ライフサイエンスコーパス: galectin

1 the carbohydrate-recognition domains of each galectin.

2 s into design-functionality relationships of galectins.

3 promoting activity of beta-galactose-binding galectins.

4 relatively low, signaling preferences among galectins.

5 Preincubation of exosomes with anti-galectin 1 antibody decreased their neuroprotective effe

6 es likely impart their effect via binding of galectin 1 to cells.

7 Galectin 1 was highly expressed on the surface of PMSCs

8 It was recently described that Galectin-1 (Gal-1) promotes axonal growth after spinal c

9 Galectin-1 (Gal-1), a member of a family of evolutionari

10 In this article, we show that galectin-1 (Gal-1), an immunoregulatory lectin widely ex

11 dy, we identified a new fibrosis gene called galectin-1 (Gal-1), which is highly expressed in tubular

12 We noted that tumor galectin-1 (Gal1) levels were inversely correlated with

13 Galectin-1 (Gal1), an endogenous glycan-binding protein,

14 The homodimeric adhesion/growth-regulatory galectin-1 and a set of covalently linked homo-oligomers

15 Using the example of homodimeric galectin-1 and monomeric galectin-3, the mutual design c

16 mmunosuppressive microenvironment, including galectin-1 and PD-L1/2.

17 increased cathepsin-V (CTSV) expression and galectin-1 expression and secretion in human glomerular

18 Galectin-1 is a new fibrosis protein in type 1 and type

19 ated in solid phase assays using recombinant galectin-1, -3, -8, confirming selectivity for galectin-

20 polypeptide, apolipoproteins A-Ib and A-II, galectin-1, and vitellogenin-6 during degeneration when

21 es (actin and myosin), ECM genes (Collagens, Galectin-1, Fibronectin, Heparan Sulfate, LOX, FAK1), ce

22 eficient cells displayed enhanced binding to galectin-1, indicating that changes in GNE activity can

23 The proteomic analysis revealed upregulated galectin-1, which is an immunomodulatory protein linked

24 relevant and exploitable for PET imaging of galectin-1-overexpressing bladder tumors.

25 umulation of the carbohydrate radiotracer in galectin-1-overexpressing UMUC3 orthotopic tumors when i

26 otrophoblast of the human placenta expresses galectins-1, -3, and -8 in vivo and in vitro.

27 confirmed the found abundance differences in galectin 10 and protein S100-A9 between the groups.

28 he Galectin superfamily and is also known as galectin-10 (Gal-10).

29 Moreover, recombinant galectin-10 by itself was able to suppress T cell prolif

30 Moreover, we show that galectin-10 functions as a T cell-suppressive molecule i

31 children with EoE also had higher levels of galectin-10 mRNA and lower levels of FOXP3 mRNA.

32 We found that Ab-mediated neutralization of galectin-10 partially abrogated the suppressive function

33 Charcot-Leyden crystals (CLCs) are Galectin-10 protein crystals that can form after eosinop

34 Finally, we detected galectin-10-containing immune synapses between eosinophi

35 evels of CD23, CD44, CD54, CRTH2, FOXP3, and galectin-10.

36 ntain stores of the immunoregulatory protein galectin-10.

37 LGALS2 encodes the glycan-binding protein Galectin 2 (Gal2), which is predominantly expressed in t

38 er from each of the three subtype galectins, galectin-2 (proto-), galectin-3 (chimera-) and galectin-

39 Increased levels of galectin 3 have been associated with nonalcoholic steato

40 GR-MD-02 (belapectin) is an inhibitor of galectin 3 that reduces liver fibrosis and portal hypert

41 ovascular disease, respectively, followed by galectin-3 <25th percentile (DLR 0.44 and 0.43, respecti

42 I 0.23) and CAC <=10 (NRI 0.28), followed by galectin-3 <25th percentile (NRI 0.14) and absence of ca

43 Colocalization of alphaS pathology with galectin-3 (a marker of endo-lysosomal membrane rupture)

44 hree subtype galectins, galectin-2 (proto-), galectin-3 (chimera-) and galectin-4 (tandem repeat-type

