Difference between revisions of "Iyer 2009 Mitochondrion"
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|abstract=We developed a scalable procedure to produce human mitochondrial transcription factor A (TFAM) modified with an N-terminal protein transduction domain (PTD) and mitochondrial localization signal (MLS) that allow it to cross membranes and enter mitochondria through its āmitochondrial transduction domainā (MTD = PTD + MLS). Alexa488-labeled MTDāTFAM rapidly entered the mitochondrial compartment of cybrid cells carrying the G11778A LHON mutation. ''MTDāTFAM'' reversibly increased respiration and levels of respiratory proteins. ''In vivo'' treatment of mice with MTDāTFAM increased motor endurance and complex I-driven respiration in mitochondria from brain and skeletal muscle. MTDāTFAM increases mitochondrial bioenergetics and holds promise for treatment of mitochondrial diseases involving deficiencies of energy production. | |abstract=We developed a scalable procedure to produce human mitochondrial transcription factor A (TFAM) modified with an N-terminal protein transduction domain (PTD) and mitochondrial localization signal (MLS) that allow it to cross membranes and enter mitochondria through its āmitochondrial transduction domainā (MTD = PTD + MLS). Alexa488-labeled MTDāTFAM rapidly entered the mitochondrial compartment of cybrid cells carrying the G11778A LHON mutation. ''MTDāTFAM'' reversibly increased respiration and levels of respiratory proteins. ''In vivo'' treatment of mice with MTDāTFAM increased motor endurance and complex I-driven respiration in mitochondria from brain and skeletal muscle. MTDāTFAM increases mitochondrial bioenergetics and holds promise for treatment of mitochondrial diseases involving deficiencies of energy production. | ||
|keywords=TFAM, Respiration, Mitochondrial gene expression, Respiratory proteins | |keywords=TFAM, Respiration, Mitochondrial gene expression, Respiratory proteins | ||
|mipnetlab=US VA Richmond Bennett JP | |mipnetlab=US VA Richmond Bennett JP, US VA Richmond Virginia Commonwealth Univ | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
}} | }} | ||
Revision as of 14:22, 7 December 2012
| Iyer S, Thomas R, Portell F, Dunham L, Quigley C, Bennett JP (2009) Recombinant mitochondrial transcription factor A with N-terminal mitochondrial transduction domain increases respiration and mitochondrial gene expression. Mitochondrion 9: 196-203. |
Ā» PMID: 19460293; PDF
Iyer S, Thomas R, Portell F, Dunham L, Quigley C, Bennett JP (2009) Mitochondrion
Abstract: We developed a scalable procedure to produce human mitochondrial transcription factor A (TFAM) modified with an N-terminal protein transduction domain (PTD) and mitochondrial localization signal (MLS) that allow it to cross membranes and enter mitochondria through its āmitochondrial transduction domainā (MTD = PTD + MLS). Alexa488-labeled MTDāTFAM rapidly entered the mitochondrial compartment of cybrid cells carrying the G11778A LHON mutation. MTDāTFAM reversibly increased respiration and levels of respiratory proteins. In vivo treatment of mice with MTDāTFAM increased motor endurance and complex I-driven respiration in mitochondria from brain and skeletal muscle. MTDāTFAM increases mitochondrial bioenergetics and holds promise for treatment of mitochondrial diseases involving deficiencies of energy production. ā¢ Keywords: TFAM, Respiration, Mitochondrial gene expression, Respiratory proteins
ā¢ O2k-Network Lab: US VA Richmond Bennett JP, US VA Richmond Virginia Commonwealth Univ
Labels:
Stress:Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Skeletal muscle, Neurons; Brain"Neurons; Brain" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Enzyme: Complex I
Coupling state: OXPHOS
HRR: Oxygraph-2k
