ライフサイエンスコーパス: renal tubular cell

1 nal protection required both macrophages and renal tubular cells.

2 iates albumin-induced profibrotic effects in renal tubular cells.

3 und accumulated in the lysosomes of proximal renal tubular cells.

4 rker for detecting ER stress in podocytes or renal tubular cells.

5 abundantly expressed in podocytes but not in renal tubular cells.

6 nction caused by ischemic or toxic injury to renal tubular cells.

7 ion and fibrosis that is highly expressed in renal tubular cells.

8 ot induce apoptosis or regulated necrosis of renal tubular cells.

9 Gas6 receptor Axl in the apical membrane of renal tubular cells.

10 pathways leading to apoptosis or survival in renal tubular cells.

11 l-mesenchymal transition induced by FGF-2 in renal tubular cells.

12 n in mouse inner medullary collecting duct-3 renal tubular cells.

13 rkers of M2 macrophages when cocultured with renal tubular cells.

14 ithelial sodium channel alpha, ENaCalpha, in renal tubular cells.

15 s a critical role in TGF-beta-induced EMT of renal tubular cells.

16 created by knocking out Tsc1 in a subset of renal tubular cells.

17 glucose-induced mitochondrial dysfunction in renal tubular cells.

18 s on the viability of islets, podocytes, and renal tubular cells.

19 the mechanism that enables viral entry into renal tubular cells.

20 eases in GAPDH and pax2 abundance in NRK-52E renal tubular cells.

21 ss 1 phosphatidylinositol 3-kinase (PI3K) in renal tubular cells.

22 or against oxidative and apoptotic damage in renal tubular cells.

23 lates membrane potential and K+ secretion in renal tubular cells.

24 beta-tubulin colocalize to primary cilia of renal tubular cells.

25 ) crystal-binding proteins on the surface of renal tubular cells.

26 a occludens (ZA) induced by ATP depletion of renal tubular cells.

27 Similar results were obtained in cultured renal tubular cells.

28 In cultured renal tubular cells, 20 microM cisplatin induced approxi

29 chemia is characterized by disruption of the renal tubular cell actin cytoskeleton, this study was co

30 ysiological osmoregulatory mechanism whereby renal tubular cells adjust to the intraluminal hyperosmo

31 beta 1 integrin-mediated adhesion between renal tubular cells after anoxic injury.

32 port to show that HSC can differentiate into renal tubular cells after I/R injury.

33 in the kidney and most likely is degraded in renal tubular cells after reabsorption.

34 was found for cell fusion between indigenous renal tubular cells and BMDC, but this was infrequent an

35 ll types including the vascular endothelium, renal tubular cells and erythrocytes.

36 Whereas murine renal tubular cells and freshly isolated renal tubules r

37 sue remodeling using cultured human proximal renal tubular cells and half-nephrectomized mice treated

38 cisplatin accumulates preferentially in the renal tubular cells and is a frequent cause of drug-indu

39 NGAL is a glycoprotein released by damaged renal tubular cells and is a sensitive maker of both cli

40 ciated with the apical membranes of cultured renal tubular cells and is bound to membrane skeletal el

41 ecific receptors located on osteoblastic and renal tubular cells and is fully functional as the N-ter

42 ologic analysis revealed Pals1 expression in renal tubular cells and podocytes of human kidneys.

43 asure the significant uptake of polymyxin in renal tubular cells and provides crucial information for

44 d ADV may cause mitochondrial dysfunction in renal tubular cells and reprogramming of glucose metabol

45 = 3) showed increased elastin expression in renal tubular cells and the interstitium but not glomeru

46 e proteins shows a predominant expression in renal tubular cells and the localization of immunoreacti

47 present on the surface of oligodendrocytes, renal tubular cells, and certain tumor cells.

48 production during the cold storage of human renal tubular cells, and to define the roles of extrinsi

49 Bax and Bak from proximal tubules attenuated renal tubular cell apoptosis and suppressed renal inters

50 delivery of HSP72 inhibits ischemia-induced renal tubular cell apoptosis by preventing NF-kappaB act

51 ll death per se, it dramatically potentiated renal tubular cell apoptosis initiated by other death cu

52 production, with increased kidney injury and renal tubular cell apoptosis.

53 utralization also inhibited ischemia-induced renal tubular cell apoptosis.

54 anscription, and subsequent ischemia-induced renal tubular cell apoptosis.

55 common in sepsis but presents focally; most renal tubular cells appear normal.

56 Myofibroblasts produced from EMT of renal tubular cells are responsible for the deposition o

57 y involved in the circadian clock system, in renal tubular cells (Bmal1(lox/lox)/Pax8-rtTA/LC1 mice).

