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Difference between revisions of "Iyer 2009 Mitochondrion"

From Bioblast
Line 14: Line 14:
|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
|tissues=Skeletal Muscle, Neurons; Brain
|tissues=Skeletal muscle, Neurons; Brain
|enzymes=Complex I
|enzymes=Complex I
|kinetics=ADP; Pi
|kinetics=ADP; Pi

Revision as of 02:26, 5 April 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.

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

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, 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