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1 ranulocyte subpopulations and calgranulin C (S100A12).
2 (SAA), and S100 calcium-binding protein A12 (S100A12).
3 cits and decreased expression and storage of S100A12.
4 ssed genes: FKBP5, S100P, SAMSN1, CLEC4E and S100A12.
5 ns that is recognized by S100A8, S100A9, and S100A12.
6 ed high and consequently unopposed levels of S100A12; a potent mucosa- and neutrophil-derived DAMP.
7         A global gene expression analysis of S100A12-activated monocytes revealed that human S100A12
8 r, our results delve into specific effect of S100A12 against Fusariumspp. with an aim to investigate
9 ic acid, HMGB1, S100A8, cell-free fetal DNA, S100A12 and HSP70.
10 ttributed to a release of interleukin-10 and S100A12 and increased PD-L1 expression.
11  assessed by bead-based multiplex assay, and S100A12 and MMP-7 by ELISA.
12   Plasma levels of MDSC mediators S100A8/A9, S100A12, and arginase 1 were significantly increased.
13         High glucose increased RAGE, S100A8, S100A12, and HMGB1 expression, which was normalized by o
14 kappaB p65 (RAGE promoter) and AP-1 (S100A8, S100A12, and HMGB1 promoters).
15 EARCH DESIGN AND Expression of RAGE, S100A8, S100A12, and HMGB1 was evaluated in human aortic endothe
16 kdown of activated protein-1 (AP-1) (S100A8, S100A12, and HMGB1), and chromatin immunoprecipitation (
17  calprotectin (CP) (S100A8/S100A9 oligomer), S100A12, and S100A7 play key roles in the innate immune
18  analyses; and serum S100A7, S100A8, S100A9, S100A12, and S100A8/A9 levels).
19 ity Mn(II) binding; the S100A7, S100A9(C3S), S100A12, and S100B homodimers do not exhibit such Mn(II)
20 gene expression include those of KYNU, OAS2, S100A12, and SERPINB3, whose strong transcriptional upre
21 on of human monocytes by granulocyte-derived S100A12 as a key function of early inflammatory processe
22 tes such as atherosclerosis, but the role of S100A12 as its ligand is less clear.
23 ructures of the metal-free apo form of human S100A12 at 1.77 A resolution and of the zinc complex in
24                    On the contrary, blocking S100A12 binding to its second proposed receptor (recepto
25                                     Blocking S100A12 binding to TLR4 on monocytes or TLR4 expressing
26 h initial levels of G-MDSCs, arginase 1, and S100A12 but not M-MDSCs were associated with subsequent
27 nt increased the expression and secretion of S100A12 by nearly 70%, which in turn activated dermal fi
28 e hypothesized that the zinc-binding protein S100A12 (calgranulin C) is induced in response to H. pyl
29 (calgranulin A), S100A9 (calgranulin B), and S100A12 (calgranulin C) proteins were also elevated in t
30 DEFB4B, DEFB103A, S100 proteins like S100A7, S100A12), chemotactic factors for neutrophils (e.g. CXCL
31                              Serum levels of S100A12 correlate with disease activity in juvenile idio
32  pathway (IL-17, IL-22, and downstream genes S100A12, DEFB-2, IL-1beta, SEPRINB3, LCN2, and CCL20).
33 e, we demonstrate that antimicrobial peptide S100A12 directly binds to the phospholipids of the funga
34             However, the exact role of human S100A12 during early steps of immune activation and seps
35 f both zinc and calcium in target binding by S100A12 during host-parasite responses is confirmed by e
36 aspase 3 and smooth muscle cell apoptosis in S100A12-expressing cells.
37               By establishing a link between S100A12 expression and apoptosis of aortic smooth muscle
38 human aortic aneurysmal disease, we examined S100A12 expression in aortic tissue from patients with t
39                                 Reduction of S100A12 expression in human aortic smooth muscle cells u
40 thoracic aortic aneurysm and found increased S100A12 expression in vascular smooth muscle cells.
41                                              S100A12 expression is sufficient to activate pathogenic
42 this study was to determine the relevance of S100A12 expression to human thoracic aortic aneurysms an
43 . pylori-positive and -negative patients for S100A12 expression.
44  immature phenotype of CB-LDG with decreased S100A12 expression.
45  zinc-calcium interplay in the transition of S100A12 from a dimer through a tetramer to a hexamer.
46                         The release of human S100A12 from granulocytes as well as the promotion of in
47                   Our findings indicate that S100A12 functions as a proinflammatory cytokine and sugg
48 oding antimicrobial peptides (AMPs) (S100A7, S100A12, human beta-defensin 2, and elafin), as well as
49 creased epidermal staining for AMPs (S100A7, S100A12, human beta-defensin 2, and elafin).