58 e also demonstrated a role for endostatin in renal tubular cell branching morphogenesis and show that

59 growth factor (EGF) causes proliferation in renal tubular cells but, when it is combined with transf

60 -beta) plays an essential role in the EMT of renal tubular cells, but the molecular mechanism governi

61 he regenerative capacity of actively cycling renal tubular cells by decreasing the number of cells in

62 In summary, activation of renal tubular cells by infiltrating T cells can amplify

63 altered exposure of Ax-II on the surface of renal tubular cells could promote crystal retention and

64 t of miR-26a on apoptosis was evaluated in a renal tubular cell culture.

65 ional intervention reduced hemolysis-related renal tubular cell damage, hepatocyte damage, ileal leak

66 f mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, rem

67 nistered to donor or recipient decreased the renal tubular cell death, inflammation, and MHC II expre

68 f persistent Cav-EGFR-ERK signaling mediates renal tubular cell dedifferentiation and identifies a no

69 with acute tubular necrosis, apoptosis, and renal tubular cell desquamation, with toxic vacuolizatio

70 Renal tubular cells do not express any of the known HIV-

71 mmed necrosis (necroptosis), which occurs in renal tubular cells during AKI.

72 Renal tubular cells elicit adaptive responses following

73 e of C5b-9 in complement-mediated effects on renal tubular cells exposed to proteinuric urine, equiva

74 obin, resulting in increased endothelial and renal tubular cell free iron, which is associated with r

75 t mediates internalization of the virus into renal tubular cells, from which the virus can be rescued

76 n of renal vessels and induces hypertension, renal tubular cell hypertrophy, and podocyte apoptosis.

77 he expression of membrane sodium channels in renal tubular cells in a manner dependent on the metabol

78 owed iron accumulation on the apical side of renal tubular cells in Heph/Cp KO mice.

79 Factor H was present on the urinary side of renal tubular cells in proteinuric, but not in normal re

80 d secreted by immune cells, hepatocytes, and renal tubular cells in various pathologic states.

81 is effects of kaempferol and esculetin using renal tubular cells in vitro and in vivo in a mouse Unil

82 viability of islets and HK-2 human proximal renal tubular cells in vitro.

83 renal tubular cells, penetrated live murine renal tubular cells in vivo, and localized in the cell n

84 Renal tubular cell injury causes dysregulation of SR-B1,

85 lation and concentration of polymyxin within renal tubular cells is essential for the development of

86 primary cultures treated with cyclosporin A, renal tubular cells isolated from Nupr1-deficient mice e

87 using fluorescence-activated cell sorting of renal tubular cells labeled with segment-specific fluore

88 found on the surface of lysosomes and that a renal tubular cell line deficient in OCRL accumulated su

89 in a doxycycline-regulated Smad7-expressing renal tubular cell line.

90 ced (thermal stress, 43 degrees Cx1 hour) in renal tubular cells (LLC-PK1) with Western blot confirma

91 Renal biopsy data further suggest that renal tubular cells may serve as reservoir for HIV-1.

92 ATP depletion or cisplatin treatment of rat renal tubular cells, mitochondrial fragmentation was obs

93 entified that bound membranes of fixed human renal tubular cells, penetrated live murine renal tubula

94 Primary cilia dysfunction alters renal tubular cell proliferation and differentiation and

95 ulated proinflammatory macrophages, promoted renal tubular cell proliferation.

96 Knockdown of Fat1 in renal tubular cells reduces migration, decreases active

97 r in situ We now show that EV from adult rat renal tubular cells significantly improved renal functio

98 indices of glomerular injury or to suppress renal tubular cell TGF-beta in D.

99 parameters in D, as well as the increases in renal tubular cell TGF-beta seen in D.

100 2-OHE had no effects on renal tubular cell TGF-beta, but it significantly reduce

101 In renal tubular cells, TGF-beta1 administration upregulate

102 In all cases, renal cysts arise from renal tubular cells that lose the capacity to produce Pk

103 HIF-2alpha activation in renal tubular cells upregulated mRNA and protein express

104 Human renal tubular cells were cold-stored at 4 degrees C for

105 s of patients shedding polyomavirus-infected renal tubular cells were compared with those of patients

106 ransforming growth factor-beta (TGF-beta) in renal tubular cells were significantly higher in PAN nep

107 The objective was to determine in human renal tubular cells whether apoptosis is specific for re

108 of the native kidneys of this patient showed renal tubular cells with intranuclear inclusions charact

109 on of cell cycle pathways was seen in murine renal tubular cells with NOTCH overexpression, and molec