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 can effectively silence disease-causing genes and m

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

6 PMOs may thus form a distinct population that is fundame

7 PMOs share several conserved features, including a monoc

8 PMOs show great promise in reducing the cost of conversi

9 ighting role in allorecognition of the CWR-1 PMO domain.

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

11 old mdx mice with the most effective let-7c PMO (i.e. S56) resulted in ca. two-fold higher utrophin

12 te blocking efficiency of a series of let-7c PMOs in vitro.

13 gonucleotide conjugate (AOC) that combines a PMO-targeting exon 44 with an antibody against the trans

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

15 o further test our platform, we synthesize a PMO that targets the genomic mRNA of SARS-CoV-2 and demo

16 h-active polysaccharide monooxygenases (AA13 PMOs) oxidatively degrade starch and can potentially be

17 e that spans the active-site surface of AA13 PMOs favors the binding of helical amylose substrates ov

18 These findings establish that AA13 PMOs preferentially bind and oxidize the helical starch

19 different from previously characterized AA9 PMOs.

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

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

22 he oxidative activities of the starch-active PMOs from the fungi Neurospora crassa and Myceliophthora

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

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

25 iodontitis, and current therapeutics against PMO prevent the aggravated alveolar bone loss of periodo

26 To access the 3'-alkyne PMO fragment, we synthesized 3'-N-propargyl chlorophosph

27 transferrin receptor 1 antibody (alphamTfR1)-PMO conjugates: cleavable and noncleavable linkers, link

28 Our results show that alphamTfR1-PMO conjugates are a potentially effective approach for

29 We demonstrate that alphamTfR1-PMO conjugates induce dystrophin protein restoration in

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

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

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

33 also incorporated to generate PMO-psDNA and PMO-DNA using commercially available 5'-DNA phosphoramid

34 t ASO design modalities, such as PMO-TMO and PMO-MO, which were inaccessible otherwise.

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

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

37 ally relevant ASO design modalities, such as PMO-TMO and PMO-MO, which were inaccessible otherwise.

38 ergent, involving the ligation of a 5'-azide PMO fragment to a 3'-alkyne fragment both in solution an

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

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

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

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

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

44 We show that the catalytic (PMO) domain of CWR-1 was sufficient for checkpoint funct

45 confirm that CWR-1 is a C1-oxidizing chitin PMO.

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

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

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

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

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

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

52 as compared with cells treated with control PMO.

53 kipping potency compared with a conventional PMO control and other widely used nucleotide analogs, su

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

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

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

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

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

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

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

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

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

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

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

65 We designed PMO-based SBOs complementary to the let-7c binding site

66 These findings highlight DG9-PMO as a promising next-generation exon-skipping therapy

67 manized DMD mouse model (hDMDdel45;mdx), DG9-PMO significantly increases exon skipping, restores dyst

68 Mechanistically, DG9-PMO enhances intracellular uptake through multiple endoc

69 Compared to the benchmark R6G peptide, DG9-PMO exhibits greater efficacy in cardiac tissue with no

70 Different PMOs isolated from Neurospora crassa were found to gener

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

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

73 linker with a DAR9.7 were the most effective PMO delivery vehicles in preclinical studies.

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

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

76 re identified in a representative AA9 family PMO from Myceliophthora thermophila (MtPMO9E).

77 hydrodynamic simulations that free-floating PMOs have a unique formation channel via the fragmentati

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

79 fers an innovative therapeutic candidate for PMO with a dual anabolic-antiresorptive profile and oral

80 Mutations of sites in CWR-1 essential for PMO catalytic activity abolished the block in cell fusio

81 istry into PMOs opens up the possibility for PMO synthesis in commercial peptide synthesizers for fut

82 gnized as a promising therapeutic target for PMO.

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

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

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

86 cleotides were also incorporated to generate PMO-psDNA and PMO-DNA using commercially available 5'-DN

87 s is long awaited to explore next-generation PMO chimeras with other therapeutically proven oligonucl

88 perception-hemi-prosopometamorphopsia (hemi-PMO)-to investigate these reference frames.

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

90 However, PMO synthesis has remained challenging for a variety of

91 oses resulted in dose-dependent increases in PMO concentration and exon 44 skipping across a range of

92 lin-stimulated glucose uptake was reduced in PMO-treated muscles of HFD-fed mice.

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

94 The resulting triazole-incorporated PMOs (TzPMOs) have exhibited comparable or improved bind

95 lly, the introduction of Fmoc chemistry into PMOs opens up the possibility for PMO synthesis in comme

96 heart, respectively, with a single 30 mg/kg PMO-equivalent dose.

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

98 Full-length PMOs and TMOs in exceptional overall yields were obtaine

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

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

101 he efficacy of antisense oligonucleotide M12-PMO on dystrophin expression and skeletal muscle enduran

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

103 These results suggest that a modest PMO-induced reduction in myostatin transcript levels is

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

105 Polysaccharide monooxygenase (PMO) catalysis involves the chemically difficult hydroxy

106 wr-1 encodes a polysaccharide monooxygenase (PMO), a class of enzymes associated with extracellular d

107 des a putative polysaccharide monooxygenase (PMO).

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

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

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

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

112 to other AA9 polysaccharide monooxygenases (PMOs), MoPMO9A is not active on cellulose but showed act

113 Moreover, PMOs with longer than 20-mer sequences, including FDA-ap

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

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

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

117 Free-floating multiple PMOs also naturally emerge when neighboring PMOs are cau

118 or intravenous injections of anti-myostatin PMOs.

