ライフサイエンスコーパス: PMO

1 PMO CTG25 reduced HTT-induced cytotoxicity in vitro and

2 PMO localization is sustained in inflammatory foci where

3 PMO with or without reperfusion hemorrhage led to chroni

4 PMOs have an unusual surface-exposed active site with a

5 PMOs share several conserved features, including a monoc

6 PMOs show great promise in reducing the cost of conversi

7 ginine-rich peptides conjugated to the 5TERM PMO sequence in order to evaluate efficacy and toxicity

8 h-active PMOs, supporting the existence of a PMO superfamily with a much broader range of substrates.

9 biological redox partner of cellulose-active PMOs, can serve as the electron donor for NCU08746.

10 more than 20 genes encoding cellulose-active PMOs, suggesting a diversity of biological activities.

11 Starch-active PMOs provide an expanded perspective on studies of starc

12 that NCU08746 and homologs are starch-active PMOs, supporting the existence of a PMO superfamily with

13 erize the spatiotemporal relationships among PMO, iron deposition, infarct resorption, and left ventr

14 Using this method, the AMO and PMO are found to explain a large proportion of internal

15 Phosphorodiamidate morpholinos (PMOs) and PMO-DNA chimeras have been prepared on DNA synthesizers

16 multidecadal variability (termed "AMO" and "PMO," respectively).

17 The results suggest that antisense PMO-mediated blocking of cis-acting elements of flavivir

18 ucting property of the novel porphyrin-based PMO film, indicating the potential of PMO materials as a

19 inal capillaries was greater after TGF-beta1-PMO treatment compared with control PMO-treated cells.

20 TGF-beta1-PMO treatment of diabetic CD34(+) cells resulted in incr

21 orodiamidate morpholino oligomers (TGF-beta1-PMOs) and analyzed for cell surface CXCR4 expression, ce

22 f oxidative depolymerization of cellulose by PMOs and considers their biological function and phyloge

23 )-morpholino oligonucleotide (MO) conjugate (PMO) that has an antibiotic effect in culture had some c

24 n, effect of transductive peptide conjugated PMO (PPMO) on tachyzoite protein expression and replicat

25 gle low-dose injection of peptide-conjugated PMO AO.

26 Peptide-conjugated PMOs (PPMOs) were developed to target acpP, which encode

27 ured in the presence of antisense or control PMO for 72 hours and analyzed.

28 GF-beta1-PMO treatment compared with control PMO-treated cells.

29 as compared with cells treated with control PMO.

30 mRNA targets when compared to individual CPP-PMO conjugates both in cell culture and in vivo in the m

31 se activity and serum-binding profile of CPP-PMO.

32 llular toxicity and serum binding for 24 CPP-PMOs.

33 The most active bi-specific CPP-PMOs demonstrated comparable exon skipping levels for bo

34 nreducing end product formed by an N. crassa PMO is a 4-ketoaldose.

35 The 3'CSI PMO also inhibited mosquito-borne flaviviruses other tha

36 hibited viral translation, whereas the 3'CSI PMO did not significantly affect viral translation but s

37 N virus were treated with the 5'End or 3'CSI PMO, virus titers were reduced by approximately 5 to 6 l

38 ion analyses showed that the 5'End and 3'CSI PMOs suppressed viral infection through two distinct mec

39 CTGn PMOs also suppressed HTT expression, with the extent of

40 For more than a decade, PMOs were incorrectly annotated as family 61 glycoside h

41 Different PMOs isolated from Neurospora crassa were found to gener

42 Additionally the N,N-dimethylamino PMO-DNA chimeras were found to stimulate RNaseH1 activit

43 ovel Arg-rich peptide was conjugated to each PMO for efficient cellular delivery.

44 We conclude that efficient PMO delivery into muscle requires two concomitant events

45 The 5'End PMO inhibited viral translation, whereas the 3'CSI PMO d

46 efficient production of dystrophin following PMO administration coincide with areas of myofiber regen

47 Clinical trials for PMO show variable and sporadic dystrophin rescue.

48 Crystallized iron deposition from PMO is directly related to proinflammatory burden, infar

49 analyses, showed that the majority of fungal PMOs fall into three major groups with distinctive activ

50 But it remains unclear how PMO, a phenomenon limited to the acute/subacute period o

51 b cells activated Wnt canonical signaling in PMOs and that DKK1 blocked osteoblast proliferation and

52 ent of HeLa cells with fluorescently labeled PMO chimeras demonstrated that these analogues were effi

53 e monooxygenases (PMOs), also known as lytic PMOs (LPMOs), enhance the depolymerization of recalcitra

54 They are also known collectively as lytic PMOs, or LPMOs, and individually as AA9 (formerly GH61),

55 is attributed to enhancement of GF-mediated PMO uptake in the muscle.

