ライフサイエンスコーパス: TUDCA

1 TUDCA abolished TG-induced markers of ER stress; reduced

2 TUDCA has the potential to lead to the development of a

3 TUDCA is a prime candidate for treatment of humans with

4 TUDCA is efficacious and safe in preserving vision in th

5 TUDCA might stimulate Ca(2+)-dependent hepatocellular ex

6 TUDCA treatment increased PrP(C) expression, which was r

7 TUDCA treatment preserved ERG b-waves and the outer nucl

8 TUDCA treatment preserved ERG b-waves and the outer nucl

9 TUDCA treatment reduced ER stress and apoptosis in Lrat(

10 TUDCA treatments did not alter retinal function or morph

11 TUDCA, 50 micromol/L (P <.001) and TCDCA up to 200 micro

12 TUDCA, but not taurocholic acid, selectively induced tra

13 TUDCA-treated rd10 retinas had fivefold more photorecept

14 UDCA (up to 100 micromol/L, P <.0001), TUDCA (up to 400 micromol/L, P <.0001), and TCDCA (up to

15 he chemical chaperone taurodeoxycholic acid (TUDCA), which can facilitate protein folding and traffic

16 c acid (GCA), and tauroursodeoxycholic acid (TUDCA) all activated ERK1/2 in primary rat hepatocytes t

17 ion of the UPR by tauroursodeoxycholic acid (TUDCA) diminishes Mst1/2 mutant-driven liver overgrowth

18 ly, the bile acid tauroursodeoxycholic acid (TUDCA) has been shown to have antiapoptotic properties i

19 essed the role of tauroursodeoxycholic acid (TUDCA) in inhibition of caspase-12 activation and its ef

20 stress inhibitor tauroursodeoxycholic acid (TUDCA) into the lateral cerebroventricle.

21 rine in vivo, and tauroursodeoxycholic acid (TUDCA) is a potent hepatocellular Ca2+ agonist and stimu

22 in ER stress with tauroursodeoxycholic acid (TUDCA) partially reversed obesity-associated metabolic a

23 lecular chaperone tauroursodeoxycholic acid (TUDCA) significantly inhibits influenza A viral replicat

24 leretic effect of tauroursodeoxycholic acid (TUDCA) was impaired in InsP(3)R2 KO mice.

25 nd treatment with tauroursodeoxycholic acid (TUDCA), a bile acid derivative that acts as a chemical c

26 tective effect of tauroursodeoxycholic acid (TUDCA), a bile acid, on ER stress in MSCs in vitro and i

27 Tauroursodeoxycholic acid (TUDCA), a chemical chaperone that alleviates ER stress,

28 at treatment with tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, prevented neuropatholog

29 treated mice with tauroursodeoxycholic acid (TUDCA), a specific inhibitor of ER stress.

30 Tauroursodeoxycholic acid (TUDCA), an endogenous bile acid, modulates cell death by

31 olic acid (TDCA), tauroursodeoxycholic acid (TUDCA), glycocholic acid (GCA), glycodeoxycholic acid (G

32 emical chaperone, tauroursodeoxycholic acid (TUDCA), in preserving cones in the Lrat(-/-) model.

33 Administration of tauroursodeoxycholic acid (TUDCA), which reportedly inhibits apoptosis, significant

34 hemical chaperone, tauroursodexycholic acid (TUDCA).

35 In addition, TUDCA induced a significant increase in hepatocellular D

36 esults showed that systemically administered TUDCA led to a significant reduction in striatal neuropa

37 Two chemical chaperones, 4PBA and TUDCA, were used to ameliorate the cellular stress and i

38 ry, we show for the first time that SAMe and TUDCA can exert an additive effect in the amelioration o

39 We determined if UDCA and TUDCA activate PKC, increase [Ca(2+)](i), and alter the

40 om 1-week BDL rats, we evaluated if UDCA and TUDCA directly inhibit cholangiocyte proliferation and s

41 in bile duct-ligated (BDL) rats, if UDCA and TUDCA effects are associated with increased cholangiocyt

42 UDCA and TUDCA inhibited in vivo the cholangiocyte proliferation,

43 In vitro UDCA and TUDCA inhibition of cholangiocyte growth and secretion r

44 dependent PKC alpha is required for UDCA and TUDCA inhibition of cholangiocyte growth and secretion.

45 Chemical chaperones such as TUDCA and PBA alleviate different forms of colitis in mi

46 neurons that can be reduced or abolished by TUDCA.

47 he ER stress protective mechanism induced by TUDCA treatment, TUDCA-mediated cellular prion protein (

48 hat administration of the chemical chaperone TUDCA helped to maintain lymphocyte homeostasis by signi

49 In conclusion, TUDCA is a nontoxic, endogenously produced hydrophilic b

50 In ER stress conditions, TUDCA treatment of MSCs reduced the activation of ER str

51 e did not change after treatment with either TUDCA or placebo.

