Our Anti-TFAM (Transcription Factor A, mitochondrial) primary antibody from PhosphoSolutions is rabbit polyclonal. It detects human, mouse, and rat TFAM (Transcription Factor A, motochondrial) and is neat serum. It is great for use in WB.
Western blot of rat kidney lysate showing specific immunolabeling of the ~24 kDa TFAM protein.
Anti-TFAM (Transcription Factor A, Mitochondrial) Antibody
Bulk Order Anti-TFAM (Transcription Factor A, Mitochondrial) Antibody
TFAM (Transcription Factor A, motochondrial)
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).
Native recombinant mouse TFAM protein with c-terminal 6-his tag
Human, Mouse, Rat
Recommended that the undiluted antibody be aliquoted into smaller working volumes (10-30 uL/vial depending on usage) upon arrival and stored long term at -20° C or -80° C, while keeping a working aliquot stored at 4° C for short term. Avoid freeze/thaw cycles. Stable for at least 1 year.
Specific for endogenous levels of the ~24 kDa TFAM protein.
Western blots performed on each lot.
For research use only. Not intended for therapeutic or diagnostic use. Use of all products is subject to our terms and conditions, which can be viewed on our website.
After date of receipt, stable for at least 1 year at -20°C.
Kozhukhar, N, et al. 2023. The C-Terminal Tail of Mitochondrial Transcription Factor A Is Dispensable for Mitochondrial DNA Replication and Transcription In Situ. International Journal of Molecular Sciences, 9430.
Hayashi, Y., Yoshida, M., Yamato, M., Ide, T., Wu, Z., Ochi-Shindou, M., Kanki, T., Kang, D., Sunagawa, K., Tsutsui, H. and 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. Journal of Neuroscience, 28(34), pp.8624-8634. PMID: 18716221
Morimoto, N., Miyazaki, K., Kurata, T., Ikeda, Y., Matsuura, T., Kang, D., Ide, T. and Abe, K., 2012. Effect of mitochondrial transcription factor a overexpression on motor neurons in amyotrophic lateral sclerosis model mice. Journal of Neuroscience Research, 90(6), pp.1200-1208. PMID: 22354563
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