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1 evealing CLEC-2 as a physiological target of fucoidan.
2 ted polysaccharide showed characteristics of fucoidan.
3 luding f-Alb, maleylated bovine albumin, and fucoidan.
4 tes is inhibited in the presence of EDTA and fucoidan.
5 the presence of EDTA and the polysaccharide fucoidan.
6 oidan (Fysk) and those of previously studied fucoidans.
7 In particular, administration of 2 doses of fucoidan (25 mg/kg) over 6 hours produces profound mobil
8 gregation and Syk phosphorylation induced by fucoidan, a CLEC-2 agonist, were unaffected in RhoG-defi
15 itive reconstitution experiments reveal that fucoidan also elicits long-term (more than 6 months) rep
20 f soluble glycoconjugates, of which heparin, fucoidan, and dextran sulfate were the most effective.
21 h as different glycosaminoglycans, alginate, fucoidan, and glycans were profiled by this comprehensiv
22 ulfate 500K, dextran sulfate 5K, sulfatides, fucoidan, and heparin but not by chondroitin sulfate A.
23 sigargin and the scavenger receptor A ligand fucoidan, and restoring iPLA(2)betaexpression with recom
24 fated polysaccharides from brown algae - the fucoidans - are known to be a topic of numerous studies,
26 ger receptor inhibitors, dextran sulfate and fucoidan, attenuated monocyte migration toward stressed
28 RNA for macrophage scavenger receptor A, and fucoidan blocking of macrophage scavenger receptors inhi
29 sulfated polysaccharides dextran sulfate and fucoidan, but not others, reduce endothelial cell-surfac
35 In addition, it binds the polysaccharide fucoidan, consistent with its C-type lectin homology and
38 vidence for further exploring the use of the fucoidans from S. cichorioides, F. evanescens, and U. pi
39 ifferent than those of commercial food grade fucoidan (Fysk) and those of previously studied fucoidan
43 apidly and dramatically after treatment with fucoidan in monkeys and in mice, coinciding with decreas
45 c release, and we find that thapsigargin and fucoidan induce mitochondrial phospholipid loss and cyto
51 ffect on platelets and the receptor by which fucoidan induces cellular processes has not been elucida
53 Sulfated polysaccharides (e.g. heparin and fucoidan) inhibited binding of soluble DC-HIL-Fc and adh
57 e, evidence is provided that the addition of fucoidan or dextran sulfate to unfractionated plasma res
58 t treatment with the sulfated polysaccharide fucoidan or the structurally similar dextran sulfate inc
60 l inhibitors of class A scavenger receptors (fucoidan, polyinosinic acid, and dextran sulfate) reveal
62 the antioxidant butylated hydroxytoluene nor fucoidan, suggesting that lipid accumulation did not inv
63 haM-/- HPCs were preferentially mobilized by fucoidan, suggesting that the enhanced mobilization is c
64 trations of a highly charged polysaccharide, fucoidan, the microscale ordering of Fmoc-FRGDF peptide
65 enon we found that BM myeloid cells bound to fucoidan through the integrin alphaMbeta2 (macrophage an
66 and the binding was inhibited by heparin and fucoidan, thus supporting the hypothesis that P97 was ac
67 erpretation of results from studies that use fucoidan to "block" either scavenger receptors or L- or
69 ng of acetylated low density lipoprotein and fucoidan to MSR-A in human THP-1 macrophages triggered t
70 kin-8, MCP1, or MMP9 were also present after fucoidan treatment, studies in gene-ablated mice (GCSFR(
74 in FcRgamma-chain null mice, indicating that fucoidan was not acting primarily through GPVI receptor.
78 utination activity (i.e. dextran sulfate and fucoidan) whereas high concentrations inhibited parasite
79 reated with anti-P-selectin antibody or with fucoidan (which inhibits P- and L-selectin function).
81 that Fsar has fundamental characteristics of fucoidan with different structural conformation i.e. var
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