45 Galectin-3 (Gal-3) can cross-link surface glycoproteins

46 ing were used to investigate the function of galectin-3 (Gal-3) during the process of leukocyte recru

47 Galectin-3 (Gal-3) has been linked to cardiac remodeling

48 We studied the role of galectin-3 (Gal-3) in the expression of alternative acti

49 Galectin-3 (gal-3) is expressed in well-differentiated a

50 Galectin-3 (Gal-3) is implicated in cardiac fibrosis, bu

51 Mammalian beta-galactoside-binding protein Galectin-3 (Gal-3) modulates the host innate and adaptiv

52 nflammation markers soluble (s)CD163, sCD14, galectin-3 (Gal-3), and Gal-3 binding protein (Gal-3BP)

53 At inclusion, Galectin-3 (Gal-3), N-terminal proB-type natriuretic pep

54 -1, matrix metalloproteinase (MMP)-2, MMP-9, Galectin-3 (Gal-3), N-terminal propeptide of collagen I

55 ion of the beta-galactoside binding protein, Galectin-3 (Gal-3).

56 n/growth-regulatory galectins, in particular galectin-3 (Gal-3).

57 Here, we show that galectin-3 (Gal3), a beta-galactoside-binding cytosolic

58 etween a C-terminal domain fragment of human galectin-3 (hGal-3C) and three human serum GPs, alpha-1-

59 by a failure of numerous PSCs to upregulate galectin-3 (MAC-2), a marker of glial axonal debris phag

60 ration and invasion, using recombinant human galectin-3 (rhgalectin-3), small molecule galectin inhib

61 These results show that galectin-3 acts as a pro-invasive autocrine/paracrine fa

62 Using two different galectin-3 affinity purification processes, we extracted

63 is was characterized by marked expression of galectin-3 and an enhanced number of proliferating RV fi

64 onic anhydrase-12, and NC markers brachyury, galectin-3 and CD24 in cells of the NP irrespective of a

65 ges, including fractional area of liver fat, galectin-3 and Col1a1.

66 Soluble recombinant galectin-3 and endogenous galectin-3 of epithelial origi

67 alidated CaRe by purifying recombinant human galectin-3 and five other known lectins and also tested

68 The impact of galectin-3 and protease expression on S. aureus virulenc

69 Both the level of galectin-3 and the galectin-3 interactions with synovial

70 Conclusions: We identified extrapulmonary galectin-3 as an important mediator that drives RV fibro

71 -based gene knockout approach, we identified galectin-3 as the major counterreceptor of GPVI on tumor

72 the self-association-related multivalency of galectin-3 at the residue-specific level.

73 IgG(4) galectin-3 autoantibodies are present in a subset of pat

74 IgG(4) anti-galectin-3 autoantibodies correlated with increased plas

75 Anti-galectin-3 autoantibody responses were predominantly of

76 Galectin-3 binding protein could be considered as potent

77 ucin-type O-glycoprotein displayed increased galectin-3 binding.

78 d phase separation, and we demonstrated that galectin-3 can also undergo liquid-liquid phase separati

79 We report that galectin-3 can bind to TLR-4, and that administration of

80 nt interactions of transmembrane mucins with galectin-3 contribute to maintenance of the epithelial b

81 istration of a neutralizing antibody against galectin-3 decreases the expression of IL-1beta, IL-6, T

82 ns and clinical isolates of S. aureus caused galectin-3 degradation.

83 nhibition in NSCLC, we tested the effects of galectin-3 depletion using genetic and pharmacologic app

84 vidence for the hypothesis that chimera-type galectin-3 design makes functional antagonism possible,

85 Taking all together, galectin-3 emerges as a clinically relevant target for T

86 No changes of galectin-3 expression were observed in the lungs.

87 leomorphism, fibrous septation and increased galectin-3 expression, consistent with atypical parathyr

88 vity troponin I (hsTnI), soluble (s)ST2, and galectin-3 from baseline to 26, 52, and 104 weeks.

