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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                                              Receptor for AGE (RAGE) and the polypeptide amphoterin a
7 vanced glycation end products (AGEs) and the receptor for AGE (RAGE) are implicated in the vascular c
8                              The AGE-induced receptor for AGE (RAGE) expression is required for the p
9 f advanced glycation end products (AGEs) and receptor for AGE (RAGE) expression were present in pancr
10 t (AGE) activation of the signal-transducing receptor for AGE (RAGE) has been linked to a proinflamma
11 citating ROS-generating NADPH oxidase or the receptor for AGE (RAGE) has beneficial effects.
12 vanced glycation end products (AGEs) and the receptor for AGE (RAGE) in development of this repair de
13                          We report here that receptor for AGE (RAGE) is a central cell surface recept
14 ified proteins, upregulate expression of the receptor for AGE (RAGE), and consequently bias the immun
15 (AGEs), with the signal-transducing receptor receptor for AGE (RAGE), by administration of the solubl
16 f mesangial cell (MC) receptors, such as the receptor for AGE (RAGE), which promote oxidant-stress-de
17                         In the present study receptor for AGE (RAGE)-mediated cellular activation was
18 all, and are signal transduction ligands for Receptor for AGE (RAGE).
19 tors, the best characterized of which is the receptor for AGE (RAGE).
20 tors, the best characterized of which is the receptor for AGE (RAGE).
21 , histology, and immunohistochemistry of the receptor for AGE (RAGE).
22 is is also placed the modulatory role of the receptor for AGEs (RAGE) and how its activation could ev
23                                          The receptor for AGEs (RAGE) is such a receptor and is a new
24 tress-advanced glycation end products (AGEs) receptor for AGEs (RAGE) pathway, and (3) enalapril (whi
25  We report here that AGEs signal through the receptor for AGEs (RAGE) to induce TEMT, as determined b
26 cts (AGEs), an increase in expression of the receptor for AGEs (RAGE), and activation of ERK1/2 MAP k
27 of diabetic nephropathy that act through the receptor for AGEs (RAGE), as well as other mechanisms, t
28 oduct (AGE) deposition and expression of the receptor for AGEs (RAGE), tartrate-resistant acid phosph
29 nd inflammation through interaction with the receptor for AGEs (RAGE).
30 ssments of inflammatory cells, expression of receptors for AGEs (RAGE), tartrate-resistant acid phosp
31                 When stimulated by AGEs, the receptors for AGEs (RAGEs) induce inflammation and are t
32 , apoptosis was shown to be mediated through receptor for AGE signaling.
33 incubation of AGE-treated cells with soluble receptor for AGE (sRAGE).
34 tem cells (hBD-MSCs) with or without soluble receptor for AGEs (sRAGE).
35                                              Receptor for AGE was demonstrated to selectively interac
36  8-isoprostane, leptin, circulating AGEs and receptor for AGEs were reduced after consumption of low

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