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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 imine (BSO) and pyrrolidine dithiocarbamate (PDTC) on the efflux of GSH and Cys from HepG2 cells.
60 paB inhibitors (pyrrolidine dithiocarbamate (PDTC) or BAY11-7082 (BAY)), p65 short interference RNA (
61 ologically with pyrrolidine dithiocarbamate (PDTC) prevented cytokine, but not IL6R, induction by Jun
62 ne (beta-NF) or pyrrolidine dithiocarbamate (PDTC) resulted in the up-regulation of the gamma-glutamy
63 ce of GH and/or pyrrolidine dithiocarbamate (PDTC), a known NF-kappaB inhibitor.
64 th IGF-I and/or pyrrolidine dithiocarbamate (PDTC), a known NF-kappaB inhibitor.
65 re treated with pyrrolidine dithiocarbamate (PDTC), a NFkappaB inhibitor, or l-1-tosylamido-2-phenyle
66                 Pyrrolidine dithiocarbamate (PDTC), a presumed antioxidant, induced JNK activation on
67 sence of either pyrrolidine dithiocarbamate (PDTC), a selective inhibitor of NF-kappaB, or Genistein,
68  the ability of pyrrolidine dithiocarbamate (PDTC), an agent that inhibits the nuclear localization o
69 t of cells with pyrrolidine dithiocarbamate (PDTC), an antioxidant that inhibits NF-kappaB activation
70                 Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappa B effective in cellular
71 dant scavenger, pyrrolidine dithiocarbamate (PDTC), inhibited iNOS expression at the transcriptional
72 f antioxidants [pyrrolidine dithiocarbamate (PDTC), N-acetyl l-cysteine (NAC)] or Ca2+ chelators (EGT
73 he antioxidants pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine (NAC), and vitamin E (VE) decrea
74 with TNF-alpha, pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine, and dexamethasone prevented I k
75  an antioxidant pyrrolidine dithiocarbamate (PDTC), whereas cytochrome c release was only inhibited b
76 xidant, such as pyrrolidine dithiocarbamate (PDTC), would attenuate HO-1 induction in response to NO.
77 teine (NAC) and pyrrolidine dithiocarbamate (PDTC).
78 th two doses of pyrrolidine dithiocarbamate (PDTC, 100 mg/kg, i.p.) 24 and 1 h prior to the acute exe
79 pplemented with pyrrolidine dithiocarbamate (PDTC, an NF-kappaB inhibitor) or SB203580 (a MAPK inhibi
80 tor), 3) 7-NI + pyrrolidine dithiocarbamate (PDTC, NF-kappaB inhibitor), or 4) PDTC.
81 r of NF-kappaB, pyrrolidine dithiocarbamate (PDTC; 250 mg/kg s.c.) was administered daily from transp
82 the antioxidant pyrrolidine-dithiocarbamate (PDTC)-prevented poly IC + IFN-gamma-induced iNOS express
83                                         Each PDTC was able to correctly identify the sensitive, resis
84 n 1 (AP-1) regulatory element is crucial for PDTC-induced HO-1 gene transcription.
85 on intracellular reduced sulfur/cysteine for PDTC biosynthesis and that pseudomonads utilize sulfite
86 ida DSM 3601 to identify genes necessary for PDTC production (Pdt phenotype).
87 tor, MG132 or inhibitors of NF-kappa B (e.g. PDTC and gliotoxin), decreased PMA-induced up-regulation
88                                     However, PDTC and NAC induced increased expression of ICAM-1 in H
89 ed in PTC and expressed at highest levels in PDTC and anaplastic thyroid cancer.
90 ression was increased and E-cadherin lost in PDTC compared with adjacent PTC.
91 f BRAF(V600E) on tumor glucose metabolism in PDTC needs further study in larger groups of patients.
92 opism for nodal versus distant metastases in PDTC.
93 al different NF-kappaB inhibitors, including PDTC, CAPE, BAY 11-7085, and lactacystin.
94  inhibitor SB 203580, or NF-kappaB inhibitor PDTC.
95 nt of RPE cells with a NF-kappa B inhibitor, PDTC, resulted in dose-dependent decrease in IL-1 beta-i
96 98 (0.1 microM), or the NF-kappaB inhibitor, PDTC (10 microM), significantly reduced the permeability
97                        NF-kappaB inhibitors, PDTC or Bay 11-7082, abolished excessive p65 phosphoryla
98  NF kappaB activation in astrocytes; instead PDTC itself induces NF kappaB activation in astrocytes,
99                      To provide insight into PDTC signaling, we constructed a conditionally active ST
100 nhancer plays an important role in mediating PDTC-induced HO-1 gene transcription.
101 us 13%; P = 0.04) in PET-positive metastatic PDTC.
102 tion was blocked by either GF109203x, MG132, PDTC, or gliotoxin.
103                                    Moreover, PDTC stained positively for phospho-Smad2, suggesting a
104 ined by the Turin (PDTC-Turin) versus MSKCC (PDTC-MSK) criteria, respectively.
105                         In contrast, neither PDTC nor NAC reduced viability in human aortic endotheli
106                 Consistent with this notion, PDTC and two other antioxidants, N-acetyl cysteine and 2
107 e studies are consistent with the ability of PDTC to down-regulate IL-6-induced STAT3 activation by a
108 ed tumor growth in vivo, coadministration of PDTC and SC 58125 resulted in actual tumor regression.
109                                The effect of PDTC and NAC on smooth muscle cells was not species spec
110 capability, we decided to test the effect of PDTC on p53 activation.
