ライフサイエンスコーパス: Topo I

1 Topo I activity in prostates of Nkx3.1+/- and Nkx3.1-/-

2 Topo I and II appear to be essential for viral DNA repli

3 Topo I and Topo IIalpha levels decreased at > 24 h.

4 Topo I binding also stimulates the production of large m

5 Topo I cleavage during necrosis was assessed by immunobl

6 Topo I could be coimmunoprecipitated with Zta, but this

7 Topo I could play an active role in strand exchange, eit

8 Topo I fragments were generated as fusion proteins using

9 Topo I hyperphosphorylation also increases its interacti

10 Topo I is a class 1B DNA-resolving enzyme that is ubiqui

11 Topo I is a ubiquitous enzyme which can be converted to

12 Topo I is also stored maternally in early embryos.

13 Topo I is required for larval growth and cell proliferat

14 Topo I likely functions during activation by enhancing t

15 Topo I, in turn, appeared to be involved in recruiting R

16 Topo I- and IIalpha-mediated relaxation and cell viabili

17 Topo I-containing sera induced significantly higher leve

18 Topo I-reactive T cell lines generated from the twins ha

19 Topo I-reactive T cell lines were generated from the twi

20 Topo I-specific T cell clones derived from SSc subjects

21 The complete gene encoding Topoisomerase 1 (Topo I) from Mycobacterium tuberculosis (MTb), Erdman st

22 in p53/p21 and 2-5-fold decreases in bcl-2, Topo I, Topo IIalpha, and cyclins A and B1, with no chan

23 3d inhibited 47% Topo I (camptothecin, 34%) and 20% Topo II (etoposide 24

24 reatment of prostate cancer cells with 2-5A, Topo I inhibitors, and TRAIL.

25 nsformation by EBV, produced IgM Abs against Topo I.

26 n addition, our results suggest that altered Topo-I function may be associated with repression of HIF

27 cipitated from LNCaP cells, where NKX3.1 and Topo I were found to colocalize in the nucleus and comig

28 e showed that the interaction between E1 and Topo I is decreased in the presence of DNA.

29 EFb, and these factors resolve from Spt6 and Topo I.

30 ns stabilize the interaction between Zta and Topo I.

31 Autoreactive anti-DNA topoisomerase I (anti-Topo I) Abs are commonly detected in sera of systemic sc

32 ific activation of B cells resulting in anti-Topo I Ab production in vitro and therefore are believed

33 The molecular targets of anti-Topo I Ab on Topo I domains remain to be further defined

34 molecular recognition pattern of serum anti-Topo I Ab in 52 SSc patients.

35 molecular recognition pattern of serum anti-Topo I Ab in SSc suggests the presence of a unique antig

36 e N-terminal domain (aa 1-213) by serum anti-Topo I Ab.

37 correlation between the levels of serum anti-Topo I Abs and both disease severity and activity of SSc

38 The highest reactivity of serum anti-Topo I Abs was against the core subdomains I and II (aa

39 The stimulation of E1's origin binding by Topo I is not synergistic with the stimulation by E2.

40 In conclusion, after DNA damage by Topo I poisons, flavopiridol targets homologous recombin

41 lthough the enhanced origin binding of E1 by Topo I requires ATP and Mg2+ for optimal efficiency, ATP

42 omerase I (Topo I) with seven other cellular Topo I enzymes reveal that the enzyme can be divided int

43 rom sequence comparisons with other cellular Topo I enzymes.

44 Unlike the more well-characterized E. coli Topo I, MTb Topo I does not contain a zinc-finger DNA-bi

45 vents that initiates in the nucleus with CPT-Topo I interaction and continues in the cytoplasm result

46 d other observations indicate that active CT Topo I catalyzes the equilibration of a metastable secon

47 ith increasing time of exposure to active CT Topo I.

48 After a third addition of fresh CT Topo I at 240 min, there is no further change in either

49 t up to at least 360 min, when no further CT Topo I is added.

