ライフサイエンスコーパス: PDTC

1 PDTC alone had no effect.

2 PDTC also blocked UV-induced accumulation of wild-type p

3 PDTC also prevented the decrease in arterial blood press

4 PDTC and BAY suppressed metatarsal linear growth.

5 PDTC prolonged graft survival as compared with untreated

6 PDTC treatment had no effect on the extent of infiltrate

7 PDTC-induced HO-1 gene expression correlated with a rise

8 Forty-eight DTC and 34 PDTC patients who underwent (18)F-FDG PET/CT for tumor s

9 eyed in 31 cell lines, 52 primary tumors (34 PDTC and 18 ATC), and 55 RAIR, FDG-PET-positive recurren

10 carbamate (PDTC, NF-kappaB inhibitor), or 4) PDTC.

11 the NF-kappaB pathway (e.g., by BAY 11-7082, PDTC, or SN-50) or molecular dysregulation of NF-kappaB

12 ng increased AP-1 DNA binding activity after PDTC treatment.

13 f the two proteins was greatly reduced after PDTC treatment or after exposure to geldanamycin, an Hsp

14 translocation and accumulation resumed after PDTC removal.

15 ALLN, PDTC, or sodium salicylate decreased P-selectin expressi

16 e treated with the NFkappaB inhibitors ALLN, PDTC, NAC, and MG132.

17 Although PDTC, BAY, and p65 siRNA reduced the expression of BMP-2

18 beta-NF and PDTC exposure also increased steady-state levels of MafG

19 hypothesize that, in response to beta-NF and PDTC, the GCS subunit genes are transcriptionally up-reg

20 d activity (by p65 short interfering RNA and PDTC, respectively) in chondrocytes reversed the IGF-I-m

21 SB203580 and PDTC blocked the increased expression of iNOS and increa

22 nding activity was inhibited by SB203580 and PDTC.

23 ion and activity (by NF-kappaB p65 siRNA and PDTC, respectively) in chondrocytes reversed the GH-medi

24 r, our data demonstrate that the antioxidant PDTC enhances HO-1 gene transcription and that the induc

25 e proteasome inhibitor ALLN, the antioxidant PDTC, or sodium salicylate, but not the glucocorticoid d

26 Although normally used as an antioxidant, PDTC has been shown to exert pro-oxidant activity on pro

27 In astrocytes PDTC also dramatically induces the NF kappaB-dependent e

28 At PDTC concentrations of 50, 100, and 200 mg/kg, the reduc

29 uscle cells was not species specific because PDTC and NAC both caused dose-dependent reductions in vi

30 signaling cascade was partially abolished by PDTC treatment.

31 appaB and iNOS), which could be abrogated by PDTC.

32 e inhibition of NF-kappaB p65 activation (by PDTC and BAY) and expression (by p65 siRNA) led to the s

33 vascular smooth muscle cell death caused by PDTC and NAC.

34 heximide partially decreased inducibility by PDTC or beta-NF and resulted in significant increases in

35 s cytochrome c release was only inhibited by PDTC.

36 es NF kappaB activation that is inhibited by PDTC.

37 The activation of JNK by PDTC, in the presence or absence of exogenous H(2)O(2),

38 owth plate chondrogenesis was neutralized by PDTC.

39 owth plate chondrogenesis was neutralized by PDTC.

40 Poorly differentiated thyroid cancer (PDTC) and anaplastic thyroid cancer (ATC) are rare and f

41 C) and poorly differentiated thyroid cancer (PDTC).

42 ess to poorly differentiated thyroid cancer (PDTC).

43 with poorly differentiated thyroid cancers (PDTC), anaplastic thyroid cancers (ATC), and radioactive

44 paB inhibitor, pyrrolidine dithio-carbamate (PDTC), and calphostin C.

45 of poorly differentiated thyroid carcinoma (PDTC).