89 Galectin-3 genetic and pharmacologic inhibition or antif

90 the requisite glycan epitopes needed to bind galectin-3 have long been elucidated, the cellular glyco

91 (hematoxylin-eosin staining), inflammation (galectin-3 immunohistochemistry (IHC); gal-3), and fibro

92 f perfluorcarbon-labeled immune cells, Mac-2/Galectin-3 immunostaining, and FACS (fluorescence-activa

93 y aimed to investigate the potential role of galectin-3 in cell migration and invasion, using recombi

94 the glycan and glycoprotein interactors for galectin-3 in live human hepatic stellate cells and peri

95 e show a large increase in the expression of galectin-3 in microglia and also an increase in the rele

96 and also an increase in the released form of galectin-3 in the cerebrospinal fluid (CSF) 24 h after h

97 mes detected the presence of fibronectin and galectin-3 in those derived from DCs, whereas T-cell exo

98 Silencing of galectin-3 induced significant reduction in cell migrati

99 To examine the role of galectin-3 inhibition in NSCLC, we tested the effects of

100 ral administration of a novel small molecule galectin-3 inhibitor GB1107 reduced human and mouse lung

101 The novel galectin-3 inhibitor presented could provide an effectiv

102 In this work, two galectin-3 inhibitors were radiolabeled with fluorine-18

103 ctively reacted to give rise to a library of galectin-3 inhibitors.

104 actions was further validated by analysis of galectin-3 interaction with a semisynthetic ligand, F3.

105 ore 2 O-linked glycans mediate this lubricin-galectin-3 interaction, shown by surface plasmon resonan

106 Both the level of galectin-3 and the galectin-3 interactions with synovial lubricin were foun

107 Galectin-3 is a beta-galactoside-binding lectin that is

108 Galectin-3 is a glycan-binding protein (GBP) that binds

109 for these proteases and that proteolysis of galectin-3 is a novel immune evasion mechanism.

110 In summary, galectin-3 is an important regulator of lung adenocarcin

111 The galactoside-binding protein galectin-3 is increasingly recognized as an important pl

112 enabling multivalency for various functions, galectin-3 is monomeric, and its functional multivalency

113 Using novel co-culture model systems, galectin-3 is shown to facilitate basophil secretion of

114 europrotection in the cortical region in the galectin-3 knockout animals in response to TBI.

115 chocardiographic assessment was performed on galectin-3 knockout or inhibitor-treated mice.

116 oantibodies correlated with increased plasma galectin-3 levels (P = .001), lymphadenopathy (P = .04),

117 We propose that galectin-3 may achieve multivalency through this multisi

118 suggest that following head trauma, released galectin-3 may act as an alarmin, binding, among other p

119 hat CD146/MCAM interactions with circulating galectin-3 may have an important influence on cancer pro

120 Serum galectin-3 modestly increased from baseline with canagli

121 oluble recombinant galectin-3 and endogenous galectin-3 of epithelial origin both stimulated MMP9 act

122 inding ligand and strongly co-localized with galectin-3 on endothelial cell surfaces treated with exo

123 f patients with IgG(4)-RD and correlate with galectin-3 plasma levels.

124 atment with galectin-3 siRNA both LGALS3 and galectin-3 protein were dramatically decreased.

125 on of membrane-damage signals as detected by galectin-3 recruitment.

126 small molecule galectin inhibitor I(47), and galectin-3 silencing.

