ライフサイエンスコーパス: gapmer

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1 '-O-methoxyethyl (2'-O-ME) phosphorothioate 'gapmer'.

2 hepatoxicity observed with some LNA-modified gapmers.

3 acy, BalbC mice were treated with 2'-O-DMAOE gapmers and a dose-dependent reduction in the targeted C

4 ), enhances the potency of second-generation gapmer antisense oligonucleotides (ASOs) 6-10-fold in mo

5 orothioate (PS)-modified tricycloDNA (tcDNA) gapmer antisense oligonucleotides (ASOs) in T(m), cell c

6 e a series of phosphorothioate (PS)-modified gapmer antisense oligonucleotides (ASOs) with control of

7 OE second generation ASOs, we have evaluated gapmer antisense oligonucleotides containing BNAs having

8 In contrast, similarly targeted MOE-gapmer antisense oligonucleotides that degrade RNA but d

9 2.) In an animal experiment, a 16-mer F-CeNA gapmer ASO showed similar RNA affinity but significantly

10 ver compared with the parent single-stranded gapmer ASO.

11 creening of fully phosphorothioated (PS)-LNA gapmer ASOs designed against the BACH1 transcript.

12 S-cEt (S-2'-O-Et-2',4'-bridged nucleic acid) gapmer ASOs, approximately 60-fold enhancement in potenc

13 BMECs) were cultured and treated with Malat1 GapmeR before 16 h oxygen and glucose depravation (OGD).

14 We have shown that the ASO gapmers can interact with the Ago-2 PAZ domain and can l

15 n of DICER or AGO2 using either siRNA or MOE-gapmer chemistries resulted in the induction of DUX4 exp

16 We designed chimeric ASOs, termed gapmers, containing modified nucleic acid residues to in

17 avage patterns (both human and E. coli) in a gapmer context.

18 HNA and 2'-O-ME gapmers displayed similar potency, but a pure HNA antise

19 A DNA/locked nucleotide acid gapmer duplex with an alpha-tocopherol-conjugated comple

20 ncing of MALAT1 by small interfering RNAs or GapmeRs induced a promigratory response and increased ba

21 ing of MANTIS with small interfering RNAs or GapmeRs inhibited angiogenic sprouting and alignment of

22 Thus, HNA gapmers may provide a valuable additional tool for antis

23 GapmeR-mediated silencing of Meg3 in CFs resulted in the

24 red the antisense effects of a chimeric HNA 'gapmer' oligonucleotide comprising a phosphorothioate ce

25 'Gapmer' oligonucleotides have one or two 2'-O-modified r

26 Pharmacological inhibition of MALAT1 by GapmeRs reduced blood flow recovery and capillary densit

27 Treatment with anti-MDR1 HNA gapmer resulted in increased cellular accumulation of th

28 The gapmers selectively knockdown expanded CUG transcripts a

29 Silencing of Malat1 by Malat1 GapmeR significantly increased OGD-induced cell death an

30 tive cytoplasmic mechanism through which ASO gapmers silence their targets when transfected or delive

31 nistration of FII antisense oligonucleotide "gapmer" to Berkeley SCD mice to selectively reduce circu

32 -methyluracil nucleoside (S)-cEt-BNA, a key "gapmer" unit in a number of biologically relevant antise

33 The anti-MDR1 HNA gapmer was substantially more potent than a phosphorothi

34 Furthermore, combination of gapmers with morpholino ASOs that help release binding o

35 The phosphorothioate oligonucleotide 'gapmers', with 2'-O-DMAOE- modified nucleoside residues

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