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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.
|authors=Iyer S, Thomas R, Portell F, Dunham L, Quigley C, Bennett JP Ā 
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19460293 PMID: 19460293 Open Access]
|authors=Iyer S, Thomas R, Portell F, Dunham L, Quigley C, Bennett JP
|year=2009
|year=2009
|journal=Mitochondrion
|journal=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.
|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, US VA Richmond Iyer S
|discipline=Biomedicine
}}
}}
{{Labeling
{{Labeling
|area=Respiration, Genetic knockout;overexpression
|organism=Human
|tissues=Skeletal muscle, Nervous system
|enzymes=Complex I
|diseases=Inherited
|couplingstates=ROUTINE
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|topics=Respiration; OXPHOS; ETS Capacity
|discipline=Biomedicine
}}
}}

Latest revision as of 13:42, 20 March 2015

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 Open Access

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, US VA Richmond Iyer S


Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Inherited 

Organism: Human  Tissue;cell: Skeletal muscle, Nervous system 

Enzyme: Complex I 

Coupling state: ROUTINE 

HRR: Oxygraph-2k