biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
28 kDa
species reactivity
human
concentration
0.5 mg - 1 mg/mL
technique(s)
western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
Gene Information
human ... TFAM(7019)
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Immunogen
Synthetic peptide directed towards the middle region of human TFAM
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Other Notes
Synthetic peptide located within the following region: LGKPKRPRSAYNIYVSESFQEAKDDSAQGKLKLVNEAWKNLSPEEKQAYI
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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存储类别
12 - Non Combustible Liquids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Daniel A Pulliam et al.
The Biochemical journal, 462(2), 359-371 (2014-06-10)
Mutations in SURF1 (surfeit locus protein 1) COX (cytochrome c oxidase) assembly protein are associated with Leigh's syndrome, a human mitochondrial disorder that manifests as severe mitochondrial phenotypes and early lethality. In contrast, mice lacking the SURF1 protein (Surf1-/-) are
Rahul Agrawal et al.
Biochimica et biophysica acta, 1842(9), 1313-1323 (2014-05-21)
The rising prevalence of type-2 diabetes is becoming a pressing issue based on emerging reports that T2DM can also adversely impact mental health. We have utilized the UCD-T2DM rat model in which the onset of T2DM develops spontaneously across time
Kent Z Q Wang et al.
Mitochondrion, 17, 132-140 (2014-04-29)
Mitochondrial transcription factor A (TFAM) regulates mitochondrial biogenesis, which is downregulated by extracellular signal-regulated protein kinases (ERK1/2) in cells treated chronically with the complex I inhibitor 1-methyl-4-phenylpyridinium (MPP+). We utilized mass spectrometry to identify ERK1/2-dependent TFAM phosphorylation sites. Mutation of
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