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1 -glycans able to establish interactions with Galectin-1.
2 were measured in the presence and absence of galectin-1.
3 (nanoplexes) to inhibit gene expression for galectin-1.
4 ginex, we had yet to prove that 0118 targets galectin-1.
5 e-host cell interaction via binding to human galectin-1.
6 ender thymocytes susceptible or resistant to galectin-1.
7 for a ubiquitous galactoside-binding lectin galectin-1.
8 as mediators of the DC activation effects of galectin-1.
9 e 2 O-glycan expression or susceptibility to galectin-1.
10 om a patient with MF, were also resistant to galectin-1.
11 that allow recognition and cross-linking by galectin-1.
12 equired for maximal T cell susceptibility to galectin-1.
13 te BCR signaling through an association with galectin-1.
14 n receptors distinct from that recognized by galectin-1.
15 n contrast to the CD45 clustering induced by galectin-1.
16 pressing the beta-galactoside-binding lectin galectin-1.
17 toplasmic levels of the nanocluster scaffold galectin-1.
18 dothelial cells against apoptosis induced by Galectin-1.
19 e-arene interactions for galectin-3 than for galectin-1.
20 galectin family of glycan binding proteins (galectins-1, -2, and -4) induce PS exposure in a carbohy
21 ated in solid phase assays using recombinant galectin-1, -3, -8, confirming selectivity for galectin-
29 at complexes containing H-ras conformers and galectin-1 affect both the number and lifetime of nanocl
32 many of the same DC maturation genes as LPS, galectin-1 also uniquely up-regulated a significant subs
35 ozoan derivatives to dissect the function of galectin-1 and -3 in the context of Trichomonas infectio
37 The homodimeric adhesion/growth-regulatory galectin-1 and a set of covalently linked homo-oligomers
38 there was a significant correlation between galectin-1 and CA IX staining (P = .01) and a strong inv
40 s and revealed concomitant overexpression of galectin-1 and CXCR4 associated adversely with overall a
41 ignificance and positive correlation between galectin-1 and CXCR4 expression levels and revealed conc
49 the specificity of Gal-3BP interacting with galectin-1 and the role of Gal-3BP in cancer cell aggreg
50 ghly up-regulated genes include SOX5, CD11C, galectin-1, and FGR, similar to a previously described F
52 that nanoplexes silenced gene expression for galectin-1, and they reversed the effects of morphine on
53 polypeptide, apolipoproteins A-Ib and A-II, galectin-1, and vitellogenin-6 during degeneration when
58 Our results also support a critical role for galectin-1 as a GM1 cross-linking counter-receptor that
61 R of OT-1 thymocytes, these studies identify galectin-1 as a tuner of TCR binding, signaling, and fun
62 general, our data indicate that 0118 targets galectin-1 as an allosteric inhibitor of glycan/carbohyd
63 oscopy demonstrates that 0118 indeed targets galectin-1 at a site away from the lectin's carbohydrate
65 -mediated glycosylation of RPTPbeta promotes galectin-1 binding and RPTPbeta levels of retention on t
67 ts in decreased RPTP retention, showing that galectin-1 binding contributes to the increased retentio
70 lated, contributes a significant fraction of galectin-1 binding sites on T cells, as T cells lacking
76 studies showed that after klotho treatment, galectin-1 binds the TRPV5 N-glycan and thereby increase
79 in-1-induced cross-linking and T cell death, galectin-1 bound to CD43 fusion proteins modified with e
