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1 on and attachment of the A-B disaccharide in mithramycin.
2 assays and treatment with the Sp-1 inhibitor mithramycin.
3 and D-mycarose, of the anticancer antibiotic mithramycin.
4 strategies, and it showed less toxicity than mithramycin.
5 rsor, premithramycin B, into the active drug mithramycin.
6 tent of TAC hypertrophy and was inhibited by mithramycin.
7 eloping 24 hours after the third infusion of mithramycin (25 mcg/kg, 6 hours/infusion, every day x7,
8 ffects of the GC-selective DNA-binding drug, Mithramycin A (MA) on hdm2 mRNA transcription, trafficki
9 ugs, mitomycin C (MIC(50) = 0.25 mug/ml) and mithramycin A (MIC(50) = 0.015 mug/ml), and the naturall
10      Herein, we show for the first time that mithramycin A (Mit-A) can successfully inhibit CSC proli
11           In addition, both BA treatment and mithramycin A (MMA) treatment inhibited lung tumor growt
12                                              Mithramycin A (MTM) inhibits the oncogenic transcription
13                                              Mithramycin A (trade name Plicamycin) is an aureolic aci
14                                              Mithramycin A also reduced Sp1- and GR-mediated transact
15                                              Mithramycin A and aureomycin were further found to inhib
16                     Here we demonstrate that mithramycin A and its structural analog chromomycin A3 a
17         Together, these results suggest that mithramycin A and its structural analogs may be effectiv
18              Binding to DNA was inhibited by mithramycin A and was greater in nuclear extracts from c
19                    The protective effects of mithramycin A cannot be attributed to global inhibition
20 A treatment and inhibition of the binding by mithramycin A decreased TPA-induced promoter activity as
21 ed previously differ in their sensitivity to mithramycin A inhibition; the hypoxia-mimic-induced expr
22                    Sp1 inhibition in vivo by mithramycin A leads to down-regulation of a luciferase r
23  Sp family factors binding to this GC box by mithramycin A led to a significant increase in the endog
24  by the observation that Sp1 knockdown using mithramycin A or shRNA decreases DNMT1 protein levels, w
25                                              Mithramycin A or Sp1-specific short interfering RNA down
26      Combined treatment with bevacizumab and mithramycin A produced synergistic tumor suppression, wh
27 f Sp1-mediated transcriptional activation by mithramycin A reduced endogenous P2X7 receptor levels in
28 rference RNA or inhibition of Sp1 binding by mithramycin A repressed Fyn protein expression.
29 moter and inhibition of Sp1 DNA binding with mithramycin A suppressed the ABCA1 promoter activity and
30 tion of Sp1 by IFI16 or pharmacologically by Mithramycin A suppresses reactivation of latent HIV-1 in
31                    Sp1/Sp3 RNA silencing and mithramycin A treatment significantly inhibited GLTP pro
32  site-directed mutagenesis, ChIP assays, and mithramycin A treatment, we identified the core promoter
33       We correlate the protective effects of mithramycin A with its ability to inhibit enhanced DNA b
34 t potent FDA-approved drugs (mitomycin C and mithramycin A) and a promising natural product (aureomyc
35 ced expression of Galpha(i2) is inhibited by mithramycin A, a compound that interferes with Sp1 bindi
36 RNA, a heterozygous Sp1 knock-out mouse, and mithramycin A, a DNA-intercalating agent that inhibits S
37 lencing Sp1 protein expression with siRNA or mithramycin A, a drug that preferentially binds GC-rich
38                               Interestingly, mithramycin A, a neuroprotective antibiotic that prefere
39  following Sp1 and Sp3 overexpression, while Mithramycin A, a selective Sp1 inhibitor, reduced the pr
40                Sp1 small interfering RNA and mithramycin A, a Sp1 binding site inhibitor, resulted in
41 C5AC-luc activity, whereas co-treatment with mithramycin A, a Sp1 inhibitor, abolished CS-induced MUC
42                                              Mithramycin A, a specific inhibitor of Sp1 oligonucleoti
43                                     Further, mithramycin A, an inhibitor of HDAC inhibition, reduced
44           Treatment of MDA MB 231 cells with mithramycin A, an inhibitor of Sp1 binding, or siRNA kno
45                                              Mithramycin A, an inhibitor of Sp1-DNA interaction, redu
46                               Treatment with mithramycin A, an Sp1 inhibitor, suppressed the expressi
47         Furthermore, dominant negative SP-1, mithramycin A, and SP-1 shRNA decreased VEGF promoter ac
48      Chemical inhibition of Sp1 binding with mithramycin A, or deletion of the GC boxes, inhibited CO
49 rter gene transfection, and was sensitive to mithramycin A, suggesting the involvement of a specifici
50 rated by the inhibition of Sp1 binding using mithramycin A.
