ライフサイエンスコーパス: S100A12

1 (SAA), and S100 calcium-binding protein A12 (S100A12).

2 ns that is recognized by S100A8, S100A9, and S100A12.

3 ed high and consequently unopposed levels of S100A12; a potent mucosa- and neutrophil-derived DAMP.

4 A global gene expression analysis of S100A12-activated monocytes revealed that human S100A12

5 ttributed to a release of interleukin-10 and S100A12 and increased PD-L1 expression.

6 assessed by bead-based multiplex assay, and S100A12 and MMP-7 by ELISA.

7 Plasma levels of MDSC mediators S100A8/A9, S100A12, and arginase 1 were significantly increased.

8 High glucose increased RAGE, S100A8, S100A12, and HMGB1 expression, which was normalized by o

9 kappaB p65 (RAGE promoter) and AP-1 (S100A8, S100A12, and HMGB1 promoters).

10 EARCH DESIGN AND Expression of RAGE, S100A8, S100A12, and HMGB1 was evaluated in human aortic endothe

11 kdown of activated protein-1 (AP-1) (S100A8, S100A12, and HMGB1), and chromatin immunoprecipitation (

12 ity Mn(II) binding; the S100A7, S100A9(C3S), S100A12, and S100B homodimers do not exhibit such Mn(II)

13 gene expression include those of KYNU, OAS2, S100A12, and SERPINB3, whose strong transcriptional upre

14 on of human monocytes by granulocyte-derived S100A12 as a key function of early inflammatory processe

15 tes such as atherosclerosis, but the role of S100A12 as its ligand is less clear.

16 ructures of the metal-free apo form of human S100A12 at 1.77 A resolution and of the zinc complex in

17 On the contrary, blocking S100A12 binding to its second proposed receptor (recepto

18 Blocking S100A12 binding to TLR4 on monocytes or TLR4 expressing

19 h initial levels of G-MDSCs, arginase 1, and S100A12 but not M-MDSCs were associated with subsequent

20 nt increased the expression and secretion of S100A12 by nearly 70%, which in turn activated dermal fi

21 e hypothesized that the zinc-binding protein S100A12 (calgranulin C) is induced in response to H. pyl

22 (calgranulin A), S100A9 (calgranulin B), and S100A12 (calgranulin C) proteins were also elevated in t

23 Serum levels of S100A12 correlate with disease activity in juvenile idio

24 pathway (IL-17, IL-22, and downstream genes S100A12, DEFB-2, IL-1beta, SEPRINB3, LCN2, and CCL20).

25 However, the exact role of human S100A12 during early steps of immune activation and seps

26 f both zinc and calcium in target binding by S100A12 during host-parasite responses is confirmed by e

27 aspase 3 and smooth muscle cell apoptosis in S100A12-expressing cells.

28 By establishing a link between S100A12 expression and apoptosis of aortic smooth muscle

29 human aortic aneurysmal disease, we examined S100A12 expression in aortic tissue from patients with t

30 Reduction of S100A12 expression in human aortic smooth muscle cells u

31 thoracic aortic aneurysm and found increased S100A12 expression in vascular smooth muscle cells.

32 S100A12 expression is sufficient to activate pathogenic

33 this study was to determine the relevance of S100A12 expression to human thoracic aortic aneurysms an

34 . pylori-positive and -negative patients for S100A12 expression.

35 zinc-calcium interplay in the transition of S100A12 from a dimer through a tetramer to a hexamer.

36 The release of human S100A12 from granulocytes as well as the promotion of in

37 Our findings indicate that S100A12 functions as a proinflammatory cytokine and sugg

38 oding antimicrobial peptides (AMPs) (S100A7, S100A12, human beta-defensin 2, and elafin), as well as

39 creased epidermal staining for AMPs (S100A7, S100A12, human beta-defensin 2, and elafin).

40 viously, we reported the structures of human S100A12 in both low (dimeric) and high (hexameric) calci

41 We found increased expression of S100A12 in the epidermis of human hypertrophic and keloi

42 f S100A12 receptors, RAGE, or TLR4 inhibited S100A12-induced fibroblast activation.

43 0A12-activated monocytes revealed that human S100A12 induces inflammatory gene expression.

44 a proinflammatory cytokine and suggest that S100A12 is a potential therapeutic target for dermal sca

45 Human S100A12 is an endogenous TLR4 ligand that induces monocy

46 S100A12 is enriched in human thoracic aortic aneurysms a

47 These assays showed that S100A12 is induced in response to H. pylori infection an

48 S100A12 is overexpressed during inflammation and is a ma

49 Calgranulin C (S100A12) is a member of the S100 family of proteins that

50 amyloid A, myeloid-related protein 8/14, and S100A12 levels compared with those seen outside attacks.

51 g a few immune response genes such as NLRC5, S100A12, LILRA4 and FCGBP, as well as an assortment of n

52 100A12 signaling pathways and indicates that S100A12 may be a useful molecular marker and possible ta

53 eurysm dissection and to study mechanisms of S100A12-mediated dysfunction of aortic smooth muscle cel

54 loperoxidase, and caspase 3 was examined and S100A12-mediated pathways were studied in cultured prima

55 c smooth muscle cell cultures, we found that S100A12 mediates increased interleukin-6 production, act

56 histochemistry of aortic tissue (n = 50) for S100A12, myeloperoxidase, and caspase 3 was examined and

57 Reduction of S100A12 or genetic ablation of its cell surface receptor

58 trations of MMP-7, ICAM-1, IL-8, VCAM-1, and S100A12 predicted poor overall survival, poor transplant

59 We found S100A12 protein expressed in all cases of acute thoracic

60 Transgenic expression of proinflammatory S100A12 protein in murine aortic smooth muscle causes th

61 ablish that the zinc-binding activity of the S100A12 protein represses the activity of the cag T4SS,

62 reover, genetic ablation of the receptor for S100A12, receptor for advanced glycation end products (R

63 Pharmacological blockade of S100A12 receptors, RAGE, or TLR4 inhibited S100A12-induc

64 scopy (FEG-SEM) was used to demonstrate that S100A12 represses biogenesis of the cag T4SS.

65 Local delivery of S100A12 resulted in a marked hypertrophic scar formation

66 S100A12 rises during sepsis, and its expression and rele

67 6, S100A7, S100A8, S100A9, S100A10, S100A11, S100A12, S100A15, S100B, and S100P) are expressed in nor

68 Genetic polymorphism in S100A9-S100A12-S100A8 locus affects serum and plasma MMP-8 and

69 ved in MDSC suppressive functions, including S100A12, S100A9, MMP8, and ARG1, were up-regulated in th

70 th muscle cells, this study identifies novel S100A12 signaling pathways and indicates that S100A12 ma

71 1q21.3, containing genes S100A8, S100A9, and S100A12 (strongest association: rs1560833; P=5.3x10(-15)

72 es from those of both calcium-loaded and apo-S100A12 structures, and comparisons suggest an explanati

73 S100A12 tissue expression was associated with increased

74 Circulating S100A12 was determined in patients with sepsis and in he

75 his fibroblast activation was not found when S100A12 was knocked down by RNA interference in keratino

76 One such protein is S100A12, which is implicated in inflammation and host-pa

77 e effects are triggered by an interaction of S100A12 with Toll-like receptor 4 (TLR4).