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Difference between revisions of "Iyer 2009 Mitochondrion"

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{{Publication
{{Publication
|title=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.
|title=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.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19460293 PMID: 19460293]
|authors=Iyer S, Thomas R, Portell F, Dunham L, Quigley C, Bennett JP
|authors=Iyer S, Thomas R, Portell F, Dunham L, Quigley C, Bennett JP
|year=2009
|year=2009
Line 6: Line 7:
|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 ā€œmitochondrial transduction domainā€ (MTD = PTD + MLS). Alexa488-labeled MTDā€“TFAM rapidly entered the mitochondrial compartment of cybrid cells carrying the G11778A LHON mutation. ''MTDā€“TFAM'' reversibly increased respiration and levels of respiratory proteins. ''In vivo'' treatment of mice with MTDā€“TFAM increased motor endurance and complex I-driven respiration in mitochondria from brain and skeletal muscle. MTDā€“TFAM 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 ā€œmitochondrial transduction domainā€ (MTD = PTD + MLS). Alexa488-labeled MTDā€“TFAM rapidly entered the mitochondrial compartment of cybrid cells carrying the G11778A LHON mutation. ''MTDā€“TFAM'' reversibly increased respiration and levels of respiratory proteins. ''In vivo'' treatment of mice with MTDā€“TFAM increased motor endurance and complex I-driven respiration in mitochondria from brain and skeletal muscle. MTDā€“TFAM 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
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19460293 PMID: 19460293]
|mipnetlab=US VA Richmond Bennett JP
|discipline=Biomedicine
}}
}}
{{Labeling
{{Labeling
|discipline=Biomedicine
|instruments=Oxygraph-2k
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression
|injuries=Mitochondrial Disease; Degenerative Disease and Defect, Genetic Defect; Knockdown; Overexpression
|organism=Human
|organism=Human
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|kinetics=ADP; Pi
|kinetics=ADP; Pi
|topics=Respiration; OXPHOS; ETS Capacity
|topics=Respiration; OXPHOS; ETS Capacity
|instruments=Oxygraph-2k
|discipline=Biomedicine
}}
}}

Revision as of 13:17, 23 February 2012

Publications in the MiPMap
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

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 ā€œmitochondrial transduction domainā€ (MTD = PTD + MLS). Alexa488-labeled MTDā€“TFAM rapidly entered the mitochondrial compartment of cybrid cells carrying the G11778A LHON mutation. MTDā€“TFAM reversibly increased respiration and levels of respiratory proteins. In vivo treatment of mice with MTDā€“TFAM increased motor endurance and complex I-driven respiration in mitochondria from brain and skeletal muscle. MTDā€“TFAM 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


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"Skeletal Muscle" 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., 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  Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k