51 a, and 4) inhibition of Sp1 DNA binding with mithramycin A.
52  primary striatal cultures were inhibited by mithramycin A.
53 ndent inhibitory effect of the SP1 inhibitor mithramycin A.
54 ors of the ESET promoter in neurons and that mithramycin, a clinically approved guanosine-cytosine-ri
55 gned to explore the therapeutic potential of mithramycin, a clinically approved guanosine-cytosine-ri
56 alpha-induced TP mRNA levels were reduced by mithramycin, a DNA-binding transcription inhibitor speci
57                                              Mithramycin, a Sp1 inhibitor, decreased minimal promoter
58  with RU 486 or ablation of Sp1 binding with mithramycin abrogated MAO-A mRNA induction.
59 geting Sox2(+) cells with the antineoplastic mithramycin abrogated tumor growth.
60                                           As mithramycin affects cellular response to bile acid treat
61 eemingly involved in the biosynthesis of the mithramycin aglycon, respectively.
62 one deacetylase inhibitors was attenuated by mithramycin, an inhibitor of Sp1 binding to GC-rich DNA
63  PaCa-2 Sp1 transfectants) when treated with mithramycin, an inhibitor of Sp1 binding, showed a reduc
64 e-induced ubiquitin expression is blocked by mithramycin, an inhibitor of Sp1 binding.
65 factors and are functionally important since mithramycin, an inhibitor of Sp1/Sp3 binding, blocks MUC
66   Initial studies in IEC-6 cells showed that mithramycin, an Sp1 inhibitor, reduced expression of Atp
67 e we use structure-activity relationships of mithramycin analogs to discover that selective DNA-bindi
68 ilitate the generation of chemically diverse mithramycin analogues through combinatorial biosynthesis
69 illaceus mutant, which accumulated three new mithramycin analogues, namely mithramycin SA, demycarosy
70                        Furthermore, selected mithramycin analogues, namely, premithramycin B, mithram
71 he production of the D-mycarose (sugar E) of mithramycin and as a ketoreductase seemingly involved in
72 gomer complexes and Ni(2+) > Co(2+) for both mithramycin and chromomycin complexes.
73  The combined pharmacological treatment with mithramycin and cystamine down-regulates ESET gene expre
74 luding antitumour aromatic compounds such as mithramycin and macrolide antibiotics such as erythromyc
75 to MtmOIV and OxyS, which are enzymes in the mithramycin and oxytetracycline biosynthetic pathways, r
76 A-binding drugs, including chromomycin A(3), mithramycin and the novel compound UK-1, were examined v
77                                              Mithramycin binding sites in the human c-Ki-ras promoter
78                                              Mithramycin binding within the c-Ki-ras promoter complet
79 atalyzes the key frame-modifying step of the mithramycin biosynthetic pathway and currently the only
80 trate flexibility of post-PKS enzymes of the mithramycin biosynthetic pathway.
81                            The Sp1 inhibitor mithramycin blocked stimulation of alpha2(I) collagen mR
82                            The Spl inhibitor mithramycin blocked stimulation of the alpha2(I) collage
83  B into the tricyclic immediate precursor of mithramycin, can act on a substrate analogue with a modi
84                   These results suggest that mithramycin causes hepatotoxicity through derangement of
85                                              Mithramycin demonstrates preclinical anticancer activity
86                             However, the new mithramycin derivatives bear unexpectedly shorter 3-side
87      Instead of obtaining premithramycin and mithramycin derivatives with a modified E-sugar upon ina
88 s, two premithramycin-type molecules and two mithramycin derivatives, were isolated from mutant strai
89 esis approaches, we have generated seven new mithramycin derivatives, which differ from the parental
90 potentially achievable in clinical settings, mithramycin diminished basal as well as CSC-mediated inc
91 cterize the interaction of DNA binding drugs mithramycin, distamycin, and berenil with an intermolecu
92 to identify patients who may tolerate higher mithramycin doses.
