Amido-bridged nucleic acid (AmNA)-modified antisense oligonucleotides targeting α-synuclein as a novel therapy for Parkinson’s disease
- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
2045-2322
- Extent
-
Online-Ressource
- Language
-
Englisch
- Notes
-
online resource.
- Bibliographic citation
-
Amido-bridged nucleic acid (AmNA)-modified antisense oligonucleotides targeting α-synuclein as a novel therapy for Parkinson’s disease ; volume:9 ; number:1 ; day:21 ; month:5 ; year:2019 ; pages:1-13 ; date:12.2019
Scientific reports ; 9, Heft 1 (21.5.2019), 1-13, 12.2019
- Creator
-
Uehara, Takuya
Choong, Chi-Jing
Nakamori, Masayuki
Hayakawa, Hideki
Nishiyama, Kumiko
Kasahara, Yuuya
Baba, Kousuke
Nagata, Tetsuya
Yokota, Takanori
Tsuda, Hiroshi
Obika, Satoshi
Mochizuki, Hideki
- Contributor
-
SpringerLink (Online service)
- DOI
-
10.1038/s41598-019-43772-9
- URN
-
urn:nbn:de:101:1-2019062420381044643851
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 10:56 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Uehara, Takuya
- Choong, Chi-Jing
- Nakamori, Masayuki
- Hayakawa, Hideki
- Nishiyama, Kumiko
- Kasahara, Yuuya
- Baba, Kousuke
- Nagata, Tetsuya
- Yokota, Takanori
- Tsuda, Hiroshi
- Obika, Satoshi
- Mochizuki, Hideki
- SpringerLink (Online service)
Other Objects (12)
An antisense Alu transposon insertion/deletion polymorphism of ALDH1A1 may functionally associate with Parkinson’s disease
Tritium labeling of antisense oligonucleotides via different conjugation agents
Minimal structural modifications of antisense oligonucleotides conveying stability towards endonucleases
Gephyrin antisense oligonucleotides prevent glycine receptor clustering in spinal neurons
Splice-Modulating Antisense Oligonucleotides as Therapeutics for Inherited Metabolic Diseases
Respirable antisense oligonucleotides: a new drug class for respiratory disease
Antisense oligonucleotides: recent progress in the treatment of various diseases
Splicing modulation via antisense oligonucleotides in recessive dystrophic epidermolysis bullosa
Parkinson
Parkinson
Mismatched single stranded antisense oligonucleotides can induce efficient dystrophin splice switching
Intracellular Delivery of Antisense Oligonucleotides by Tri‐Branched Cyclic Disulfide Units
An antisense Alu transposon insertion/deletion polymorphism of ALDH1A1 may functionally associate with Parkinson’s disease
Tritium labeling of antisense oligonucleotides via different conjugation agents
Minimal structural modifications of antisense oligonucleotides conveying stability towards endonucleases
Gephyrin antisense oligonucleotides prevent glycine receptor clustering in spinal neurons
Splice-Modulating Antisense Oligonucleotides as Therapeutics for Inherited Metabolic Diseases
Respirable antisense oligonucleotides: a new drug class for respiratory disease
Antisense oligonucleotides: recent progress in the treatment of various diseases
Splicing modulation via antisense oligonucleotides in recessive dystrophic epidermolysis bullosa
Parkinson
Parkinson
Mismatched single stranded antisense oligonucleotides can induce efficient dystrophin splice switching
Intracellular Delivery of Antisense Oligonucleotides by Tri‐Branched Cyclic Disulfide Units
An antisense Alu transposon insertion/deletion polymorphism of ALDH1A1 may functionally associate with Parkinson’s disease
Tritium labeling of antisense oligonucleotides via different conjugation agents
Minimal structural modifications of antisense oligonucleotides conveying stability towards endonucleases
Gephyrin antisense oligonucleotides prevent glycine receptor clustering in spinal neurons
Splice-Modulating Antisense Oligonucleotides as Therapeutics for Inherited Metabolic Diseases
Respirable antisense oligonucleotides: a new drug class for respiratory disease
Antisense oligonucleotides: recent progress in the treatment of various diseases
Splicing modulation via antisense oligonucleotides in recessive dystrophic epidermolysis bullosa
Parkinson
Parkinson
Mismatched single stranded antisense oligonucleotides can induce efficient dystrophin splice switching