50 he action of calf-thymus topoisomerase I (CT Topo I) on a native supercoiled DNA and, if so, whether

51 The action of CT Topo I on supercoiled p30delta DNA was examined over a r

52 The action of CT Topo I was also examined in the presence of 20 and 40 w/

53 Serially diluted Topo I relaxation reactions at constant DNA/ligand ratio

54 s possessing a deletion of the gene encoding Topo I (topA) are only viable in the presence of an addi

55 Endogenous Topo I and NKX3.1 could be coimmunoprecipitated from LNC

56 In bulk experiments Topo I is more efficient at DNA relaxation, whereas Topo

57 These Abs had low affinity for Topo I and reacted equally to all domains of Topo I.

58 d affinity or no affinity, respectively, for Topo I.

59 are indistinguishable from the native human Topo I purified from HeLa cells.

60 ids of Escherichia coli DNA topoisomerase I (Topo I) and III (Topo III) play in catalysis was examine

61 poisomerase activities, DNA topoisomerase I (Topo I) and III (Topo III).

62 Topoisomerase I (Topo I) and Topo II inhibitors can selectively inhibit E

63 toantibody responses to DNA topoisomerase I (Topo I) are highly specific to patients with systemic sc

64 (CPT), impaired CPT-induced topoisomerase I (Topo I) degradation and ubiquitination, thereby suggesti

65 ffinity column, we isolated topoisomerase I (Topo I) from a PC-3 prostate cancer cell extract.

66 ase I clinical trial of the topoisomerase I (Topo I) poison CPT-11 followed by the cyclin-dependent k

67 quence comparisons of human topoisomerase I (Topo I) with seven other cellular Topo I enzymes reveal

68 t uses closed circular DNA, topoisomerase I (Topo I), and two-dimensional agarose gel electrophoresis

69 autoantigens, including DNA topoisomerase I (Topo I), have been implicated.

70 (ADP-ribose) polymerase and topoisomerase I (Topo I), were observed in endothelial cells after detach

71 ), and more recently, human topoisomerase I (Topo I).

72 volves titration of E. coli topoisomerase I (Topo I).

73 nt tumor biopsies to assess topoisomerase-I (Topo-I) activity were obtained from 11 patients.

74 silon, PCNA, RFC, RFA, DNA ligase I, NDH II, Topo I and Topo II) and cell cycle proteins (Cyclins A,

75 Escherichia coli topoisomerases I and III (Topo I and Topo III) relax negatively supercoiled DNA an

76 generalized DNA binding domain of Topo III, Topo I, and a hybrid topoisomerase polypeptide containin

77 e combination of these properties results in Topo I having an overall faster total relaxation rate, e

78 on of the Topo I-DNA complex and to increase Topo I cleavage of DNA.

79 s of beta-lap or camptothecin (CPT), a known Topo I poison.

80 he circular dichroism spectra of full-length Topo I and Topo70 demonstrates that residues 1-174 (appr

81 f the hydrodynamic properties of full-length Topo I, Topo70, and Topo58 demonstrates that the core, l

82 more well-characterized E. coli Topo I, MTb Topo I does not contain a zinc-finger DNA-binding motif

83 Recombinant MTb Topo I is enzymatically active, relaxing negatively supe

84 asts and in CEM/C2 cells expressing a mutant Topo I protein that fails to bind CPT.

85 In the presence of compensatory mutations, Topo I deletion strains grow normally; however, if Topo

86 roliferative responses to full-length native Topo I unless exogenous IL-2 was added.

87 which encodes amino acids 209 through 386 of Topo I, but not to F10, which encodes amino acids 209 th

88 ainst the core subdomain III (aa 433-636) of Topo I.

89 nhibitor against the catalytic activities of Topo I and Topo IIalpha.

90 meodomain protein can modify the activity of Topo I and may have implications for organ-specific DNA

91 Tnp, inhibits the DNA relaxation activity of Topo I in vivo as well as in vitro.

92 The binding of equimolar amounts of Topo I to NKX3.1 caused displacement of NKX3.1 from its

93 Noncovalent binding of Topo I to plasmid DNA or to short duplex oligonucleotide

94 Small interfering RNA depletion of Topo I also inhibited the Zta-dependent activation of ly

95 e putative generalized DNA binding domain of Topo I.

