|Reactivity||Human, Mouse, Rat|
|Calculated MW||24 KDa|
|Other Names||Transcription factor A, mitochondrial, mtTFA, Testis-specific high mobility group protein, TS-HMG, Tfam, Hmgts|
|Target/Specificity||Native recombinant mouse TFAM protein with c-terminal 6-his tag.|
|Antibody Specificity||Specific for the ~24 kDa TFAM protein.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||TFAM (Transcription Factor A, mitochondrial) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
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Provided below are standard protocols that you may find useful for product applications.
Mitochondrial Transcription Factor A (TFAM) is a key activator of mitochondrial (mt) DNA transcription as well as a participant in mitochondrial genome replication. mtDNA is highly susceptible to oxidative stress leading to mitochondrial dysfunction. Overexpression of TFAM has been implicated in the amelioration of age dependent impairment of brain functions through the prevention of oxidative stress and mitochondrial dysfunction in microglia (Hayashi et al., 2008). More recently, TFAM overexpression has been shown to potentially reduce oxidative stress in motor neurons and delay onset of amyotrophic lateral sclerosis (ALS) in ALS model mice (Morimoto et al., 2012).
Hayashi Y, Yoshida M, Yamato M, Ide T, Wu Z, Ochi-Shindou M, Kanki T, Kang D, Sunagawa K, Tsutsui H, Nakanishi H (2008) Reverse of age-dependent memory impairment and mitochondrial DNA damage in microglia by an overexpression of human mitochondrial transcription factor a in mice. J Neurosci. 28(34):8624-34
Morimoto N, Miyazaki K, Kurata T, Ikeda Y, Matsuura T, Kang D, Ide T, Abe K (2012) Effect of mitochondrial transcription factor a overexpression on motor neurons in amyotrophic lateral sclerosis model mice. J Neurosci Res. 90(6):1200-8. Epub 2012 Feb 22
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