46 In A1-5 cells, PDTC abrogated UV- and temperature shift-induced TSp53 n

47 Contrary to the results in Jurkat cells, PDTC did not inhibit tumor necrosis factor-alpha-induced

48 In rat aortic smooth muscle cells, PDTC induced cell shrinkage, chromatin condensation, and

49 In contrast, PDTC inhibited Cox-2 expression at the post-transcriptio

50 oxidant, either pyrrolidine dithiocarbamate (PDTC) (200 mg/kg s.c. daily) or N-acetylcysteine (NAC) (

51 the antioxidant pyrrolidine dithiocarbamate (PDTC) also reduces intracellular ROS levels in associati

52 appaB inhibitor pyrrolidine dithiocarbamate (PDTC) and by NF-kappaB silencing.

53 Pyrrolidine dithiocarbamate (PDTC) blocked activation of NF-kappaB and led to promine

54 ble antioxidant pyrrolidine dithiocarbamate (PDTC) decreased the intracellular levels of ROS and inhi

55 monstrated that pyrrolidine dithiocarbamate (PDTC) exerts protection against inflammatory responses,

56 The antioxidant pyrrolidine dithiocarbamate (PDTC) greatly diminished the intracellular oxidation and

57 Pyrrolidine dithiocarbamate (PDTC) is a thiol compound widely used to study the activ

58 Pyrrolidine dithiocarbamate (PDTC) is an inhibitor of NF kappaB in most cells; howeve

59 paB inhibitors (pyrrolidine dithiocarbamate (PDTC) or BAY11-7082 (BAY)), p65 short interference RNA (

60 ologically with pyrrolidine dithiocarbamate (PDTC) prevented cytokine, but not IL6R, induction by Jun

61 ne (beta-NF) or pyrrolidine dithiocarbamate (PDTC) resulted in the up-regulation of the gamma-glutamy

62 ce of GH and/or pyrrolidine dithiocarbamate (PDTC), a known NF-kappaB inhibitor.

63 th IGF-I and/or pyrrolidine dithiocarbamate (PDTC), a known NF-kappaB inhibitor.

64 re treated with pyrrolidine dithiocarbamate (PDTC), a NFkappaB inhibitor, or l-1-tosylamido-2-phenyle

65 Pyrrolidine dithiocarbamate (PDTC), a presumed antioxidant, induced JNK activation on

66 sence of either pyrrolidine dithiocarbamate (PDTC), a selective inhibitor of NF-kappaB, or Genistein,

67 the ability of pyrrolidine dithiocarbamate (PDTC), an agent that inhibits the nuclear localization o

68 t of cells with pyrrolidine dithiocarbamate (PDTC), an antioxidant that inhibits NF-kappaB activation

69 Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappa B effective in cellular

70 dant scavenger, pyrrolidine dithiocarbamate (PDTC), inhibited iNOS expression at the transcriptional

71 f antioxidants [pyrrolidine dithiocarbamate (PDTC), N-acetyl l-cysteine (NAC)] or Ca2+ chelators (EGT

72 he antioxidants pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine (NAC), and vitamin E (VE) decrea

73 with TNF-alpha, pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine, and dexamethasone prevented I k

74 an antioxidant pyrrolidine dithiocarbamate (PDTC), whereas cytochrome c release was only inhibited b

75 xidant, such as pyrrolidine dithiocarbamate (PDTC), would attenuate HO-1 induction in response to NO.

76 teine (NAC) and pyrrolidine dithiocarbamate (PDTC).

77 th two doses of pyrrolidine dithiocarbamate (PDTC, 100 mg/kg, i.p.) 24 and 1 h prior to the acute exe

78 pplemented with pyrrolidine dithiocarbamate (PDTC, an NF-kappaB inhibitor) or SB203580 (a MAPK inhibi

79 tor), 3) 7-NI + pyrrolidine dithiocarbamate (PDTC, NF-kappaB inhibitor), or 4) PDTC.

80 r of NF-kappaB, pyrrolidine dithiocarbamate (PDTC; 250 mg/kg s.c.) was administered daily from transp

81 the antioxidant pyrrolidine-dithiocarbamate (PDTC)-prevented poly IC + IFN-gamma-induced iNOS express

82 n 1 (AP-1) regulatory element is crucial for PDTC-induced HO-1 gene transcription.