80 was blocked by intracellular Bcl-2, whereas galectin-1, but not galectin-9, T cell death was blocked
84 s, in the present study, we demonstrate that galectin-1 can enhance NiV attachment to and infection o
88 s of bivalent constructs with galectin-9 and galectin-1 carbohydrate recognition domains connected by
90 itated with galectin antisera, we found that galectin-1 containing spliceosomes did not contain galec
91 sensitivity of GluA4 AMPA receptors to human galectin-1 could be enhanced by supplementation of cultu
92 tion of cell apoptosis, we hypothesized that Galectin-1 could interact with CD146, leading to functio
94 on, with loss of core 2 O-glycan ligands for galectin-1 created by core 2 beta1,6-N-acetylglucosaminy
95 n patients with renal cell carcinoma and the galectin-1-CXCR4 axis may serve as a therapeutic target
96 hocytes in TLR5-responsive tumors to secrete galectin-1, dampening antitumor immunity and acceleratin
99 ced ERK signaling was sustained in activated galectin-1-deficient CD8 T cells and antagonized by reco
107 y, we underscore the biological relevance of galectin-1-enhanced DC migration by showing that intrade
108 ssue of Immunity, Starossom et al. show that Galectin-1 exerts a neuroprotective function through gly
111 umor evasion of immune attack; we found that galectin-1-expressing prostate cancer cells killed bound
113 increased cathepsin-V (CTSV) expression and galectin-1 expression and secretion in human glomerular
115 unoblots and PCR studies confirmed increased galectin-1 expression by hypoxia in several cancer cell
117 B cells lacking OCA-B expression, increased galectin-1 expression, secretion, and cell surface assoc
119 es (actin and myosin), ECM genes (Collagens, Galectin-1, Fibronectin, Heparan Sulfate, LOX, FAK1), ce
121 s had no surface galectin-3 but used surface galectin-1 for interaction with Gal-3BP to form large ol
123 t interactions between the regulatory lectin galectin-1 (Gal-1) and specific target N-glycans link tu
125 hort, which revealed that increased lymphoma galectin-1 (Gal-1) expression strongly correlated with r
131 By binding cell surface glycoconjugates, galectin-1 (gal-1) is involved in cell adhesion and migr
134 fabricated for the quantitative detection of Galectin-1 (Gal-1) protein, a biomarker for the onset of
136 fferent stages of the disease, we found that galectin-1 (Gal-1) was the most abundantly expressed gal
146 dy we evaluated the therapeutic potential of galectin-1 (gal-1), an endogenous lectin that in some au
153 dy, we identified a new fibrosis gene called galectin-1 (Gal-1), which is highly expressed in tubular
154 a binding partner for the endogenous lectin galectin-1 (Gal-1), which is known to ameliorate symptom
156 lopment, bone marrow stromal cells secreting galectin-1 (GAL1) constitute a specific niche for pre-BI
161 l lines (LCLs) and primary PTLDs overexpress galectin-1 (Gal1), a carbohydrate-binding lectin that in
167 the immunoregulatory glycan-binding protein, galectin-1 (Gal1), through an AP1-dependent enhancer.
168 ace glycome selectively regulated binding of galectin-1 (Gal1), which upon recognition of complex N-g
169 core 2 O-glycans (high affinity ligands for galectin-1), galectin-1 signaling in cells expressing a
170 osis similar to that of a known nonselective galectin-1/galectin-3 inhibitor, which strongly suggests
173 tor, TGF-beta, hepatocyte growth factor, and galectin-1 gene expression levels varied among donors.