127 Upon HTR-8/SVneo cell treatment with galectin-3 siRNA both LGALS3 and galectin-3 protein were

128 trated that the carbohydrate-binding protein galectin-3 stimulated microenvironment remodeling in the

129 tween platelet GPVI and tumor cell-expressed galectin-3 uses ITAM-signaling components in platelets a

130 Galectin-3 was identified as the antigen specifically re

131 Galectin-3 was increased in TSC-related skin tumors, ang

132 Signature component Lgals3 encoding galectin-3 was increased in Tsc2-deficient cells and ser

133 Serum levels of galectin-3 were increased in patients with idiopathic pu

134 is partly attributable to the interaction of galectin-3 with unknown receptor(s) on vascular endothel

135 iguingly, YopK limited the colocalization of Galectin-3 with YopD, suggesting that YopK limits the in

136 We also characterise a subpopulation of galectin-3(+) (Gal3(+)) myeloid cells within the develop

137 overall showed smaller lesion sizes than the galectin-3(+/+) animals.

138 In galectin-3(+/+) mice, SspB-expressing S. aureus caused l

139 Galectin-3(-/-) mice developed significantly smaller and

140 ositive bone marrow restored tumor growth in galectin-3(-/-) mice, indicating that macrophages were a

141 acterial load or lesion size was detected in galectin-3(-/-) mice, which overall showed smaller lesio

142 (macrophage surface glycoproteins binding to galectin-3) and an increase of renal epithelial damage m

143 5 (growth differentiation factor 15), GAL-3 (galectin-3), and Cys-C (cystatin-C) were assessed before

144 s in biomarkers of immunity (S100A8, S100A9, galectin-3), tissue injury and repair (Serpine1/PAI-1) a

145 erminal pro-B-type natriuretic peptide], and galectin-3).

146 We hypothesized that human galectin-3, a beta-galactoside-binding lectin involved i

147 the staphylococcal protease SspB inactivates galectin-3, abrogating its stimulation of oxygen radical

148 neutrophil gelatinase-associated lipocalin, galectin-3, and lipocalin-like prostaglandin D2 synthase

149 brogated by bacterium-derived proteolysis of galectin-3, and SspB was identified as the major proteas

150 lomerular filtration rate, creatinine, NGAL, galectin-3, and urea.

151 dimer, fibrinogen, C-reactive protein, sST2, galectin-3, cystatin-C, and urinary albumin-to-creatinin

152 id intima-media thickness, apolipoprotein B, galectin-3, high-sensitivity C-reactive protein, lipopro

153 tumorgenicity 2, highly sensitive troponin, galectin-3, midregional proadrenomedullin, cystatin-C, i

154 erly individuals with CAC = 0, CAC <=10, low galectin-3, or no carotid plaque had remarkable low card

155 mple of homodimeric galectin-1 and monomeric galectin-3, the mutual design conversion caused qualitat

156 ty to the carbohydrate recognition domain of galectin-3, using a combination of isothermal titration

157 We have shown previously that circulating galectin-3, which is increased up to 30-fold in cancer p

158 CD146 was the major galectin-3-binding ligand and strongly co-localized with

159 Thus, CD146/MCAM is the functional galectin-3-binding ligand on endothelial cell surfaces r

160 Here we sought to identify the galectin-3-binding molecule(s) on the endothelial cell s

161 chymotrypsin, ficolin-2, 14-3-3 protein, and galectin-3-binding protein were considered potential bio

162 roteinase 9, S100A8/S100A9, cathepsin D, and galectin-3-binding protein) improved risk prediction and

163 00A8), S100A9, cathepsin B, fibronectin, and galectin-3-binding protein.

164 Moreover, corneas of galectin-3-deficient mice failed to stimulate IL-1beta a

165 cretion systems into PV membranes stimulates Galectin-3-dependent recruitment of antimicrobial GBPs t

166 ates but not in Staphylococcus saprophyticus Galectin-3-induced activation of the neutrophil NADPH ox

167 on endothelial cell surfaces responsible for galectin-3-induced secretion of metastasis-promoting cyt

168 d develop selective therapeutics to mitigate galectin-3-mediated biological events.