83 on intracellular reduced sulfur/cysteine for PDTC biosynthesis and that pseudomonads utilize sulfite

84 ida DSM 3601 to identify genes necessary for PDTC production (Pdt phenotype).

85 tor, MG132 or inhibitors of NF-kappa B (e.g. PDTC and gliotoxin), decreased PMA-induced up-regulation

86 However, PDTC and NAC induced increased expression of ICAM-1 in H

87 ed in PTC and expressed at highest levels in PDTC and anaplastic thyroid cancer.

88 ression was increased and E-cadherin lost in PDTC compared with adjacent PTC.

89 f BRAF(V600E) on tumor glucose metabolism in PDTC needs further study in larger groups of patients.

90 opism for nodal versus distant metastases in PDTC.

91 al different NF-kappaB inhibitors, including PDTC, CAPE, BAY 11-7085, and lactacystin.

92 inhibitor SB 203580, or NF-kappaB inhibitor PDTC.

93 nt of RPE cells with a NF-kappa B inhibitor, PDTC, resulted in dose-dependent decrease in IL-1 beta-i

94 98 (0.1 microM), or the NF-kappaB inhibitor, PDTC (10 microM), significantly reduced the permeability

95 NF-kappaB inhibitors, PDTC or Bay 11-7082, abolished excessive p65 phosphoryla

96 NF kappaB activation in astrocytes; instead PDTC itself induces NF kappaB activation in astrocytes,

97 To provide insight into PDTC signaling, we constructed a conditionally active ST

98 nhancer plays an important role in mediating PDTC-induced HO-1 gene transcription.

99 us 13%; P = 0.04) in PET-positive metastatic PDTC.

100 tion was blocked by either GF109203x, MG132, PDTC, or gliotoxin.

101 Moreover, PDTC stained positively for phospho-Smad2, suggesting a

102 ined by the Turin (PDTC-Turin) versus MSKCC (PDTC-MSK) criteria, respectively.

103 In contrast, neither PDTC nor NAC reduced viability in human aortic endotheli

104 Consistent with this notion, PDTC and two other antioxidants, N-acetyl cysteine and 2

105 e studies are consistent with the ability of PDTC to down-regulate IL-6-induced STAT3 activation by a

106 ed tumor growth in vivo, coadministration of PDTC and SC 58125 resulted in actual tumor regression.

107 The effect of PDTC and NAC on smooth muscle cells was not species spec

108 capability, we decided to test the effect of PDTC on p53 activation.

109 The pathway of PDTC biosynthesis has not been defined.

110 s effect was not reversed in the presence of PDTC and was not accompanied with DNA fragmentation when

111 Continual presence of PDTC was required for its effect as both UV-induced nucl

112 harmacological and biochemical properties of PDTC.

113 ay analysis using RNA from paired samples of PDTC and PTC collected from the same animals by laser ca

114 tida and that the effect of finR mutation on PDTC production was due to deficient expression of fprA

115 signaling pathways revealed that IL-1beta or PDTC activated extracellular signal-regulated kinase-2 (

116 ne splenic B lymphocytes with either TPCK or PDTC also resulted in apoptosis.

117 s slower in cells treated with H(2)O(2) plus PDTC compared with the rate in cells treated with ultrav

118 strong JNK-activating ability, H(2)O(2) plus PDTC did not induce significant activation of the upstre

119 suggest that JNK activation by H(2)O(2) plus PDTC resulted from the down-regulation of JNK phosphatas

120 Treatment of H(2)O(2) plus PDTC significantly decreased the expression levels of a

121 n BRAF (44 versus 12%; P = 0.002) in primary PDTC, whereas BRAF was more common than RAS (39 versus 1

122 e constructs of adhesion molecule promoters, PDTC inhibited VCAM-1 and E-selectin, but to a lesser ex

123 To investigate the PTC-PDTC progression, we performed a microarray analysis usi

124 itor, and pyrrolidinediethyldithiocarbamate (PDTC), the NF-kappaB inhibitor, but not by PD 98059, a s

