ライフサイエンスコーパス: mithramycin

1 assays and treatment with the Sp-1 inhibitor mithramycin.

2 and D-mycarose, of the anticancer antibiotic mithramycin.

3 strategies, and it showed less toxicity than mithramycin.

4 rsor, premithramycin B, into the active drug mithramycin.

5 tent of TAC hypertrophy and was inhibited by mithramycin.

6 on and attachment of the A-B disaccharide in mithramycin.

7 ffects of the GC-selective DNA-binding drug, Mithramycin A (MA) on hdm2 mRNA transcription, trafficki

8 In addition, both BA treatment and mithramycin A (MMA) treatment inhibited lung tumor growt

9 Mithramycin A (trade name Plicamycin) is an aureolic aci

10 Here we demonstrate that mithramycin A and its structural analog chromomycin A3 a

11 Together, these results suggest that mithramycin A and its structural analogs may be effectiv

12 Binding to DNA was inhibited by mithramycin A and was greater in nuclear extracts from c

13 The protective effects of mithramycin A cannot be attributed to global inhibition

14 A treatment and inhibition of the binding by mithramycin A decreased TPA-induced promoter activity as

15 ed previously differ in their sensitivity to mithramycin A inhibition; the hypoxia-mimic-induced expr

16 Sp1 inhibition in vivo by mithramycin A leads to down-regulation of a luciferase r

17 Sp family factors binding to this GC box by mithramycin A led to a significant increase in the endog

18 by the observation that Sp1 knockdown using mithramycin A or shRNA decreases DNMT1 protein levels, w

19 Mithramycin A or Sp1-specific short interfering RNA down

20 Combined treatment with bevacizumab and mithramycin A produced synergistic tumor suppression, wh

21 f Sp1-mediated transcriptional activation by mithramycin A reduced endogenous P2X7 receptor levels in

22 rference RNA or inhibition of Sp1 binding by mithramycin A repressed Fyn protein expression.

23 moter and inhibition of Sp1 DNA binding with mithramycin A suppressed the ABCA1 promoter activity and

24 Sp1/Sp3 RNA silencing and mithramycin A treatment significantly inhibited GLTP pro

25 site-directed mutagenesis, ChIP assays, and mithramycin A treatment, we identified the core promoter

26 We correlate the protective effects of mithramycin A with its ability to inhibit enhanced DNA b

27 ced expression of Galpha(i2) is inhibited by mithramycin A, a compound that interferes with Sp1 bindi

28 RNA, a heterozygous Sp1 knock-out mouse, and mithramycin A, a DNA-intercalating agent that inhibits S

29 following Sp1 and Sp3 overexpression, while Mithramycin A, a selective Sp1 inhibitor, reduced the pr

30 Sp1 small interfering RNA and mithramycin A, a Sp1 binding site inhibitor, resulted in

31 C5AC-luc activity, whereas co-treatment with mithramycin A, a Sp1 inhibitor, abolished CS-induced MUC

32 Mithramycin A, a specific inhibitor of Sp1 oligonucleoti

33 Treatment of MDA MB 231 cells with mithramycin A, an inhibitor of Sp1 binding, or siRNA kno

34 Mithramycin A, an inhibitor of Sp1-DNA interaction, redu

35 Treatment with mithramycin A, an Sp1 inhibitor, suppressed the expressi

36 Furthermore, dominant negative SP-1, mithramycin A, and SP-1 shRNA decreased VEGF promoter ac

37 Chemical inhibition of Sp1 binding with mithramycin A, or deletion of the GC boxes, inhibited CO

38 rter gene transfection, and was sensitive to mithramycin A, suggesting the involvement of a specifici

39 a, and 4) inhibition of Sp1 DNA binding with mithramycin A.

40 primary striatal cultures were inhibited by mithramycin A.

41 ndent inhibitory effect of the SP1 inhibitor mithramycin A.

42 rated by the inhibition of Sp1 binding using mithramycin A.

43 ors of the ESET promoter in neurons and that mithramycin, a clinically approved guanosine-cytosine-ri

44 gned to explore the therapeutic potential of mithramycin, a clinically approved guanosine-cytosine-ri

45 alpha-induced TP mRNA levels were reduced by mithramycin, a DNA-binding transcription inhibitor speci

46 Mithramycin, a Sp1 inhibitor, decreased minimal promoter

47 with RU 486 or ablation of Sp1 binding with mithramycin abrogated MAO-A mRNA induction.

48 geting Sox2(+) cells with the antineoplastic mithramycin abrogated tumor growth.

49 eemingly involved in the biosynthesis of the mithramycin aglycon, respectively.

50 one deacetylase inhibitors was attenuated by mithramycin, an inhibitor of Sp1 binding to GC-rich DNA

51 PaCa-2 Sp1 transfectants) when treated with mithramycin, an inhibitor of Sp1 binding, showed a reduc

52 e-induced ubiquitin expression is blocked by mithramycin, an inhibitor of Sp1 binding.