169 endothelial cell surface responsible for the galectin-3-mediated cytokine secretion.

170 ed tumor growth, whereas reconstitution with galectin-3-positive bone marrow restored tumor growth in

171 lectin-1, -3, -8, confirming selectivity for galectin-3.

172 y mediating interaction between lubricin and galectin-3.

173 ors become upregulated, including the lectin galectin-3.

174 thelial cell surfaces treated with exogenous galectin-3.

175 ore 2 structures did not bind to recombinant galectin-3.

176 are positive for the membrane damage marker Galectin-3.

177 growth factor-binding protein-7], and GAL-3 [galectin-3]) were assessed.

178 lectin-2 (proto-), galectin-3 (chimera-) and galectin-4 (tandem repeat-type), was selected and analys

179 cident diabetes and 3 proteins (Cathepsin D, Galectin-4, Paraoxonase type 3) with a novel association

180 Galectin-4, with an increased risk of diabetes, and Para

181 re screened against the family 51 CBM, human galectin-7, and CTB(5) to illustrate the potential of NG

182 The sensor of this mechanism, galectin-8 (encoded by LGALS8), detects permeated endoso

183 We also found that the danger receptor galectin-8 detects damaged endomembranes and activates a

184 y analysis that alpha-tubulin interacts with galectin-8 during mitosis.

185 Galectin-8 is a beta-galactoside-recognizing protein hav

186 We conclude that galectin-8 is upregulated in psoriasis and contributes t

187 In addition, we show that galectin-8 levels in keratinocytes are positively correl

188 staining and immunoblotting the presence of galectin-8 within the mitotic apparatus.

189 In this study, we demonstrate that galectin-8, a beta-galactoside-binding lectin, is upregu

190 cytosolic exposure of glycans, which recruit galectin-8, indicating bacterial entry into the cytosol.

191 Finally, we show that in the absence of galectin-8, pericentrin compactness is lessened and mito

192 Inhibition of galectin-8- and NDP52-dependent autophagy increased seed

193 lated with the compounds' ability to inhibit galectin-8-induced expression of chemokines and proinfla

194 ing from mitosis into G1 phase is delayed in galectin-8-knockout HaCaT cells after cell-cycle synchro

195 atinocyte proliferation is less prominent in galectin-8-knockout mice after intradermal IL-23 treatme

196 at these monosaccharide-based compounds bind galectin-8N by engaging its unique arginine (Arg59) and

197 e with particular amino acid residues of the galectin-8N extended carbohydrate-binding site.

198 mpounds had in vitro binding affinity toward galectin-8N in the range of 5-33 muM, as evaluated by is

199 Absence of Galectin 9 (Gal9) or loss of its capacity to recognize l

200 Upon disruption of the dectin 1-galectin 9 axis, CD4(+) and CD8(+) T cells, which are di

201 We found that dectin 1 can ligate the lectin galectin 9 in mouse and human PDA, which results in tole

202 We report significant upregulation of Galectin-9 (Gal-9) and VISTA on both CD4(+) and CD8(+) T

203 ly been studied, and our results reveal that galectin-9 (Gal-9) can potently inhibit HCMV infection.

204 Galectin-9 (Gal-9) is highly expressed in the liver and

205 pproach to understand the role of endogenous galectin-9 (Gal-9), a mucosal galectin that has been lin

206 so can bind to the tandem repeat-type lectin galectin-9 (Gal-9), and signaling through mouse (m)4-1BB

207 a member of the galectin family of proteins, galectin-9 (Gal-9), is upregulated during natural HCMV-r

208 gnaling through mouse (m)4-1BB is reduced in galectin-9 (Gal-9)-deficient mice, suggesting a pivotal

209 inhibitor Tim3 and its physiological ligand galectin-9 (Gal9).