125 Pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) have been used as antio

126 nown antioxidant pyrrolidinedithiocarbamate (PDTC) leads to time and dose dependent activation of hea

127 sed antioxidants pyrrolidinedithiocarbamate (PDTC) and butylated hydroxyanisole (BHA), indicating tha

128 The antioxidants pyrrolidinedithiocarbamate (PDTC), N-acetylcysteine, 6-hydroxy-2,5,7,8-tetramethylch

129 appaB inhibitors pyrrolidinedithiocarbamate (PDTC; 100 microM), caffeic acid phenethyl ester (CAPE; 9

130 ls with 10(-7) M pyrrolidinedithiocarbamate (PDTC), an inhibitor of nuclear factor (NF)-kappaB, aboli

131 ith low doses of pyrrolidinedithiocarbamate (PDTC) selectively inhibited NF-kappaB/Rel factor binding

132 e ROS scavengers pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) significantly inhibited

133 ct inhibited by the oxygen radical scavenger PDTC.

134 pression at the transcriptional level, since PDTC abolished iNOS mRNA accumulation.

135 ion at the post-transcriptional level, since PDTC did not affect IL-1beta-induced Cox-2 mRNA levels b

136 Spionolactone, PDTC, and NAC each attenuated these responses suggesting

137 Co-treatment with spironolactone, PDTC, or NAC attenuated these molecular and cellular res

138 Surprisingly, PDTC was a very potent inducer of HO-1 gene expression,

139 We further demonstrate that PDTC activates heat-shock factor 1 (HSF1), one of severa

140 We found that PDTC increased p53 cysteine residue oxidation in vivo.

141 We report here that PDTC and NAC induce apoptosis in rat and human smooth mu

142 In this communication, we report that PDTC inhibits the activation of temperature-sensitive mu

143 eterologous promoter construct revealed that PDTC inhibited VCAM-1 and E-selectin, but to a lesser ex

144 kappaB in most cells; however, we show that PDTC is also a potent scavenger of NO through formation

145 The PDTC concentration-dependent reductions in iNOS activity

146 cavenging of endogenously produced NO by the PDTC iron complex.

147 In the PDTC group, only 5 tumors were BRAF(V600E)-positive, and

148 Pyridine-2,6-bis(thiocarboxylate) (PDTC), produced by certain pseudomonads, is a sulfur-con

149 m mice lacking nNOS responds more rapidly to PDTC compared with astrocytes from wild-type mice.

150 nguished between PDTCs defined by the Turin (PDTC-Turin) versus MSKCC (PDTC-MSK) criteria, respective

151 All of these changes were abolished when PDTC was given together with 7-NI.

152 We next investigated whether PDTC treatment altered the p53 redox state.

153 With PDTC administration, a threefold decrease in NF-kappaB a

154 Combined treatment of HCA-7 cells with PDTC and SC 58125 resulted in an additive decrease in PG

155 atment of cultured HepG2 hepatoma cells with PDTC inhibits IL-6-stimulated tyrosine phosphorylation a

156 Pretreatment of cells with PDTC reduced and delayed the activation of Syk kinases a

157 Pretreatment of AGS cells with PDTC, which blocks NF-kappa B activation, inhibited H. p

158 ead genomic disruptions in ATC compared with PDTC underscore their greater virulence and higher morta

159 ormation of mononitrosyl iron complexes with PDTC.

160 nd a primary culture of rat hepatocytes with PDTC restored insulin responsiveness that was abrogated

161 In vivo, rabbits pretreated with PDTC before LPS infusion showed significantly less neutr

162 ession was blocked in HUVECs pretreated with PDTC before TNF-alpha, IL-1, or LPS stimulation.

163 edly enhanced in lymphocytes pretreated with PDTC, and another antioxidant, N-acetylcysteine, did not

164 in TNF-alpha-treated HUVECs pretreated with PDTC.

165 cells decreased within 3 h of treatment with PDTC and was reduced to 30% at 12 h.

166 ation-independent manner, and treatment with PDTC mitigated the response.

167 ssayed for CAT activity after treatment with PDTC.