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

1 Dicarbonyls are reactive precursors of advanced glycation endproducts.

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

3 Advanced glycation endproduct (AGE) formation is a trigg

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

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

6 Advanced glycation endproduct (AGE) levels are elevated

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

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

9 Forty-five glycated, 48 advanced glycation endproduct (AGE-) modified, and 20 ox

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

11 Advanced glycation endproducts (AGE) contribute to kidne

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

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

14 Advanced glycation endproducts (AGEs) accumulate in pati

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

16 Advanced glycation endproducts (AGEs) and their precurso

17 Advanced glycation endproducts (AGEs) are believed to pl

18 Advanced glycation endproducts (AGEs) are derivatives of

19 Advanced glycation endproducts (AGEs) are formed in a se

20 Advanced glycation endproducts (AGEs) have been linked t

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

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

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

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

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

26 Advanced glycation endproducts (AGEs), a pathogenic fact

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

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

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

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

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

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

33 Dicarbonyls are major reactive precursors of advanced glycation endproducts (AGEs).

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

35 tion is mediated in part by the receptor for advanced glycation endproducts and Toll-like receptor pr

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

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

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

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

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

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

42 These advanced glycation endproducts engage their receptor in

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

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

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

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

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

48 on products (protein carbonyl compound), and advanced glycation endproducts (N(epsilon)-(carboxymethy

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

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

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

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

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

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

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

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

57 The receptor for advanced glycation endproducts (RAGE) has been implicate

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

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

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

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

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

63 The receptor for advanced glycation endproducts (RAGE) is critically invo

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

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

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

67 tal studies have found that the receptor for advanced glycation endproducts (RAGE) plays a significan

68 hich subsequently activated the receptor for advanced glycation endproducts (RAGE) receptor to promot

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

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

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

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

73 a heteromeric complex with the receptor for advanced glycation endproducts (RAGE).

74 markers of alveolar (including receptor for advanced glycation endproducts [RAGE]), endothelial (inc

75 oxia-inducible factor 1 [HIF1], receptor for advanced glycation endproducts [RAGE], angiopoietin 2 [A

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

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

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

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

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

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

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

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

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

85 Advanced glycation endproducts were measured using SDS-P