210 I 0.16-0.86, p = 0.011) and high circulating Galectin-9 (HR 0.11, 95%CI 0.15-0.85, p = 0.010) levels

211 L1 (HR 0.33, 95%CI 0.16-0.68, p = 0.002) and Galectin-9 (HR 0.27, 95%CI 0.13-0.57, p = 0.001) resulte

212 tion between circulating levels of PD-L1 and Galectin-9 and their intra-tumoral expression levels.

213 ially CD3(+) T cells, showed upregulation of galectin-9 compared with immune cells from matched blood

214 we identified a positive correlation between galectin-9 expression and colitis severity.

215 The patients with high Galectin-9 expression in recurrent NPC frequently also h

216 Using flow cytometry, we determined galectin-9 expression on immune cells from tumor and mat

217 adelta T cells from PDAC patients had higher galectin-9 expression than gammadelta T cells from healt

218 intra-tumoral expression levels of PD-L1 or Galectin-9 further improves the prognostic values of the

219 ficance of circulating PD-L1 and circulating Galectin-9 in patients with resected HCC, and to compare

220 nner, indicating a complicated regulation of galectin-9 in T cells.

221 CD4, Foxp3 and Tim-3 in lymphocytes, and of Galectin-9 in tumour cells between paired primary and re

222 Galectin-9 is a new biomarker for the detection of PDAC.

223 r, these findings suggest that intracellular galectin-9 is a positive regulator of T cell activation

224 Galectin-9 is a risk gene in inflammatory bowel disease.

225 We found that galectin-9 is expressed mainly inside T cells, and its s

226 In conclusion, circulating PD-L1 and Galectin-9 levels prognostically differentiate resected

227 Galectin-9 polarized macrophages toward a protumoral M2

228 Furthermore, we analyzed galectin-9 serum levels by enzyme-linked immunosorbent a

229 r, several mouse-based studies reported that galectin-9 treatment induces T cell apoptosis and amelio

230 Furthermore, serum concentration of galectin-9 was able to discriminate PDAC from benign pan

231 Galectin-9 was highly expressed in human PDAC compared w

232 Endogenous galectin-9 was recruited to immune synapses upon T cell

233 In fact, circulating levels of PD-L1 and Galectin-9 were predictive of HCC-specific survival inde

234 DAC showed the highest expression of LGALS9 (galectin-9) mRNA.

235 as significant increase in the expression of Galectin-9+ tumour cells (p < 0.001) and Foxp3+ lymphocy

236 patients (60%) had increased percentages of Galectin-9+ tumour cells and of Foxp3+ lymphocytes, resp

237 Galectin-9, a beta-galactoside-binding lectin, promotes

238 over, the C-terminal region of SNX3 recruits galectin-9, a lectin implicated in protein and membrane

239 une co-inhibitory ligands, such as PD-L1 and Galectin-9, have potential prognostic value in Hepatocel

240 ermine intra-tumoral expression of PD-L1 and Galectin-9, while ELISA was used to quantify their respe

241 We observed that galectin-9-deficient T cells were less able to induce T

242 over, proximal TCR signaling was impaired in galectin-9-deficient T cells, and proliferation of these

243 17 cell differentiation was downregulated in galectin-9-deficient T cells, and this impairment can be

244 imens from 83 patients with PDAC stained for galectin-9.

245 urface programmed death ligand 1 (PD-L1) and galectin-9.

246 c advantage than primary NPC, especially the Galectin-9/Tim-3 pathway.

247 The immunotherapies targeting Galectin-9/Tim-3/Foxp3 interaction may serve as a potent

248 Galectins, an evolutionarily conserved family of glycan-

249 Thus, galectin and ubiquitin systems converge to activate AMPK

250 ealed marked selectivity among the family of galectins and bridging potency of homodimers.

