio

186 of the most mobile population of nonliganded Con A receptors is estimated to be about 2 x 10(-3) micr

187 toxicity both in the presence and absence of Con A.

188 brogated BoNT-A action; however, addition of Con A after 40 min was no longer protective.

189 Addition of Con A at times up to 15 min after toxin exposure abrogat

190 Intravenous administration of Con A (20 mg/kg) caused 100% mortality in C57BL/6 CD44-k

191 Administration of Con A induces severe injury to hepatocytes in mice and i

192 ll-mediated hepatitis: the administration of Con A or of Pseudomonas aeruginosa exotoxin A (PEA).

193 More importantly, taking advantage of Con A-gold nanoprobe catalyzed silver enhancement, the p

194 an unexpected role of SRA in attenuation of Con A-induced, T-cell-mediated hepatic injury.

195 The multivalent binding of Con A to the E. coli surface O-antigen favors the strong

196 ubercidin has no effect on either capping of Con A receptors or phagocytosis in Dictyostelium.

197 um (growth in suspension culture, capping of Con A receptors, and development to fruiting bodies) and

198 motile, and dividing cells and under caps of Con A receptors but has no effect on myosin II-dependent

199 In turn, the slow structural change of Con A induced by TFE provides a useful model system for

200 this conserved water in the complexation of Con A with a synthetic analog of the natural trisacchari

201 MD simulations of the complexes of Con A with 1 and 2 demonstrated that the hydroxyethyl si

202 The apparent affinity constant of Con A binding to mannose was (8.7 +/- 2.8) x 10(5) and (

203 ange of manno-PANI film for the detection of Con A.

204 Administration of lower doses of Con A (12 mg/kg body weight) into CD44 WT mice induced h

205 CD44 KO mice injected with similar doses of Con A exhibited more severe acute suppurative hepatitis.

206 k implicates a novel innate immune driver of Con A hepatitis and, more broadly, suggests a potential

207 SCs demonstrated potent immunosuppression of Con A-stimulated splenocytes in vitro, even at a 1:320 M

208 as equal potency to CsA in the inhibition of Con A and alloantigen stimulated rat spleen cell prolife

209 lyvalent ligands are effective inhibitors of Con A binding, whereas linear oligomeric ligands generat

210 rtality than controls after the injection of Con A and in a model of cerebral malaria.

211 The interactions of Con A with surface glycans were quantified with both AFM

212 rticularly those from regenerating livers of Con A-pretreated mice, induced a regulatory phenotype in

213 Using the murine model of Con A-induced immune-mediated hepatitis, we showed that

214 croscopy (CLSM) revealed numerous patches of Con A and SYTO 9 staining structures covering the surfac

215 ferative response and the IL-2 production of Con A-stimulated autologous CD4(+)CD25(-) T cells compar

216 urrent work reports the crystal structure of Con A with this synthetic ligand and shows that even tho

217 Instead, we demonstrate that the effects of Con-A on macroscopic responses reflect a shift in the re

218 Identical inhibition of Con-A-stimulated cultures occurred in both serum free an

219 media, indicating that AT-III inhibition of Con-A-stimulated rat spleen cell proliferation is indepe

220 on the AuNCs@ew and glycan binding sites on Con A.

221 glycoproteineous properties when applied on Con-A Sepharose column.

222 action of two or more chains of PPE with one Con A molecule leading to a quenched sugar-PPE-Con A con

223 adsorbing the ER-glycosylated peptides onto Con A-coupled Sepharose beads.

224 by treatment with nicotine, anti-TCR Abs, or Con A.

225 cells or on splenic LPS-activated B cells or Con A-activated T cells.

226 ition, by modifying the amount of dextran or Con A used in nanoparticle fabrication, we can to some e

227 he presence of rCIL-2, PMA plus ionomycin or Con A stimulated CD4(+)CD25(+) cell proliferation, where

228 phorbyl myristyl acetate plus ionomycin, or Con A.

229 mmune responses (having no effect on LPS- or Con A-induced activation).

230 /+ mice on stimulation with anti-CD3 mAbs or Con A.

231 It had no effect on postoperative Con A or MLR and did not prevent mAb clearance due to th

232 n A molecule leading to a quenched sugar-PPE-Con A construct.

233 IL-18BP-Fc also prevents Con A-induced liver damage and IFN-gamma and Fas ligand

234 n anti-IL-18 antiserum significantly reduced Con A- and PEA-induced liver damage.

235 the ability of mononuclear cells to restore Con A-induced liver injury in NKT-depleted mice, whereas

236 In splenic Con A blasts from high transgene copy B27 lines that dev

237 ion stimulated by two commonly used stimuli: Con A and antibodies that crosslink surface CD3 and CD28

238 Succinylated Con A was without effect and neither Con A nor LC increa

239 First, we determined that Con A induces proMMP-2 activation in HT1080 cells by shi

240 ometry (XPS) and UV-vis results suggest that Con A binding with the manno-PANI film triggers the swit

241 s MT1-MMP remains competent, suggesting that Con A regulates MT1-MMP activity through cytoplasmic dom

242 This work suggests that Con A-mannan complex could be potentially utilized for i

243 Our results show that Con-A and PSD-95 regulate kainate receptors via distinct

244 ) = 45 +/- 9 microM, n = 6), suggesting that Con-A does not convert non-conducting channels with high

245 The Con A - mannose (or glucose) type glycans present on WM3

246 The Con A receptors appear to consist of a heterogeneous pop

247 Furthermore, a detection limit for the Con A biosensor down to 1 aM was achieved in a sandwich

248 A nonspecific binding of proteins for the Con A biosensor was only 6.1% (probed with an oxidized i

249 es a conserved water molecule present in the Con A binding site.

