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1 und to the glycosaminoglycan (GAG) chains of serglycin.
2 fects of proteases that are complex-bound to serglycin.
3 ked to the chondroitin-sulfate proteoglycan, serglycin.
4 d with the chondroitin-sulfate proteoglycan, serglycin.
5 nogen activator was distributed similarly to serglycin.
9 in granules along with other mediators using serglycin and its carried glycosaminoglycan side chains.
11 lacking mouse mast cell protease 6, a major serglycin-associated protease, exhibited similar defects
12 e mast cells underwent apoptotic cell death, serglycin(-/-) cells died predominantly by necrosis.
13 similar defects in apoptosis as observed in serglycin(-/-) cells, indicating that the pro-apoptotic
14 Targets exposed to double-labeled granzyme B-serglycin complexes show solely the uptake of granzyme B
15 molecular interaction of secreted granzyme B-serglycin complexes with target cells remains undefined.
20 the first intron may be related to the high serglycin expression in HL60 relative to HEL or CHRF cel
25 e DNase I-hypersensitive sites (DHSS) of the serglycin gene in resting and phorbol 12-myristate 13-ac
27 ry identified (i) the 25-kDa core protein as serglycin, (ii) the 90-kDa core protein as inter-alpha-i
28 vide direct evidence for a critical role for serglycin in MM pathogenesis and show that targeting ser
30 n together, this study introduces a role for serglycin in the regulation of obesity-induced adipose i
31 learn whether the physiologic effector, GrB-serglycin, initiates apoptosis primarily through caspase
34 ndicating that the pro-apoptotic function of serglycin is due to downstream effects of proteases that
35 smembrane domain, flow cytometry showed that serglycin is present on the MM cell surface, and attachm
38 LP2 and IalphaIHC2 with macrophages, whereas serglycin localizes to the underlying glycosaminoglycan-
39 ve high homology with the orthologous murine serglycin locus and are rich in potential transcription
40 e cytosol and that the necrotic phenotype of serglycin(-/-) mast cells was linked to defective degrad
44 n in MM pathogenesis and show that targeting serglycin may provide a novel therapeutic approach for M
46 how the interaction of granzyme B (GrB) with serglycin might influence the apoptotic potential of thi
51 tain regulatory sequences derived from human serglycin, preproapolipoprotein C II, and Egr1 genes.
53 om participating in extracellular processes, serglycin proteoglycan and one of its associated proteas
54 including a single consensus sequence of the serglycin proteoglycan core protein bound heparin strong
59 low mMCP-9 to form multimeric complexes with serglycin proteoglycans and other negatively charged pro
60 Cs) can reversibly alter their expression of serglycin proteoglycans and the homologous granule chyma
61 diators such as bioactive amines, cytokines, serglycin proteoglycans with negatively charged glycosam
62 anule mediators (e.g., neutral proteases and serglycin proteoglycans) and proinflammatory cytokines (
65 s multimeric complexes with the proteoglycan serglycin (SG) in cytotoxic granules, and cytotoxic cell
68 A granule-associated proteoglycan, namely serglycin, that contains chondroitin 4-sulfate (CS) glyc
70 monstrates the exchange of the granzyme from serglycin to immobilized, sulfated glycosaminoglycans.
72 teolysis through a secretory granule-derived serglycin-tryptase axis as a novel principle for histone
73 reover, it was shown that the absence of the serglycin-tryptase axis resulted in altered chromatin co
75 A core protein of the appropriate size for serglycin was detected by analysis of the chondroitinase
76 CD44 is the cell surface-binding partner for serglycin, which therefore may serve as a major ligand f