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TFAM (Transcription Factor A, mitochondrial) Antibody

Rabbit polyclonal antibody

     
  • WB - TFAM (Transcription Factor A, mitochondrial) Antibody AN1221
    Western blot of rat kidney lysate showing specific immunolabeling of the ~24k TFAM protein.
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  • SPECIFICATION
  • CITATIONS: 1
  • PROTOCOLS
  • BACKGROUND
  • detail
Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
WB
Primary Accession P40630
Reactivity Human, Mouse, Rat
Host Rabbit
Clonality polyclonal
Calculated MW 24 KDa
Additional Information
Gene ID 21780
Gene Name TFAM
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.
Dilution WB~~ 1:2000
Format serum
Antibody Specificity Specific for the ~24 kDa TFAM protein.
StorageMaintain 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.
PrecautionsTFAM (Transcription Factor A, mitochondrial) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
ShippingBlue Ice
Research Areas
Citations ( 0 )

Background

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).

References

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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$ 310.00
Cat# AN1221
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Availability: 7-10 days
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