56 to a natural DNA duplex, the amino modified PMO was found to have a higher melting temperature with

57 uitous fungal polysaccharide monooxygenases (PMOs) (also known as GH61 proteins, LPMOs, and AA9 prote

58 and bacterial polysaccharide monooxygenases (PMOs) are capable of oxidatively cleaving chitin, cellul

59 Polysaccharide monooxygenases (PMOs), also known as lytic PMOs (LPMOs), enhance the dep

60 per-dependent polysaccharide monooxygenases (PMOs), formerly known as GH61 proteins, have recently be

61 Phosphorodiamidate morpholinos (PMOs) and PMO-DNA chimeras have been prepared on DNA syn

62 ow systemic doses, we demonstrate that B-MSP-PMO restores high-level, uniform dystrophin protein expr

63 t time that a chimeric fusion peptide (B-MSP-PMO) consisting of a muscle-targeting heptapeptide (MSP)

64 ved features suggested several potential new PMO families in the fungus Neurospora crassa that are li

65 s that persistent microvascular obstruction (PMO) is more predictive of major adverse cardiovascular

66 th dystrophic lesions, and second, fusion of PMO-loaded myoblasts into repairing myofibers.

67 -based PMO film, indicating the potential of PMO materials as a basis for optoelectroactive systems.

68 events: first, accumulation and retention of PMO within inflammatory foci associated with dystrophic

69 otency, selectivity, and predicted safety of PMO conjugates make this approach attractive for the dev

70 m contributes to enhanced cellular uptake of PMO in the muscle.

71 Conjugations of PMOs to a single CPP were carried out through an amide b

72 These data demonstrate the potential of PMOs as an approach to suppressing the expression of mut

73 de) and conjugated to a morpholino oligomer (PMO) AO directs highly efficient systemic dystrophin spl

74 Unique peptide-morpholino oligomer (PMO) conjugates have been designed to bind and promote t

75 4658 phosphorodiamidate morpholino oligomer (PMO) in patients with Duchenne muscular dystrophy.

76 ense phosphorodiamidate morpholino oligomer (PMO) were used to elucidate the role of beta-catenin in

77 ip6a-morpholino phosphorodiamidate oligomer (PMO), which demonstrates potent efficacy in both the CNS

78 oth phosphorodiamidate morpholino oligomers (PMO) and 2'-O-methyl phosphorothioate.

79 Phosphorodiamidate morpholino oligomers (PMO) inhibit gene expression in a sequence-specific mann

80 delivery of antisense morpholino oligomers (PMO).

81 of phosphorodiamidate morpholino oligomers (PMOs) has shown great promise for exon-skipping therapy

82 Phosphorodiamidate morpholino oligomers (PMOs) represent a neutral class of antisense agents that

83 of phosphorodiamidate morpholino oligomers (PMOs) with glucose enhances exon-skipping activity in Du

84 on phosphorodiamidate morpholino oligomers (PMOs), ASOs that are especially stable, highly soluble a

85 of phosphorodiamidate morpholino oligomers (PMOs), whose sequences are complementary to RNA elements

86 as phosphorodiamidate morpholino oligomers (PMOs).

87 osphorodiamidate morpholino oligonucleotide (PMO) SSOs to a single CPP for simultaneous delivery and

88 oying morpholino antisense oligonucleotides (PMO-AO) to exclude disruptive exons from the mutant DMD

89 Baird using perturbation molecular orbital (PMO) theory, and since then it has been confirmed throug

90 n oriented periodic mesoporous organosilica (PMO) film has been developed.

