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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
3 ted MDMs, and these effects were reversed by calgranulin A siRNA.
4                                              Calgranulin A small interfering RNA (siRNA) abrogated rI
5        Significantly, levels of CRP, S100A8 (calgranulin A), S100A9 (calgranulin B), and S100A12 (cal
6 atinocytes (beta-2 microglobulin, betaIG-H3, calgranulin A, cathepsin B and D, E-cadherin, gelatinase
7 of other pro-atherosclerotic mediators, like Calgranulin A, Cathepsin S, and Osteopontin.
8 A, and SN), statherin, albumin, amylase, and calgranulin A.
9 sion of an intracellular signaling molecule, calgranulin A.
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
13                    RAGE ligands include S100/calgranulins, a class of low-molecular-mass, calcium-bin
14 cruitment of inflammatory cells bearing S100/calgranulins, also ligands for RAGE, augments vascular d
15 e in transcription of a single gene encoding calgranulin AMrp-8.
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
18 tion receptor triggered by inflammatory S100/calgranulins and high mobility group box-1 ligands.
19 endproduct (RAGE) ligands, specifically S100/calgranulins and high-mobility group box 1, which sustai
20                                          The calgranulins are a family of calcium- and zinc-binding p
21                                              Calgranulins are released during inflammatory responses
22           Its pro-inflammatory ligands, S100-calgranulins, are upregulated in MS and in the related r
23 acterial peptides calprotectin (P =.021) and calgranulin B (P <.0001).
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
27 tins, lysozyme, statherin, cytokeratins, and calgranulin B.
28 sequence of CO-Ag shows a high homology with calgranulin C (CaG-C) previously purified from pig granu
29                                              Calgranulin C (CaGC) is a protein released by activated
30     Recently, one of the calgranulins, human calgranulin C (CaGC), has been implicated as an importan
31                                              Calgranulin C (S100A12) is a member of the S100 family o
32                                          Apo-calgranulin C also binds to sRAGE using a completely dif
33                                     The RAGE-calgranulin C interaction mediates a pro-inflammatory re
34 on NMR spectroscopy, we identified the sRAGE-calgranulin C interaction surface.
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
39 orms tetramers that bind to hexamers of Ca2+-calgranulin C.
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
45                         Recently, one of the calgranulins, human calgranulin C (CaGC), has been impli
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
50                                    AGE, S100/calgranulin, or H(2)O(2) promoted MAPK phosphorylation i
51                                         S100/calgranulin polypeptides are present at sites of inflamm
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
54                                         S100/calgranulins share conserved calcium-binding EF-hand dom
55 GEs, amyloid-beta peptide (Abeta), and S100B/calgranulins, some of which are known components of drus
56 ing protein) and related members of the S100/calgranulin superfamily.
57 0a9 genes encode a pro-inflammatory protein (calgranulin) that has been implicated in multiple diseas

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