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1 in the induction of unique genes, including calgranulin A (S100a8), an endogenous damage-associated
2 ulosis growth inhibition by IL-22 depends on calgranulin A and enhanced phagolysosomal fusion, which
6 atinocytes (beta-2 microglobulin, betaIG-H3, calgranulin A, cathepsin B and D, E-cadherin, gelatinase
10 S100A8/S100A9 heterodimer (calprotectin, or calgranulin A/B) binds zinc and represses the elaboratio
11 in calprotectin (CP, S100A8/S100A9 oligomer, calgranulin A/calgranulin B oligomer, MRP-8/MRP-14 oligo
12 7(phox), p40(phox), IL-8, CXCL1, Nramp1, and calgranulins A and B, were up-regulated constitutively i
14 cruitment of inflammatory cells bearing S100/calgranulins, also ligands for RAGE, augments vascular d
16 esis that expression of the alternative S100/calgranulin and patterning receptor CD36, identified her
17 E interacts with the endogenous ligands S100 calgranulins and high mobility group box 1 (HMGB1) to in
19 endproduct (RAGE) ligands, specifically S100/calgranulins and high-mobility group box 1, which sustai
24 diagnostic peak in amniotic fluid identified calgranulin B and a unique fragment of insulinlike growt
25 n (CP, S100A8/S100A9 oligomer, calgranulin A/calgranulin B oligomer, MRP-8/MRP-14 oligomer) chelates
26 vels of CRP, S100A8 (calgranulin A), S100A9 (calgranulin B), and S100A12 (calgranulin C) proteins wer
28 sequence of CO-Ag shows a high homology with calgranulin C (CaG-C) previously purified from pig granu
30 Recently, one of the calgranulins, human calgranulin C (CaGC), has been implicated as an importan
35 s two symmetric hydrophobic surfaces on Ca2+-calgranulin C that allow calgranulin C to bind to the C-
36 ic surfaces on Ca2+-calgranulin C that allow calgranulin C to bind to the C-type immunoglobulin domai
37 sized that the zinc-binding protein S100A12 (calgranulin C) is induced in response to H. pylori infec
38 lin A), S100A9 (calgranulin B), and S100A12 (calgranulin C) proteins were also elevated in the serum
40 anced glycation end products (AGEs) and S100/calgranulins, demonstrated increased deposition/expressi
41 vanced glycation endproducts (AGEs) and S100/calgranulins, displays enhanced expression in podocytes
42 gands, AGE and EN-RAGEs (members of the S100/calgranulin family of pro-inflammatory cytokines), displ
43 roducts (RAGE) and its ligands AGEs and S100/calgranulins have been implicated in a range of disorder
44 ), advanced oxidation protein products, S100/calgranulins, high-mobility group box-1, amyloid-beta pe
46 dvanced glycation endproducts (AGE) and S100/calgranulins in diabetic tissues, upregulation and activ
47 AGE and immunoreactivities of RAGE and S100/calgranulins in response to balloon injury in diabetic c
48 steoarthritis (OA) cartilage, including S100/calgranulin ligands of receptor for advanced glycation e
49 s raised to either RAGE or its ligands, S100/calgranulins or amphoterin, reduced functional recovery
52 s associated with an increased expression of calgranulins, possibly through an induction of Toll-like
53 RNAs mediating lung inflammation including calgranulin-S100 family members, IL-1beta and IL-4, were
55 GEs, amyloid-beta peptide (Abeta), and S100B/calgranulins, some of which are known components of drus
57 0a9 genes encode a pro-inflammatory protein (calgranulin) that has been implicated in multiple diseas
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