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1 (IEs) that surface-express VAR2CSA and bind chondroitin sulfate A.
2 basic peptides (FS2 and NFS3) to heparin and chondroitin sulfate A.
3 the actions of these two exolytic lyases on chondroitin sulfate A.
4 gh a process that does not involve PfEMP1 or chondroitin sulfate A.
5 parin > dermatan sulfate > heparan sulfate > chondroitin sulfate A.
6 sulfatides, fucoidan, and heparin but not by chondroitin sulfate A.
7 related to HS, but not by other GAGs such as chondroitin sulfate A and C, N-acetyl heparin and de-N-s
9 turated, and saturated oligosaccharides from chondroitin sulfate A and chondroitin sulfate C, separat
10 arin, heparan sulfate, and dermatan sulfate; chondroitin sulfate A and hyaluronic acid were intermedi
13 alciparum adhesion to the placental receptor chondroitin sulfate A are associated with a reduced risk
14 f GAGs such as hyaluronic acid, heparin, and chondroitin sulfates A, B, and C induce arthritis, tendo
15 e-3-phosphate dehydrogenase aggregation, but chondroitin sulfates A, B, and C together with dextran s
16 inoglycans such as heparin, heparan sulfate, chondroitin sulfates A, B, and C, and sulfated compounds
17 ly folded PEDF bound to immobilized heparin, chondroitin sulfate-A, -B, -C, and dextran sulfate colum
19 gh molecular weight (MW) dextran sulfate and chondroitin sulfate A, but not other anionic polysacchar
20 egulated when parasites are selected to bind chondroitin sulfate A, but other PfEMP1 forms may be upr
21 chondroitin better than dermatan sulfate and chondroitin sulfates A, C, D, and E, but it does not bin
22 lycan or with addition of heparan sulfate or chondroitin sulfate A/C but did stimulate BaF/KGFR divis
23 be our results of HC transfer experiments to chondroitin sulfate A, chemically desulfated chondroitin
26 tran sulfate (LDS) and the glycosaminoglycan chondroitin sulfate A (CSA) also had significant inhibit
27 tan sulfate (KS), dermatan sulfate (DS), and chondroitin sulfate A (CSA) and C (CSC), polymerized in
28 EMP1 variant that binds to the host receptor chondroitin sulfate A (CSA) and is implicated in malaria
29 erythrocytes (IEs) that selectively bind to chondroitin sulfate A (CSA) and sequester in placental t
30 ocytes that adhere to the placental receptor chondroitin sulfate A (CSA) and sequester in the placent
31 ciparum-infected erythrocytes, and placental chondroitin sulfate A (CSA) are primarily responsible fo
33 hesion of parasites to the glycosaminoglycan chondroitin sulfate A (CSA) present on syncytiotrophobla
34 ncipal ligand associated with the binding to chondroitin sulfate A (CSA) that allows placental seques
35 alciparum-infected erythrocytes to placental chondroitin sulfate A (CSA) through the PfEMP1-VAR2CSA p
36 m falciparum-infected erythrocytes adhere to chondroitin sulfate A (CSA) to sequester in the human pl
37 the surface of iRBC selected for adhesion to chondroitin sulfate A (CSA), a placental receptor for pa
38 glycans (GAGs) include keratan sulfate (KS), chondroitin sulfate A (CSA), and hyaluronic acid (HA).
39 igenically distinct and bind receptors, like chondroitin sulfate A (CSA), that are not commonly bound
40 hesion of VAR2CSA-expressing erythrocytes to chondroitin sulfate A (CSA)-a major criterion for evalua
41 serum cross-reacted with surface proteins of chondroitin sulfate A (CSA)-binding laboratory strains (
42 chia pastoris and developed a panel of seven chondroitin sulfate A (CSA)-binding parasites from diver
43 um-infected erythrocytes (PE) to immobilized chondroitin sulfate A (CSA)-conjugated albumin at a conc
50 ed multivariate analysis, including heparin, chondroitin sulfate A, dermatan sulfate, and the infamou
51 d, partially sulfated, or fully oversulfated chondroitin sulfate A, dermatan sulfate, or heparan sulf
52 variant surface antigen that binds placental chondroitin sulfate A, have been suggested to mediate pr
53 escribes the separation of dermatan sulfate, chondroitin sulfate A, heparin, and the semisynthetic fu
54 the variant surface antigen PfEMP1 that bind chondroitin sulfate A in vitro (PfEMP1(varCSA)) are high
56 of Hic to hTSP-1 is inhibited by heparin and chondroitin sulfate A, indicating binding to the N-termi
57 nfected erythrocytes and mediates binding to chondroitin sulfate A, initiating inflammation and disru
58 e antigen VAR2CSA (variant surface antigen 2-chondroitin sulfate A) is expressed on infected erythroc
60 thereby promoting amyloid formation, whereas chondroitin sulfate A kinetically traps partially unfold
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