50 viously, we reported the structures of human S100A12 in both low (dimeric) and high (hexameric) calci
51             We found increased expression of S100A12 in the epidermis of human hypertrophic and keloi
52 protein A8, A9, and A12 [S100A8, S100A9, and S100A12]) in skin through 12 weeks.
53 f S100A12 receptors, RAGE, or TLR4 inhibited S100A12-induced fibroblast activation.
54 0A12-activated monocytes revealed that human S100A12 induces inflammatory gene expression.
55  a proinflammatory cytokine and suggest that S100A12 is a potential therapeutic target for dermal sca
56                                        Human S100A12 is an endogenous TLR4 ligand that induces monocy
57                                              S100A12 is enriched in human thoracic aortic aneurysms a
58                     These assays showed that S100A12 is induced in response to H. pylori infection an
59                                              S100A12 is overexpressed during inflammation and is a ma
60                               Calgranulin C (S100A12) is a member of the S100 family of proteins that
61 amyloid A, myeloid-related protein 8/14, and S100A12 levels compared with those seen outside attacks.
62                                Additionally, S100A12 levels correlated positively with gestational ag
63 g a few immune response genes such as NLRC5, S100A12, LILRA4 and FCGBP, as well as an assortment of n
64 100A12 signaling pathways and indicates that S100A12 may be a useful molecular marker and possible ta
65 ht) CD64(high) CD16(low) CD35(low) CD10(low) S100A12(med-low) and, based on these markers, recovered
66 eurysm dissection and to study mechanisms of S100A12-mediated dysfunction of aortic smooth muscle cel
67 loperoxidase, and caspase 3 was examined and S100A12-mediated pathways were studied in cultured prima
68 c smooth muscle cell cultures, we found that S100A12 mediates increased interleukin-6 production, act
69  However, salivary concentrations of S100A8, S100A12, MMP-8, and TCC were strongly associated with th
70            However, saliva levels of S100A8, S100A12, MMP-8, and TCC, and CFH polymorphisms were asso
71  measured salivary concentrations of S100A8, S100A12, MMP-8, and terminal complement complex (TCC) in
72 e genes affect the concentrations of S100A8, S100A12, MMP-8, or complement activation marker in saliv
73 L11/CCL17), and T(H)17/T(H)22 (IL-23p19/IL-8/S100A12) mRNA expression in lesional skin.
74 histochemistry of aortic tissue (n = 50) for S100A12, myeloperoxidase, and caspase 3 was examined and
75                                 Reduction of S100A12 or genetic ablation of its cell surface receptor
76 cant expression quantitative trait locus for S100A12 (P = 3.3 x 10(-7)).
77 trations of MMP-7, ICAM-1, IL-8, VCAM-1, and S100A12 predicted poor overall survival, poor transplant
78                                     We found S100A12 protein expressed in all cases of acute thoracic
79     Transgenic expression of proinflammatory S100A12 protein in murine aortic smooth muscle causes th
80 ablish that the zinc-binding activity of the S100A12 protein represses the activity of the cag T4SS,
81 reover, genetic ablation of the receptor for S100A12, receptor for advanced glycation end products (R
82                  Pharmacological blockade of S100A12 receptors, RAGE, or TLR4 inhibited S100A12-induc
83 scopy (FEG-SEM) was used to demonstrate that S100A12 represses biogenesis of the cag T4SS.
84                            Local delivery of S100A12 resulted in a marked hypertrophic scar formation
85                                              S100A12 rises during sepsis, and its expression and rele
86 nd validated TSPO (translocator protein) and S100A12 (S100 calcium-binding protein A12) as main molec
87 6, S100A7, S100A8, S100A9, S100A10, S100A11, S100A12, S100A15, S100B, and S100P) are expressed in nor
88               Genetic polymorphism in S100A9-S100A12-S100A8 locus affects serum and plasma MMP-8 and
89 ved in MDSC suppressive functions, including S100A12, S100A9, MMP8, and ARG1, were up-regulated in th
90 th muscle cells, this study identifies novel S100A12 signaling pathways and indicates that S100A12 ma
91 1q21.3, containing genes S100A8, S100A9, and S100A12 (strongest association: rs1560833; P=5.3x10(-15)
92 es from those of both calcium-loaded and apo-S100A12 structures, and comparisons suggest an explanati
93                                              S100A12 tissue expression was associated with increased
94                                  Circulating S100A12 was determined in patients with sepsis and in he
95             In CB serum of healthy neonates, S100A12 was found to be higher in female newborns when c
96 his fibroblast activation was not found when S100A12 was knocked down by RNA interference in keratino
97 ession of MMP-12, KRT16, S100A8, S100A9, and S100A12 was significantly decreased from baseline with a
98                          One such protein is S100A12, which is implicated in inflammation and host-pa
99 e effects are triggered by an interaction of S100A12 with Toll-like receptor 4 (TLR4).