174 1 susceptibility and synthesis of endogenous galectin-1 has been proposed to promote tumor evasion of
175 positively regulate T cell susceptibility to galectin-1, identifying a novel function for CD43 in con
178 mphatic endothelial cells, and deposition of galectin-1 in extracellular matrix selectively regulates
182 ion by showing that intradermal injection of galectin-1 in MRL-fas mice, which have a defect in skin
183 mergence of hormonal and redox regulation of galectin-1 in placental mammals may be implicated in mat
184 we show conserved placental localization of galectin-1 in primates and its predominant expression in
187 t CD8 T cells and antagonized by recombinant galectin-1, indicating galectin-1 modulates TCR feed-for
188 eficient cells displayed enhanced binding to galectin-1, indicating that changes in GNE activity can
190 ted, we propose that increased expression of galectin-1 induced by morphine may modulate HIV-1 infect
194 CD45, or if fodrin degradation is prevented, galectin-1-induced cell death is not accompanied by memb
195 other glycoprotein receptors is critical for galectin-1-induced cross-linking and T cell death, galec
196 Syk and protein kinase C signaling abrogated galectin-1-induced DC activation as monitored by interle
197 lthough roles for CD7 and CD45 in regulating galectin-1-induced death have been described, the requir
206 -immunoprecipitation experiments showed that Galectin-1 interacts with endogenous CD146 that is highl
207 ain of galectin-3 inhibited incorporation of galectin-1 into splicing complexes, explaining the domin
224 f core 1 O-glycans (low affinity ligands for galectin-1) is sufficient to overcome lack of core 2 O-g
225 between the two galectins, as galectin-9 and galectin-1 killed different subsets of murine thymocytes
226 susceptibility to the two galectins: whereas galectin-1 kills double-negative and double-positive hum
233 C migration through the ECM, suggesting that galectin-1 may be an important component in initiating a
236 onized by recombinant galectin-1, indicating galectin-1 modulates TCR feed-forward/feedback loops inv
237 In order to exhibit an enhancing effect, galectin-1 must be present during the initial phase of v
238 gonists of the effect of lung cancer-derived galectin-1 on DCs and anti-HB-EGF blocking antibodies co
242 umulation of the carbohydrate radiotracer in galectin-1-overexpressing UMUC3 orthotopic tumors when i
243 f virus attachment; in contrast, addition of galectin-1 postinfection results in reduced production o
246 dentify a complex set of mechanisms by which galectin-1 prolongs cell-surface retention of VEGF recep
249 ; however, we have found that galectin-9 and galectin-1 require different glycan ligands and glycopro
251 though MF cells are typically CD7-, and thus galectin-1 resistant, CD7+ HH cells, derived from a pati
252 minyltransferase, which is down-regulated in galectin-1-resistant PSA(-) LNCaP cells compared with ga
254 e first to indicate that lung cancer-derived galectin-1 secretion is responsible for stimulating tumo
256 d expression of glycosyltransferase genes in galectin-1-sensitive, prostate-specific antigen-positive
257 an ligands that are important for conferring galectin-1 sensitivity in these cells, and analyzed expr
259 nsferase 1 rendered LNCaP cells resistant to galectin-1, showing that specific O-glycans are critical
261 cans (high affinity ligands for galectin-1), galectin-1 signaling in cells expressing a high molecula
264 ells, and restoration of CXCR4 expression in galectin-1-silenced cells rescued cell motility and clon
265 lectin galectin-3; galectin-3 siRNA but not galectin-1 siRNA prevented MUC1-induced upregulation of
266 notechnology approach that uses gold nanorod-galectin-1 small interfering RNA complexes (nanoplexes)
268 ng galectin-1 increased and adding exogenous galectin-1 suppressed chemokine responses to Trichomonas
272 is the same glycosyltransferase required for galectin-1 susceptibility of T lymphoma cells, indicatin
274 e show that fodrin degradation occurs during galectin-1 T cell death and that CD45 is essential for f
277 lular death pathways, as galectin-9, but not galectin-1, T cell death was blocked by intracellular Bc
281 ial cells express the innate immune effector galectin-1 that we have previously shown can bind to spe
282 t the acquired immunoregulatory functions of galectin-1 then became highly conserved in eutherian lin
284 assays show that 0118 attenuates binding of galectin-1 to cell surface glycans, and the inhibition o
290 unohistochemical analysis substantiated that Galectin-1 upregulation is associated with osteoarthriti
295 of the tandem repeat galectin-9 and dimeric galectin-1, we created a series of bivalent constructs w
297 2 O-glycan expression and susceptibility to galectin-1, whereas mutant enzyme lacked activity and di
298 The proteomic analysis revealed upregulated galectin-1, which is an immunomodulatory protein linked
301 ns, and a reported inhibitory interaction of galectin-1 with CD45, the phosphatase activity of CD45 i