250 a negligible nonspecific interaction of the Con A biosensor was observed in diluted human sera (1000

251 Extensive accumulation of the Con A receptors by an electric field results in the form

252 otein hydrogels with a 2D PC embedded on the Con A protein hydrogel surface, that multivalently and s

253 The resulting crosslinks shrink the Con A protein hydrogel, reduce the 2D PC particle spacin

254 The response is proportional to the Con A concentration up to 10(-7) M in phosphate-buffered

255 f these molecules ameliorates or worsens the Con A-induced hepatic injury in vivo.

256 e addition of glucose competitively binds to Con A, reducing gold nanoparticle aggregation and theref

257 restored the responsiveness of ob/ob mice to Con A and normalized their lymphocyte and monocyte popul

258 tic SRA ablation strongly sensitizes mice to Con A-induced liver injury.

259 Remarkable response was observed to Con A at a concentration as low as 5 x 10(-10) M.

260 C was subsequently shown to be resistant to Con A treatment whereas MT1-MMP remains competent, sugge

261 acking functional caspase-1 are resistant to Con A-induced hepatitis, even after pretreatment with a

262 oups to cell surfaces, are also resistant to Con A-induced hepatitis.

263 - T cells did not proliferate in response to Con A or alloantigens but entered apoptosis within 48 h

264 rat spleen cell proliferation in response to Con A, in a dose-dependent manner.

265 d similar amounts of TNFalpha in response to Con A, PMA/ionomycin, or anti-CD3/anti-CD28.

266 hemokine stimulation, as T cell responses to Con A and PMA were also suppressed.

267 (+) cells did not affect T cell responses to Con A and to a peptide presented by MHC class II.

268 Gal-3(-/-) mice were less sensitive to Con A-induced hepatitis and had a significantly lower nu

269 hiomannose derivative binds even stronger to Con A than the natural substrate, offering opportunities

270 Binding studies to Con A have been performed by isothermal titration calori

271 imulated keratinocyte culture supernatant to Con A-stimulated spleen cells resulted in the suppressio

272 controls, which show equal susceptibility to Con A- induced injury, because IL-6/gp130 signaling has

273 We tested susceptibility to Con A-induced hepatitis in galectin-3-deficient (Gal-3(-

274 at are more resistant than wild-type (WT) to Con A killing.

275 cers display an excellent selectivity toward Con A in the presence of a large excess of bovine serum

276 odamine isothiocyanate concanavalin A (TRITC-Con A) chemically conjugated into the hydrogel network u

277 en 0 and 800 mg/dL was obtained with a TRITC-Con A/FITC-dextran mass ratio of 500:5 micrograms/mL PEG

278 In the absence of glucose, TRITC-Con A binds with FITC-dextran, and the FITC fluorescence

279 nd glucose were conducted for multiple TRITC-Con A/FITC-dextran ratios.

280 Competitive glucose binding to TRITC-Con A liberates FITC-dextran, resulting in increased FIT

281 Further purification was performed using Con-A Sepharose, Phenyl Sepharose, DEAE Sephacel, and Su

282 Using an in vivo Con A challenge model of acute hepatitis, we observed re

283 e.g. control, EC50(SS) = 31 +/- 28 microM vs Con-A, EC50(SS) = 45 +/- 9 microM, n = 6), suggesting th

284 rates and a range of lectins, including WGA, Con A, UEA-I, GS-II, PNA and SBA, were monitored in real

285 the water molecule in the complex of 1 with Con A.

286 e interactions of trimannosides 1 and 2 with Con A were studied to reveal the effects of displacement

287 Treatment of cells with Con A results in quantitative phosphorylation of the reg

288 llular location upon treatment of cells with Con A, nor does it localize to the myosin-rich caps that

289 nding between the dendrimer and glucose with Con A are presented.

290 iments: rat spleen cells were incubated with Con A or irradiated stimulator cells with/without serial

291 tran-coated gold colloids, cross-linked with Con A, by glucose.

292 affinity increase compared to free Man with Con A.

293 of the so-prepared cross-linked polymer with Con A were measured to be between 2.5 x 10(6) and 3.2 x

294 in T cells as observed by proliferation with Con A.

295 pon in vitro stimulation of splenocytes with Con A or anti-CD3, type 2 cytokine levels were reduced,

296 ), but stimulation of mouse splenocytes with Con A results in induction of delta OR mRNA and protein.

297 rotein 2, and IFNgamma upon stimulation with Con A, Toll-like receptor 2 agonist, or anti-CD3 antibod

298 ncreased after activation of the Tcells with Con A.

299 Treatment with Con A in a model of polyclonal T lymphocyte activation r

300 mma)-producing CD3 T cells but this worsened Con A hepatitis, suggesting inhibition of a suppressor c