91 Periodic Mesoporous Organosilicas (PMOs) were developed in 1999 and are basically ordered t

92 cancer cells with primary mouse osteoblasts (PMOs) or in bone organ cultures) showed that MDA PCa 2b

93 P-PMO showed low nonspecific inhibitory activity against t

94 Prophylactic 5TERM P-PMO treatment decreased the amount of weight loss associ

95 5TERM P-PMO treatment reduced viral titers in target organs and

96 ation followed by delayed treatment, 5TERM P-PMO treatment was not protective and increased morbidity

97 Active P-PMO were effective when administered at any time prior t

98 rgeted P-PMO and a random-sequence control P-PMO showed low inhibitory activity against SARS coronavi

99 ed suggests that with further development, P-PMO may provide an effective therapeutic approach agains

100 conjugated antisense morpholino oligomers (P-PMO) were designed to bind by base pairing to specific s

101 In uninfected mice, prolonged P-PMO treatment did not result in weight loss or detectabl

102 Several virus-targeted P-PMO and a random-sequence control P-PMO showed low inhib

103 Certain other virus-targeted P-PMO reduced virus-induced cytopathology and cell-to-cell

104 passages in the presence of a TRS-targeted P-PMO, partially drug-resistant SARS-CoV mutants arose whi

105 ions at the binding site of a TRS-targeted P-PMO.

106 dity in the treated group, suggesting that P-PMO may cause toxic effects in diseased mice that were n

107 The P-PMO were tested for their capacity to inhibit production

108 Two P-PMO targeting the viral transcription-regulatory sequenc

109 e phosphorodiamidate morpholino oligomers (P-PMOs).

110 Ten P-PMOs directed against various target sites in the viral

111 At 6 days after infection, a P4-PMO targeting the 3'-terminal nucleotides of the DEN-2 v

112 ed in Vero cells incubated with 20 microM P4-PMO compounds.

113 DEN-2 virus genome and a random-sequence P4-PMO showed relatively little suppression of DEN-2 virus

114 Two P4-PMO compounds, 5'SL and 3'CS (targeting the 5'-terminal

115 P4-PMOs targeting the AUG translation start site region of

116 The 5'SL and 3'CS P4-PMOs did not suppress the replication of West Nile virus

117 phosphorodiamidate morpholino oligomers (P4-PMOs) were evaluated for their ability to inhibit replic

118 rates the high clinical potential of peptide-PMO therapy for SMA.

119 AOs of morpholino phosphoroamidate (PMO) and 2'-O-methyl phosphorothioate RNA (2'Ome RNA) ch

120 Pip6a-PMO yields SMN expression at high efficiency in peripher

121 Pip6a-PMO, a recently developed conjugate, is particularly eff

122 Likewise, Pip6a-PMO mainly accumulates in cytoplasmic vesicles in primar

123 ficking and the biological activity of Pip6a-PMO in skeletal muscle cells and primary cardiomyocytes.

124 The potent systemic efficacy of Pip6a-PMO, targeting both peripheral as well as CNS tissues, d

125 Overall, Pip6a-PMO appears as the most efficient conjugate to date (low

126 Our results indicate that Pip6a-PMO is taken up in the skeletal muscle cells by an energ

127 Collectively, we show that GF potentiates PMO activity by replenishing cellular energy stores unde

128 e-fructose (GF) formulation that potentiates PMO activity, completely corrects aberrant Dmd transcrip

129 plementary DNA or RNA, whereas the remaining PMO analogues having morpholino, dimethylamino, or N-met

130 Here, we show that robust PMO uptake and efficient production of dystrophin follow

131 These results suggest PMO compounds have powerful therapeutic and investigativ

132 The synthesized PMO film has a face-centered orthorhombic porous structu

133 We demonstrate that PMO cellular uptake is energy dependent, and that ATP fr

134 We hypothesized that PMO resolves into chronic iron crystals within MI territ

135 We conclude from the emerging data that PMOs display advantageous pharmaceutical properties in c

136 linical and clinical studies have shown that PMOs demonstrate improved efficacy, excellent kinetic be

137 The PMO and the CPP can be mixed together, as has been shown

138 The effect of the PMO appears to be bacteriocidal.

139 he gene-specific effects are a result of the PMO, and the nonspecific effects are a result of the unl

140 e CTG repeat length and concentration of the PMO.

141 mproved purification procedure separates the PMO from the free CPP and MO.

142 We conclude that the PMO antisense to beta-catenin effectively inhibits synth

143 Among them, PMOs targeting the 5'-terminal 20 nucleotides (5'End) or

144 These PMOs exhibited various degrees of antiviral activity upo

145 We designed three PMOs to selectively target expanded CAG repeat tracts (C

146 necting regioselectivity of the chemistry to PMO phylogeny.

147 t of this deposition was strongly related to PMO volume (r>0.8).

148 he AMO and a substantially negative-trending PMO are seen to produce a slowdown or "false pause" in w

149 eat tracts (CTG22, CTG25 and CTG28), and two PMOs to selectively target sequences flanking the HTT CA

150 the simplistic synthesis procedures, various PMO analogues are now readily available and should there