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 did not affect the elevated ER-stress markers foun

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

4 TUDCA is a prime candidate for treatment of humans with

5 TUDCA is efficacious and safe in preserving vision in th

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

7 TUDCA prevented neurotoxic (A1) polarization of astrocyt

8 TUDCA supplementation in experimental autoimmune encepha

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

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

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

12 TUDCA treatment reduced ER stress and apoptosis in Lrat(

13 TUDCA treatments did not alter retinal function or morph

14 TUDCA was predicted to bind to the GR, in a similar fash

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

16 TUDCA, but not taurocholic acid, selectively induced tra

17 TUDCA-treated rd10 retinas had fivefold more photorecept

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

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

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

21 re, we pinpointed tauroursodeoxycholic acid (TUDCA) as an efficient therapeutic, improving the motor

22 ss-relieving drug tauroursodeoxycholic acid (TUDCA) causes long-term amelioration of body weight, foo

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

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

25 acid (GUDCA) and tauroursodeoxycholic acid (TUDCA) have long been known to have anti-apoptotic, anti

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

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

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

29 Tauroursodeoxycholic acid (TUDCA) is considered an artificial chaperone protecting

30 administration of tauroursodeoxycholic acid (TUDCA) or tolvaptan impeded these processes.

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

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

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

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

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

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

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

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

39 onists, RG239 and tauroursodeoxycholic acid (TUDCA), acutely promoted stimulus-secretion coupling (SS

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

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

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

43 genous bile acid, tauroursodeoxycholic acid (TUDCA), on astrocyte and microglial polarization.

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

45 hemical chaperone, tauroursodexycholic acid (TUDCA).

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

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

48 x(betaetageo) and w/t mice were administered TUDCA in drinking water for 4 weeks.

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

50 CA in models of bilirubin encephalopathy and TUDCA in models of depression.

51 the therapeutic potential of UDCA, GUDCA and TUDCA in neurological, neurodegenerative and neuropsychi

52 nvestigating the role of the UDCA, GUDCA and TUDCA in the regulation of brain apoptosis, oxidative st

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

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

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

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

57 UDCA and TUDCA inhibited in vivo the cholangiocyte proliferation,

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

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

60 ls of Huntington's disease, whereas UDCA and TUDCA would be more beneficial in models of Parkinson's

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

62 neurons that can be reduced or abolished by TUDCA.

63 lcification in dystrophic muscles induced by TUDCA is specific to muscles lacking dystrophin.

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

65 uence of ATXN3 dysfunction being restored by TUDCA treatment.

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

67 ing dexamethasone or the chemical chaperones TUDCA and 4PBA attenuated MMP9 expression and secretion

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

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

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

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

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

73 ed to investigate the effect of UDCA, GUDCA, TUDCA on the same mechanisms in pre-clinical models of n

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

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

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

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

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

79 dase production in neurodegenerative models; TUDCA decreases apoptosis in neurological models, reduce

80 dase production in neurodegenerative models; TUDCA decreases apoptosis in neurological models, reduce

81 , all of which are ameliorated with neonatal TUDCA treatment.

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

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

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

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

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

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

88 mechanism for the neuroprotective effects of TUDCA in SCA3 and propose this readily available drug fo

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

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

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

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

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

94 Treatment of TUDCA not only attenuated proteinuria and kidney histolo

95 t with sildenafil to inhibit mPTP opening or TUDCA to suppress ER stress.

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

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

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

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

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

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

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

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

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

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

106 6 +/- 34%, P <.025) > tauroursodeoxycholate (TUDCA) (175 +/- 28%, P <.05) of control levels.

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

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

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

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

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

112 t tissue mineralisation we hypothesised that TUDCA treatment should reduce mineral deposits in dystro

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

114 omic and functional in vivo data showed that TUDCA acts in neuronal tissue through the glucocorticoid

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

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

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

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

119 Unexpectedly, TUDCA enhanced calcification of dystrophic but not dystr

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

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

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

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

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

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

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

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

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

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

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

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

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