ライフサイエンスコーパス: advanced glycation endproduct

1 s in the accumulation of irreversibly formed advanced glycation endproducts.

2 Advanced glycation endproduct (AGE) formation is a trigg

3 l (MG), that are known to modify proteins by advanced glycation endproduct (AGE) formation.

4 or PBS subcutaneously for 8 weeks to induce advanced glycation endproduct (AGE) formation.

5 Advanced glycation endproduct (AGE) levels are elevated

6 levels are associated with the generation of advanced glycation endproduct (AGE) modifications.

7 ysis and lipid peroxidation, and they act as advanced glycation endproduct (AGE) precursors.

8 lation and expression of key ligands such as advanced glycation endproducts (AGE) and S100/calgranuli

9 Advanced glycation endproducts (AGE) contribute to kidne

10 Treatment of brain microvascular ECs with advanced glycation endproducts (AGE), a metabolite commo

11 ent in mice induces accelerated aging due to advanced glycation endproduct (AGEs) formation.

12 Advanced glycation endproducts (AGEs) accumulate in pati

13 RAGE, a receptor for advanced glycation endproducts (AGEs) and S100/calgranul

14 Advanced glycation endproducts (AGEs) are believed to pl

15 Advanced glycation endproducts (AGEs) are derivatives of

16 Advanced glycation endproducts (AGEs) have been linked t

17 (UPLC-MS/MS) method for the determination of advanced glycation endproducts (AGEs) in food items and

18 he fragmentation of triose phosphates, forms advanced glycation endproducts (AGEs) in vitro.

19 a heterogeneous group of compounds known as advanced glycation endproducts (AGEs) or Maillard reacti

20 volves formation of early (Amadori) and late advanced glycation endproducts (AGEs) together with free

21 study demonstrates that reducing sugars form advanced glycation endproducts (AGEs) with GlcN and, as

22 Advanced glycation endproducts (AGEs), a pathogenic fact

23 emodynamic changes, accelerated formation of advanced glycation endproducts (AGEs), oxidative stress,

24 c sera contain excessive amounts of reactive advanced glycation endproducts (AGEs), which accelerate

25 The inactivation of NO by advanced glycation endproducts (AGEs), which accumulate

26 rocessed nutrients, replete with pro-OS/Infl advanced glycation endproducts (AGEs), which enhance app

27 rystallin, and link them together, producing advanced glycation endproducts (AGEs).

28 king of ketoamine leads to the production of advanced glycation endproducts (AGEs).

29 se findings indicate interaction between the advanced glycation endproducts and their receptor is inv

30 reduced expression of both the receptor for advanced glycation endproducts and tumour necrosis facto

31 n endproduct signaling through receptors for advanced glycation endproducts are implicated in diabeti

32 tide (beta=-0.250; P<0.001) and receptor for advanced glycation endproducts (beta=-0.095; P<0.007) we

33 The cytoplasmic domain of the receptor for advanced glycation endproducts binds to the formin homol

34 ble extracellular domain of the receptor for advanced glycation endproducts completely suppressed dia

35 s suggest that protein crosslinks, including advanced glycation endproduct-derived crosslinks which w

36 These advanced glycation endproducts engage their receptor in

37 id modification results in the generation of advanced glycation endproduct epitopes and subsequent in

38 ocytes or blockade of the HMGB1 receptor for advanced glycation endproducts in EPCs prevents this eff

39 of mDia1; mDia1 is required for receptor for advanced glycation endproducts ligand-induced cellular m

40 le cells, mDia1 is required for receptor for advanced glycation endproducts ligand-induced membrane t

41 triggered, at least in part, by receptor for advanced glycation endproducts ligands, thereby regulati

42 versibly bound, crosslinking moieties called advanced glycation endproducts, or AGEs.

43 hese inflammatory cells release receptor for advanced glycation endproduct (RAGE) ligands, specifical

44 eta peptide (Abeta) to neuronal Receptor for Advanced Glycation Endproduct (RAGE), a cell surface rec

45 The receptor for advanced glycation endproducts (RAGE) and myeloid differ

46 Here, we show that the receptor for advanced glycation endproducts (RAGE) and one of its pri

47 infection and mutations in the receptor for advanced glycation endproducts (RAGE) are risk factors f

48 The receptor for advanced glycation endproducts (RAGE) binds diverse liga

49 Activation of the receptor for advanced glycation endproducts (RAGE) by its multiple li

50 Receptor for advanced glycation endproducts (RAGE) is a multi-ligand

51 The receptor for advanced glycation endproducts (RAGE) is a multiligand r

52 The receptor for advanced glycation endproducts (RAGE) is a scavenger rec

53 Receptor for advanced glycation endproducts (RAGE) is an Ig superfami

54 The receptor for advanced glycation endproducts (RAGE) is an ubiquitous,

55 Here we show that the receptor for advanced glycation endproducts (RAGE) is required for th

56 Receptor for advanced glycation endproducts (RAGE) is up-regulated in

57 e advanced glycation endproduct/receptor for advanced glycation endproducts (RAGE) pathway and showed

58 In this study, we examined the receptor for advanced glycation endproducts (RAGE), a multi-ligand re

59 Receptor for Advanced Glycation Endproducts (RAGE), a multiligand rec

60 We also characterized the receptor for advanced glycation endproducts (RAGE), whose homooligome

61 oll-like receptor 4 (TLR4)- and receptor for advanced glycation endproducts (RAGE)-signaling pathways

62 AGE (Advanced Glycation Endproducts)-RAGE (Receptor for AGEs)

63 excess glucose as well as the prevention of advanced glycation endproduct/receptor for advanced glyc

64 lso found substantial gene enrichment in the advanced glycation endproduct/receptor for advanced glyc

65 f advanced glycation endproduct/receptor for advanced glycation endproduct signaling may offer new th

66 hecked glucose-mediated oxidative stress and advanced glycation endproduct signaling through receptor

67 nt protein D (SP-D) and soluble receptor for advanced glycation endproduct (sRAGE) were significantly

68 trations of epithelial (soluble receptor for advanced glycation endproducts [sRAGE]) and endothelial

69 elevated blood glucose lead to generation of advanced glycation endproducts, the products of nonenzym

70 d M1 polarization of macrophages after AGEs (advanced glycation endproducts) treatment, blocking the

71 Advanced glycation endproducts were measured using SDS-P