251 Galectins are a family of beta-galactoside-binding prote

252 Galectins are a family of lectins that bind beta-galacto

253 Galectins are a widely expressed protein family that hav

254 Galectins are carbohydrate-binding proteins overexpresse

255 Within the context of the mucosal surface, galectins are established regulators of innate and adapt

256 Galectins are involved in the regulation of divergent ph

257 y, the B-galactoside binding lectins, termed galectins, are being recognized as critical regulators o

258 Glycan-binding proteins, which include galectins, are involved at all stages of immunity and in

259 Galectins bind to branched N-glycans attached to cell su

260 Moreover, TFS detected very weak galectin binding where ITC could not reliably do so.

261 ture [6GS], including Charcot-Leyden crystal galectin [CLC]; carboxypeptidase 3 [CPA3]; deoxyribonucl

262 nhibitor specificity and selectivity for the galectins expressed in extravillous trophoblast were val

263 galactose moieties have a high affinity for galectin-expressing tumor cells.

264 We conducted in vivo studies in a galectin-expressing UMUC3 orthotopic BCa model to determ

265 xpression levels of different members of the galectin family have been reported in prostate and bladd

266 first time that secretion of a member of the galectin family of proteins, galectin-9 (Gal-9), is upre

267 Understanding the roles of galectin family proteins in the development and progress

268 Galectin (Gal)-3 is a beta-galactoside-binding lectin an

269 tative member from each of the three subtype galectins, galectin-2 (proto-), galectin-3 (chimera-) an

270 Galectins have been implicated in inhibiting BCR signali

271 saccharide, was screened against three human galectin (hGal) proteins (a stable mutant of hGal1 (hGal

272 Unlike the other 14 known galectins in mammalian cells, which have dimeric or tand

273 In this review, we dissect the role of galectins in shaping cellular circuitries governing each

274 relevance of molecular recognition of KS by galectins in terms of physiological processes in situ, e

275 architecture for adhesion/growth-regulatory galectins in vertebrates, here we introduce protein engi

276 asaccharides with adhesion/growth-regulatory galectins, in particular galectin-3 (Gal-3).

277 an galectin-3 (rhgalectin-3), small molecule galectin inhibitor I(47), and galectin-3 silencing.

278 repeat-type), was selected and analysed for galectin interaction with three ligands of different aff

279 igate the possibility that alteration of the galectin intrinsic tryptophan fluorescence could be used

280 finity of cell-surface glycoproteins for the galectin lattice.

281 ace programming with a derivative of the pan-galectin ligand lactose.

282 ctures with N-acetyllactosamine, a preferred galectin ligand.

283 ple, sensitive and reliable way to determine galectin-ligand interactions and also as a drug-discover

284 ver, a simple and effective way in assessing galectin-ligand interactions is lacking.

285 The reliability of TFS in determining galectin-ligand interactions was further validated by an

286 could be used in determining the strength of galectin-ligand interactions.

287 ifically, the N-glycans that wedge between 2 galectin-like domains within the S1 subunit of FIPV S pr

288 examination of the sequence of all 12 human galectin members reveals the presence of one or more try

289 ents were revealed in ligand bindings of all galectin members.

290 ow uM range and stoichiometry of ~ 8 to ~ 20 galectin molecules binding per polysaccharide chain.

291 milk oligosaccharides (HMOs) for four human galectin proteins, a stable mutant of hGal1 (hGal-1), a

292 tional lattice formation on biomembranes and galectin-reagents with therapeutic potential.

293 The binding data show that each of the four galectins recognize the majority of the HMOs tested (hGa

294 den crystal (CLC) protein is a member of the Galectin superfamily and is also known as galectin-10 (G

295 inding energies of KS oligosaccharide-loaded galectins support experimental data on Gal-3 and -7, and

296 o as a drug-discovery platform in developing galectin-targeted therapeutic drugs.

297 of endogenous galectin-9 (Gal-9), a mucosal galectin that has been linked to inflammatory bowel dise

298 The potential for galectins to directly modulate HCMV infection has not pr

299 relationship of these adhesins to mammalian galectins was examined by computational similarity asses

300 Intrafamily diversity among human galectins was in the range of that to these viral surfac