Bridging PNAs can bind preferentially to a deleted mitochondrial DNA template but replication by mitochondrial DNA polymerase γ in vitro is not impaired
- 1 October 2003
- journal article
- Published by Elsevier in Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression
- Vol. 1629 (1-3) , 73-83
- https://doi.org/10.1016/j.bbaexp.2003.08.005
Abstract
No abstract availableKeywords
This publication has 19 references indexed in Scilit:
- An antigenomic strategy for treating heteroplasmic mtDNA disordersAdvanced Drug Delivery Reviews, 2001
- The epidemiology of pathogenic mitochondrial DNA mutationsAnnals of Neurology, 2000
- Peptide nucleic acid delivery to human mitochondriaGene Therapy, 1999
- Mitochondria in neuromuscular disordersBiochimica et Biophysica Acta (BBA) - Bioenergetics, 1998
- Selective inhibition of mutant human mitochondrial DNA replication in vitro by peptide nucleic acidsNature Genetics, 1997
- Treatment of mitochondrial disease.Journal of Bioenergetics and Biomembranes, 1997
- Stability of peptide nucleic acids in human serum and cellular extractsBiochemical Pharmacology, 1994
- PNA hybridizes to complementary oligonucleotides obeying the Watson–Crick hydrogen-bonding rulesNature, 1993
- Single base pair mutation analysis by PNA directed PCR clampingNucleic Acids Research, 1993
- MELAS mutation in mtDNA binding site for transcription termination factor causes defects in protein synthesis and in respiration but no change in levels of upstream and downstream mature transcripts.Proceedings of the National Academy of Sciences, 1992