Proteomics

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Engineered transfer RNAs for suppression of premature termination codons


ABSTRACT: PTCs cause a multitude of human diseases and there are no established therapeutic options for their therapeutic management. Herein, we report the high-throughput cloning and identification, characterization and functional analysis of anticodon-edited tRNA which display efficacious PTC reversion in eukaryotic cells and mouse skeletal muscle. Notably, our screen identifies ACE-tRNA, in total, with the potential to repair a vast majority of known human disease-causing PTC, but this therapeutic will require overcoming tissue and delivery specific challenges. However, the engineered tRNA, once delivered, faithfully encode their cognate amino acid, thus abrogating spurious effects on downstream protein stability, folding, and trafficking, and consequently negating the need for tandem therapies involving protein folding or trafficking agents. When transfected as cDNA, ACE-tRNAs rescued multiple full-length proteins via PTC suppression; a NLuc luciferase reporter, a model protein HDH, and two disease nonsense mutations in CFTR.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human) Escherichia Coli

DISEASE(S): Cystic Fibrosis

SUBMITTER: robert Pope  

LAB HEAD: Robert Marshall Pope

PROVIDER: PXD012581 | Pride | 2019-02-11

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
Blank.raw Raw
Feb03.raw Raw
John_1.raw Raw
John_1.raw_20170615_Byonic.mzid.mzid Mzid
John_1.raw_20170615_Byonic.mzid.mzid_John_1.raw_20170615_Byonic.mzid.MGF Mzid
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