ライフサイエンスコーパス: receptor for AGE

1 relates with the expression of its receptor, receptor for AGE.

2 nt of mesangial cells with AGEs and with the receptor for AGEs agonist S100 triggers activation of th

3 n end products), increased expression of the receptor for AGEs and its activating ligands, activation

4 re is evidence that AGEs, acting through the receptor for AGEs, contribute to diabetic complications.

5 AGE (Advanced Glycation Endproducts)-RAGE (Receptor for AGEs) interactions and oxidative-stress-med

6 by advanced glycation end products (AGE) and receptor for AGE (RAGE) and mediates AGE/RAGE-induced re

7 Receptor for AGE (RAGE) and the polypeptide amphoterin a

8 vanced glycation end products (AGEs) and the receptor for AGE (RAGE) are implicated in the vascular c

9 The AGE-induced receptor for AGE (RAGE) expression is required for the p

10 f advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancr

11 t (AGE) activation of the signal-transducing receptor for AGE (RAGE) has been linked to a proinflamma

12 citating ROS-generating NADPH oxidase or the receptor for AGE (RAGE) has beneficial effects.

13 vanced glycation end products (AGEs) and the receptor for AGE (RAGE) in development of this repair de

14 We report here that receptor for AGE (RAGE) is a central cell surface recept

15 ified proteins, upregulate expression of the receptor for AGE (RAGE), and consequently bias the immun

16 (AGEs), with the signal-transducing receptor receptor for AGE (RAGE), by administration of the solubl

17 f mesangial cell (MC) receptors, such as the receptor for AGE (RAGE), which promote oxidant-stress-de

18 In the present study receptor for AGE (RAGE)-mediated cellular activation was

19 all, and are signal transduction ligands for Receptor for AGE (RAGE).

20 tors, the best characterized of which is the receptor for AGE (RAGE).

21 tors, the best characterized of which is the receptor for AGE (RAGE).

22 , histology, and immunohistochemistry of the receptor for AGE (RAGE).

23 is is also placed the modulatory role of the receptor for AGEs (RAGE) and how its activation could ev

24 iated by the intricate interplay between the receptor for AGEs (RAGE) and toll-like receptor-4 (TLR4)

25 The receptor for AGEs (RAGE) is such a receptor and is a new

26 tress-advanced glycation end products (AGEs) receptor for AGEs (RAGE) pathway, and (3) enalapril (whi

27 We report here that AGEs signal through the receptor for AGEs (RAGE) to induce TEMT, as determined b

28 cts (AGEs), an increase in expression of the receptor for AGEs (RAGE), and activation of ERK1/2 MAP k

29 of diabetic nephropathy that act through the receptor for AGEs (RAGE), as well as other mechanisms, t

30 oduct (AGE) deposition and expression of the receptor for AGEs (RAGE), tartrate-resistant acid phosph

31 AGEs bind to the receptor for AGEs (RAGE), which triggers pro-inflammator

32 nd inflammation through interaction with the receptor for AGEs (RAGE).

33 ssments of inflammatory cells, expression of receptors for AGEs (RAGE), tartrate-resistant acid phosp

34 When stimulated by AGEs, the receptors for AGEs (RAGEs) induce inflammation and are t

35 , apoptosis was shown to be mediated through receptor for AGE signaling.

36 incubation of AGE-treated cells with soluble receptor for AGE (sRAGE).

37 (RvD(1), RvE(1), lipoxin A(4)), and soluble receptor for AGE (sRAGE).

38 E carboxymethyl-lysine (CML) and the soluble receptor for AGEs (sRAGE) in 2439 participants from the

39 tem cells (hBD-MSCs) with or without soluble receptor for AGEs (sRAGE).

40 Receptor for AGE was demonstrated to selectively interac

41 8-isoprostane, leptin, circulating AGEs and receptor for AGEs were reduced after consumption of low

42 ddition, CML and CEL are ligands for RAGE, a receptor for AGEs, which has been implicated in several