111                               The pathway of PDTC biosynthesis has not been defined.
112 s effect was not reversed in the presence of PDTC and was not accompanied with DNA fragmentation when
113                        Continual presence of PDTC was required for its effect as both UV-induced nucl
114 harmacological and biochemical properties of PDTC.
115 ay analysis using RNA from paired samples of PDTC and PTC collected from the same animals by laser ca
116 tida and that the effect of finR mutation on PDTC production was due to deficient expression of fprA
117 signaling pathways revealed that IL-1beta or PDTC activated extracellular signal-regulated kinase-2 (
118 ne splenic B lymphocytes with either TPCK or PDTC also resulted in apoptosis.
119 s slower in cells treated with H(2)O(2) plus PDTC compared with the rate in cells treated with ultrav
120 strong JNK-activating ability, H(2)O(2) plus PDTC did not induce significant activation of the upstre
121 suggest that JNK activation by H(2)O(2) plus PDTC resulted from the down-regulation of JNK phosphatas
122                   Treatment of H(2)O(2) plus PDTC significantly decreased the expression levels of a
123 n BRAF (44 versus 12%; P = 0.002) in primary PDTC, whereas BRAF was more common than RAS (39 versus 1
124 e constructs of adhesion molecule promoters, PDTC inhibited VCAM-1 and E-selectin, but to a lesser ex
125                       To investigate the PTC-PDTC progression, we performed a microarray analysis usi
126 itor, and pyrrolidinediethyldithiocarbamate (PDTC), the NF-kappaB inhibitor, but not by PD 98059, a s
127                  Pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) have been used as antio
128 nown antioxidant pyrrolidinedithiocarbamate (PDTC) leads to time and dose dependent activation of hea
129 sed antioxidants pyrrolidinedithiocarbamate (PDTC) and butylated hydroxyanisole (BHA), indicating tha
130 The antioxidants pyrrolidinedithiocarbamate (PDTC), N-acetylcysteine, 6-hydroxy-2,5,7,8-tetramethylch
131 appaB inhibitors pyrrolidinedithiocarbamate (PDTC; 100 microM), caffeic acid phenethyl ester (CAPE; 9
132 ls with 10(-7) M pyrrolidinedithiocarbamate (PDTC), an inhibitor of nuclear factor (NF)-kappaB, aboli
133 ith low doses of pyrrolidinedithiocarbamate (PDTC) selectively inhibited NF-kappaB/Rel factor binding
134 e ROS scavengers pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) significantly inhibited
135 ct inhibited by the oxygen radical scavenger PDTC.
136 pression at the transcriptional level, since PDTC abolished iNOS mRNA accumulation.
137 ion at the post-transcriptional level, since PDTC did not affect IL-1beta-induced Cox-2 mRNA levels b
138                               Spionolactone, PDTC, and NAC each attenuated these responses suggesting
139            Co-treatment with spironolactone, PDTC, or NAC attenuated these molecular and cellular res
140                                Surprisingly, PDTC was a very potent inducer of HO-1 gene expression,
141                  We further demonstrate that PDTC activates heat-shock factor 1 (HSF1), one of severa
142                                We found that PDTC increased p53 cysteine residue oxidation in vivo.
143                          We report here that PDTC and NAC induce apoptosis in rat and human smooth mu
144        In this communication, we report that PDTC inhibits the activation of temperature-sensitive mu
145 eterologous promoter construct revealed that PDTC inhibited VCAM-1 and E-selectin, but to a lesser ex
146  kappaB in most cells; however, we show that PDTC is also a potent scavenger of NO through formation
147                                          The PDTC concentration-dependent reductions in iNOS activity
148 cavenging of endogenously produced NO by the PDTC iron complex.
149                                       In the PDTC group, only 5 tumors were BRAF(V600E)-positive, and
150           Pyridine-2,6-bis(thiocarboxylate) (PDTC), produced by certain pseudomonads, is a sulfur-con
151 m mice lacking nNOS responds more rapidly to PDTC compared with astrocytes from wild-type mice.
152 nguished between PDTCs defined by the Turin (PDTC-Turin) versus MSKCC (PDTC-MSK) criteria, respective
153     All of these changes were abolished when PDTC was given together with 7-NI.
154                 We next investigated whether PDTC treatment altered the p53 redox state.
155                                         With PDTC administration, a threefold decrease in NF-kappaB a
156       Combined treatment of HCA-7 cells with PDTC and SC 58125 resulted in an additive decrease in PG
157 atment of cultured HepG2 hepatoma cells with PDTC inhibits IL-6-stimulated tyrosine phosphorylation a
158                   Pretreatment of cells with PDTC reduced and delayed the activation of Syk kinases a
159               Pretreatment of AGS cells with PDTC, which blocks NF-kappa B activation, inhibited H. p
160 ead genomic disruptions in ATC compared with PDTC underscore their greater virulence and higher morta
161 ormation of mononitrosyl iron complexes with PDTC.
162 nd a primary culture of rat hepatocytes with PDTC restored insulin responsiveness that was abrogated
163             In vivo, rabbits pretreated with PDTC before LPS infusion showed significantly less neutr
164 ession was blocked in HUVECs pretreated with PDTC before TNF-alpha, IL-1, or LPS stimulation.
165 edly enhanced in lymphocytes pretreated with PDTC, and another antioxidant, N-acetylcysteine, did not
166  in TNF-alpha-treated HUVECs pretreated with PDTC.
167 cells decreased within 3 h of treatment with PDTC and was reduced to 30% at 12 h.
168 ation-independent manner, and treatment with PDTC mitigated the response.
169 ssayed for CAT activity after treatment with PDTC.

 
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