96 Topo I and reacted equally to all domains of Topo I.

97 T cell responses to the full-length form of Topo I presented by dendritic cells were considerably lo

98 ponses, would present either of two forms of Topo I to T cells more efficiently than PBMC APCS: Using

99 vity cannot be attributed to inactivation of Topo I, the molecular target of camptothecin, because le

100 In contrast, inhibition of Topo I by topotecan results in a compensatory increase i

101 hat residues 1-174 (approximately 21 kDa) of Topo I are largely if not completely unfolded.

102 lar concentration (50 nM) in the presence of Topo I (37 degrees C), induces DNA cleavage between thre

103 carboxyl-terminal 312 amino acid residues of Topo I onto the truncated molecule stimulates topoisomer

104 The molecular targets of anti-Topo I Ab on Topo I domains remain to be further defined.

105 that one or more immunodominant epitopes on Topo I is located between amino acids 276 and 386.

106 the combination of 2-5A with either TRAIL or Topo I inhibitor, whereas normal prostate epithelial cel

107 f CPT-treated cells and addition of purified Topo I does not restore replication activity.

108 ation and ubiquitination, thereby suggesting Topo I to be a novel Cul4-dependent substrate.

109 entity compared to E. coli and Synechococcus Topo I is 22 and 30%, respectively.

110 We recently demonstrated that Topo I-specific T cells are components of the T cell rep

111 Here, we show that Topo I specifically stimulates the origin binding of E1

112 Our results suggest that Topo I participates in the initiation of papillomavirus

113 1 binding to OriLyt in vivo, suggesting that Topo I promotes replication protein assembly at OriLyt.

114 To characterize the Topo I-specific T cell, 15 T cell clones reactive with T

115 des are generated based upon the form of the Topo I and the APC that processes it.

116 ding to Topo I occurred independently of the Topo I NH2-terminal domain.

117 acts with Topo I to enhance formation of the Topo I-DNA complex and to increase Topo I cleavage of DN

118 We found that the Topo I inhibitor camptothecin and, to a lesser extent, t

119 F-1 and VEGF inhibition, the activity of the Topo-I inhibitors tested is associated with induction of

120 NKX3.1 binding to Topo I occurred independently of the Topo I NH2-terminal

121 68) showed enhanced apoptosis in response to Topo I inhibitor alone or in combination with TRAIL.

122 vigorous T cell proliferation in response to Topo I polypeptide fragments presented by either APC typ

123 APC may be involved in breaking tolerance to Topo I in the early stages of development of SSC:

124 es in vitro, including type I topoisomerase (Topo I); however, its exact intracellular target(s) and

125 combination treatments with a topoisomerase (Topo) I inhibitor (camptothecin, topotecan, or SN-38) an

126 cin (CPT), which inhibits DNA topoisomerase (Topo) I activity and causes DNA double-strand breaks dur

127 To elucidate the effect of topoisomerase (Topo) I inhibitors in the modulation of Topo II levels a

128 ed camptothecin analogues and topoisomerase (Topo)-I inhibitors.

129 They include topoisomerases (Topo) I and II, MSH2/6, RecQL, poly(ADP-ribose) polymera

130 en ligand and its association constant under Topo I relaxation conditions.

131 for strand annealing to a purified vaccinia Topo I-DNA (vTopo-DNA) covalent complex containing a sin

132 ed proteolysis pattern of the vaccinia viral Topo I, indicating that the two enzymes belong to separa

133 educed compared with wild-type mice, whereas Topo I activity in livers, where no NKX3.1 is expressed,

134 long pauses before relaxation runs, whereas Topo I relaxes DNA in slow processive runs but with shor

135 fectiveness of combination chemotherapy with Topo I and Topo II inhibitors.

136 Tn5 Tnp copurifies with Topo I while nonkilling derivatives of Tnp, Delta37Tnp a

137 but not sufficient, for the interaction with Topo I.

138 uggesting that RNA polymerase interacts with Topo I and not Tnp.

139 NKX3.1 interacts with Topo I to enhance formation of the Topo I-DNA complex an

140 cific T cell, 15 T cell clones reactive with Topo I were generated from two patients with SSc and thr