52 Furthermore, TUDCA promoted the degradation of cone membrane-associat

53 Furthermore, TUDCA treatment modulated expression of certain Bcl-2 fa

54 A structure of ATX simultaneously harbouring TUDCA in the tunnel and LPA in the pocket, together with

55 e of ERG b-waves was significantly higher in TUDCA-treated Bbs1 and rd10 animals than in controls.

56 ght-adapted responses were twofold larger in TUDCA-treated mice than in controls at the brightest ERG

57 ective action at the mitochondrial membrane, TUDCA also activated the Akt-1protein kinase Balpha surv

58 In a murine hindlimb ischemia model, TUDCA-treated MSC transplantation augmented the blood pe

59 Administration of TUDCA before or up to 6 h after stereotaxic collagenase

60 In addition, the effect of TUDCA on the accummulation of sn-1,2-diacylglycerol (DAG

61 The effect of TUDCA on the distribution of PKC isoenzymes within the h

62 of this study was to determine the effect of TUDCA therapy on multiorgan insulin action and metabolic

63 es the wide-range neuroprotective effects of TUDCA after ICH.

64 We examined the effects of TUDCA and PBA in cultured intestinal epithelial cells (I

65 f this study was to determine the effects of TUDCA on PKC in isolated hepatocytes.

66 s study the authors examined the efficacy of TUDCA on preserving rod and cone function and morphology

67 Systemic injection of TUDCA is effective in reducing ER stress, preventing apo

68 This novel mechanism of TUDCA action suggests new intervention methods for ER st

69 stress marker expression in the podocytes of TUDCA-treated mice.

70 Treatment of TUDCA not only attenuated proteinuria and kidney histolo

71 Oral administration of either PBA or TUDCA reduced features of DSS-induced acute and chronic

72 Immediately after BDL, rats were fed UDCA or TUDCA (both 275 micromol/d) for 1 week.

73 In particular, TUDCA inhibited the dissociation between GRP78 and PERK,

74 Specifically, R6/2 mice began receiving TUDCA at 6 weeks of age and exhibited reduced striatal a

75 he control Bbs1(M390R/M390R) while receiving TUDCA.

76 ds are absent in the rd10 mouse model of RP, TUDCA treatment preserved rod and cone function and grea

77 Thus, given its clinical safety, TUDCA may provide a potentially useful treatment in pati

78 protective bile acid, tauroursodeoxycholate (TUDCA), partially protects against the action of TLC whe

79 e chemical chaperones tauroursodeoxycholate (TUDCA) and 4-phenylbutyrate (4-PBA), as well as the iron

80 e chemical chaperones tauroursodeoxycholate (TUDCA) and 4-phenylbutyrate (PBA), which facilitate prot

81 6 +/- 34%, P <.025) > tauroursodeoxycholate (TUDCA) (175 +/- 28%, P <.05) of control levels.

82 eoxycholate (UDCA) or tauroursodeoxycholate (TUDCA) chronic feeding prevents the increased cholangioc

83 rol and the bile salt tauroursodeoxycholate (TUDCA), showing how the tunnel selectively binds steroid

84 ndary role in ER-mediated apoptosis and that TUDCA prevents apoptosis by blocking a calcium-mediated

85 These data demonstrate that TUDCA might be an effective pharmacological approach for

86 This study is the first to demonstrate that TUDCA protects MSCs against ER stress via Akt-dependent

87 We observed that TUDCA, a compound capable of restoring Tollip cellular f

88 deficits were significantly improved in the TUDCA-treated mice.

89 icantly in response to signaling through the TUDCA-Akt axis.

90 ective mechanism induced by TUDCA treatment, TUDCA-mediated cellular prion protein (PrP(C)) activatio

91 In conclusion, UDCA, TUDCA, and TCDCA but not TCA are capable of protecting h

92 In this study, we evaluated whether TUDCA can reduce brain injury and improve neurological f

93 We therefore examined whether TUDCA would also be neuroprotective in a genetic mouse m

94 /-) mice were systemically administered with TUDCA and vehicle (0.15 M NaHCO(3)) every 3 days from P9

95 Rd1 and rd16 mice showed no improvement with TUDCA treatment, and the rd1 mice did not have normal we

96 IECs, which were reduced by incubation with TUDCA or PBA.

97 nd rd10 mice were systemically injected with TUDCA (500 mg/kg) every 3 days from P6 to P30 and were c

98 db/db mice and diet-induced obese mice with TUDCA increased the cellular and serum levels of adipone

99 mice were injected daily from P6 to P30 with TUDCA or vehicle.

100 re injected every 3 days from P6 to P38 with TUDCA or vehicle (0.15 M NaHCO(3)).

101 In addition, therapy with TUDCA, but not placebo, increased muscle insulin signali

102 re twofold greater in rd10 mice treated with TUDCA than with vehicle, likewise light-adapted response

103 were randomized to 4 weeks of treatment with TUDCA (1,750 mg/day) or placebo.

104 ximately 30% (P < 0.05) after treatment with TUDCA but did not change after placebo therapy.