93 f a transgenic mouse model of HD (R6/2) with mithramycin extended survival by 29.1%, greater than any
94 phageal cancers, and support clinical use of mithramycin for repressing ABCG2 and inhibiting stem cel
95 AI-1 and p21 is blocked by the Sp1 inhibitor mithramycin, implicating Sp1 in the in vivo regulation o
96     Two such anthracyclines, chromomycin and mithramycin, improved altered nucleosome homeostasis in
97 for a genotype-directed clinical trial using mithramycin in patients with thoracic malignancies.
98 ed a binding preference for chromomycin over mithramycin in the presence of Co(2+) and Ni(2+).
99 e undertook to characterize the mechanism of mithramycin-induced acute transaminitis.
100 n bile flow transporters are associated with mithramycin-induced liver function test elevations, and
101       A pharmacogenomics characterization of mithramycin-induced transaminitis revealed that hepatoto
102 mary human hepatocytes, we hypothesized that mithramycin inhibited bile-mediated activation of the fa
103  primary human hepatocytes (P < 0.0001), and mithramycin inhibited chenodeoxycholic acid- and GW4046-
104 ated Nix promoter activity was suppressed by mithramycin inhibition of Sp1-DNA interactions.
105        A possible biological significance of mithramycin interaction with intramolecular triplex is d
106                                              Mithramycin is a FXR expression and FXR transactivation
107 it is Food and Drug Administration-approved, mithramycin is a promising drug for the treatment of HD.
108                                              Mithramycin is an antitumor compound produced by Strepto
109                                              Mithramycin is an aureolic acid-type antimicrobial and a
110 loring enzymes involved in the production of mithramycin is an effective way of gaining further infor
111 lts in a C2 stereoisomer of mithramycin, iso-mithramycin (iso-MTM).
112 ectedly this results in a C2 stereoisomer of mithramycin, iso-mithramycin (iso-MTM).
113                                              Mithramycin (MIT) and tolfenamic acid (TA) inhibit the a
114 MtmW catalyze the final two reactions in the mithramycin (MTM) biosynthetic pathway, the Baeyer-Villi
115       The aureolic acid antitumor antibiotic mithramycin (MTM) inhibits both cancer growth and bone r
116                  DNA binding natural product mithramycin (MTM) is a potent antagonist of oncogenic tr
117 nalized pentyl side chain attached at C-3 of mithramycin (MTM), we focused on a post-polyketide synth
118 nism of drug-induced hepatotoxicity in which mithramycin not only alters farnesoid X receptor (FXR) a
119 pression correlates with protective doses of mithramycin or its analogs.
120 e p21 when Sp1 was functionally inhibited by mithramycin or siRNA-mediated down-regulation.
121 W, a gene located ca. 8 kb downstream of the mithramycin-PKS genes, yielded an S. argillaceus mutant,
122                     The antitumor antibiotic mithramycin prolongs survival of mouse models of Hunting
123                                              Mithramycin promoted glycochenodeoxycholic acid-induced
124 ated three new mithramycin analogues, namely mithramycin SA, demycarosyl-mithramycin SK, and mithramy
125 hramycin SA, demycarosyl-mithramycin SK, and mithramycin SK (MTM-SK).
126 e MTM 3-pentyl side chain led to a compound (mithramycin SK) with the same DNA binding specificity bu
127 ramycin analogues, namely, premithramycin B, mithramycin SK, 7-demethylmithramycin, 4E-ketomithramyci
128 nalogues, namely mithramycin SA, demycarosyl-mithramycin SK, and mithramycin SK (MTM-SK).
129 moter activity were all readily repressed by mithramycin, suggesting regulation by GC-rich DNA sequen
130            Microarray analyses revealed that mithramycin targeted multiple stem cell-related pathways
131                 Furthermore, the addition of mithramycin to pre-formed triplex by c-Ki-ras promoter d
132                                              Mithramycin treatment prevented the increase in H3 methy
133 onal mechanism for the salubrious effects of mithramycin, we examined transcriptional dysfunction in
134                         Both chromomycin and mithramycin were shown to bind preferentially to GC-rich
135              We had correlated protection by mithramycin with its ability to bind to GC-rich DNA and

 
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