119 PMOs also naturally emerge when neighboring PMOs are caught by their mutual gravity.

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

121 ekly intravenous administrations of 100 nmol PMO did not reduce myostatin expression, and therefore h

122 The origin of planetary mass objects (PMOs) wandering in young star clusters remains enigmatic

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

124 higher after intramuscular administration of PMO in HFD- than chow-fed mice.

125 as been hampered by insufficient delivery of PMO to cardiac and skeletal muscle.

126 rapeutics, but also for rapid development of PMO candidates to treat new and emerging diseases.

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

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

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

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

131 nable to fast generation of various types of PMO chimeras for biological screening, which will expedi

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

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

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

135 zer-compatible modular synthesis protocol of PMOs is long awaited to explore next-generation PMO chim

136 DNA synthesizer to make several sequences of PMOs, demonstrating for the first time the adaptation of

137 hosphoramidite approach for the synthesis of PMOs using tert-butyl-protected 5'-(t)Bu-morpholino phos

138 The present work illustrates the utility of PMOs to study alternative splicing that could be applied

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

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

141 4658 phosphorodiamidate morpholino oligomer (PMO) in patients with Duchenne muscular dystrophy.

142 as a phosphorodiamidate morpholino oligomer (PMO) structure, suggests that the UV-260 nm extinction c

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

144 r of phosphorodiamidate morpholino oligomer (PMO)-based therapy targeting exon 44.

145 ated morpholino phosphorodiamidate oligomer (PMO) dramatically enhanced ASO delivery into striated mu

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

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

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

149 use phosphorodiamidate morpholino oligomers (PMO) to induce exon skipping in the dystrophin pre-mRNA,

150 nse phosphorodiamidate morpholino oligomers (PMO) to reduce myostatin expression in skeletal muscle a

151 delivery of antisense morpholino oligomers (PMO).

152 nse phosphorodiamidate morpholino oligomers (PMOs) are promising candidates to fill such a role, but

153 ile phosphorodiamidate morpholino oligomers (PMOs) are promising exon-skipping therapeutics aimed at

154 ody-phosphorodiamidate morpholino oligomers (PMOs) depend on several aspects of their component parts

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

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

157 ike phosphorodiamidate morpholino oligomers (PMOs) that are currently used in various splice-switchin

158 nse Phosphorodiamidate Morpholino Oligomers (PMOs) to modulate E23a alternative splicing at physiolog

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

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

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

162 as phosphorodiamidate morpholino oligomers (PMOs).

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

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

165 sphorodiamidate morpholino oligonucleotides (PMOs) constitute 3 out of the 11 FDA-approved oligonucle

166 sphorodiamidate Morpholino Oligonucleotides (PMOs) have been well established in the milieu of FDA-ap

167 sphorodiamidate morpholino oligonucleotides (PMOs) incorporating single or double triazole rings in t

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

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

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

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

172 Postmenopausal osteoporosis (PMO) is a risk factor for periodontitis, and current the

173 Postmenopausal osteoporosis (PMO) is characterized by an imbalance in bone remodeling

174 d 3-dimensional fold characteristic of other PMOs.

175 P-PMO showed low nonspecific inhibitory activity against t

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

177 5TERM P-PMO treatment reduced viral titers in target organs and

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

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

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

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

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

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

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

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

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

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

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

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

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

191 e phosphorodiamidate morpholino oligomers (P-PMOs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 Our results demonstrate that Pip6a-PMO-CAG induces long-lasting correction with high effica

210 tient-derived muscle cells showed that Pip6a-PMO-CAG specifically targets mutant CUGexp-DMPK transcri

211 Thus, low-dose treatment with Pip6a-PMO-CAG targeting pathologic expansions is sufficient to

212 e clusters like Trapezium forming metal-poor PMOs with disks.

213 To rapidly prototype potential PMO drug candidates, we report a fully automated flow-ba

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

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

216 for the first time the adaptation of regular PMOs in a commercial DNA synthesizer.

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

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

219 te enhances muscle delivery of exon skipping PMO (M23D) in mdx mice, achieving dose-dependent and rob

220 These results suggest PMO compounds have powerful therapeutic and investigativ

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

222 The synthesized PMOs using both the methods on a solid support have been

223 cking and coupling reagents for synthesizing PMOs using either trityl or Fmoc-protected chlorophospho

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

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

226 In summary, we show that PMO-based let-7c SBO has potential applicability for upr

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

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

229 Hybridization study shows that PMOs exhibit a higher binding affinity toward complement

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

231 icient may need to be re-established for the PMO based oligonucleotide.

232 The effect of the PMO appears to be bacteriocidal.

233 Swapping a portion of the PMO domain (V86 to T130) did not switch cwr haplogroup s

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

235 e CTG repeat length and concentration of the PMO.

236 noncleavable linkers, linker location on the PMO, and the impact of drug-to-antibody ratios (DARs) on

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

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

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

240 am quantities of three candidate therapeutic PMO sequences for an unserved class of Duchenne muscular

241 These PMOs exhibited various degrees of antiviral activity upo

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

243 necting regioselectivity of the chemistry to PMO phylogeny.

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

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

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

247 ministration in comparison with unconjugated PMO and other ASO strategies.

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