53 factors and are functionally important since mithramycin, an inhibitor of Sp1/Sp3 binding, blocks MUC

54 Initial studies in IEC-6 cells showed that mithramycin, an Sp1 inhibitor, reduced expression of Atp

55 e we use structure-activity relationships of mithramycin analogs to discover that selective DNA-bindi

56 ilitate the generation of chemically diverse mithramycin analogues through combinatorial biosynthesis

57 illaceus mutant, which accumulated three new mithramycin analogues, namely mithramycin SA, demycarosy

58 Furthermore, selected mithramycin analogues, namely, premithramycin B, mithram

59 he production of the D-mycarose (sugar E) of mithramycin and as a ketoreductase seemingly involved in

60 gomer complexes and Ni(2+) > Co(2+) for both mithramycin and chromomycin complexes.

61 The combined pharmacological treatment with mithramycin and cystamine down-regulates ESET gene expre

62 luding antitumour aromatic compounds such as mithramycin and macrolide antibiotics such as erythromyc

63 to MtmOIV and OxyS, which are enzymes in the mithramycin and oxytetracycline biosynthetic pathways, r

64 A-binding drugs, including chromomycin A(3), mithramycin and the novel compound UK-1, were examined v

65 Mithramycin binding sites in the human c-Ki-ras promoter

66 Mithramycin binding within the c-Ki-ras promoter complet

67 atalyzes the key frame-modifying step of the mithramycin biosynthetic pathway and currently the only

68 trate flexibility of post-PKS enzymes of the mithramycin biosynthetic pathway.

69 The Sp1 inhibitor mithramycin blocked stimulation of alpha2(I) collagen mR

70 The Spl inhibitor mithramycin blocked stimulation of the alpha2(I) collage

71 B into the tricyclic immediate precursor of mithramycin, can act on a substrate analogue with a modi

72 However, the new mithramycin derivatives bear unexpectedly shorter 3-side

73 Instead of obtaining premithramycin and mithramycin derivatives with a modified E-sugar upon ina

74 s, two premithramycin-type molecules and two mithramycin derivatives, were isolated from mutant strai

75 esis approaches, we have generated seven new mithramycin derivatives, which differ from the parental

76 potentially achievable in clinical settings, mithramycin diminished basal as well as CSC-mediated inc

77 cterize the interaction of DNA binding drugs mithramycin, distamycin, and berenil with an intermolecu

78 f a transgenic mouse model of HD (R6/2) with mithramycin extended survival by 29.1%, greater than any

79 phageal cancers, and support clinical use of mithramycin for repressing ABCG2 and inhibiting stem cel

80 AI-1 and p21 is blocked by the Sp1 inhibitor mithramycin, implicating Sp1 in the in vivo regulation o

81 Two such anthracyclines, chromomycin and mithramycin, improved altered nucleosome homeostasis in

82 ed a binding preference for chromomycin over mithramycin in the presence of Co(2+) and Ni(2+).

83 ated Nix promoter activity was suppressed by mithramycin inhibition of Sp1-DNA interactions.

84 A possible biological significance of mithramycin interaction with intramolecular triplex is d

85 it is Food and Drug Administration-approved, mithramycin is a promising drug for the treatment of HD.

86 Mithramycin is an antitumor compound produced by Strepto

87 Mithramycin is an aureolic acid-type antimicrobial and a

88 loring enzymes involved in the production of mithramycin is an effective way of gaining further infor

89 Mithramycin (MIT) and tolfenamic acid (TA) inhibit the a

90 The aureolic acid antitumor antibiotic mithramycin (MTM) inhibits both cancer growth and bone r

91 DNA binding natural product mithramycin (MTM) is a potent antagonist of oncogenic tr

92 nalized pentyl side chain attached at C-3 of mithramycin (MTM), we focused on a post-polyketide synth

93 pression correlates with protective doses of mithramycin or its analogs.

94 e p21 when Sp1 was functionally inhibited by mithramycin or siRNA-mediated down-regulation.

95 W, a gene located ca. 8 kb downstream of the mithramycin-PKS genes, yielded an S. argillaceus mutant,

96 The antitumor antibiotic mithramycin prolongs survival of mouse models of Hunting

97 ated three new mithramycin analogues, namely mithramycin SA, demycarosyl-mithramycin SK, and mithramy

98 hramycin SA, demycarosyl-mithramycin SK, and mithramycin SK (MTM-SK).

99 e MTM 3-pentyl side chain led to a compound (mithramycin SK) with the same DNA binding specificity bu

100 ramycin analogues, namely, premithramycin B, mithramycin SK, 7-demethylmithramycin, 4E-ketomithramyci

101 nalogues, namely mithramycin SA, demycarosyl-mithramycin SK, and mithramycin SK (MTM-SK).

102 moter activity were all readily repressed by mithramycin, suggesting regulation by GC-rich DNA sequen

103 Microarray analyses revealed that mithramycin targeted multiple stem cell-related pathways

104 Furthermore, the addition of mithramycin to pre-formed triplex by c-Ki-ras promoter d

105 Mithramycin treatment prevented the increase in H3 methy

106 onal mechanism for the salubrious effects of mithramycin, we examined transcriptional dysfunction in

107 Both chromomycin and mithramycin were shown to bind preferentially to GC-rich

108 We had correlated protection by mithramycin with its ability to bind to GC-rich DNA and