产品名称
Anti-ATPIF1 antibody produced in rabbit, affinity isolated antibody
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
12 kDa
species reactivity
horse, dog, bovine, rabbit, human, rat, guinea pig
concentration
0.5 mg - 1 mg/mL
technique(s)
western blot: suitable
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... ATPIF1(93974)
Biochem/physiol Actions
ATPIF1 is a mitochondrial ATPase inhibitor. It is thought to be a regulatory component of the ATP-synthesizing complex in the mitochondria.This gene encodes a mitochondrial ATPase inhibitor. Alternative splicing occurs at this locus and three transcript variants encoding distinct isoforms have been identified.
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.
Immunogen
Synthetic peptide directed towards the N terminal region of human ATPIF1
Other Notes
Synthetic peptide located within the following region: GSIREAGGAFGKREQAEEERYFRAQSREQLAALKKHHEEEIVHHKKEIER
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
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存储类别
10 - 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
Valerie Lefebvre et al.
Autophagy, 9(11), 1770-1779 (2013-09-06)
Mitochondrial dysfunction is a hallmark of aging and numerous human diseases, including Parkinson disease (PD). Multiple homeostatic mechanisms exist to ensure mitochondrial integrity, including the selective autophagic program mitophagy, that is activated during starvation or in response to mitochondrial dysfunction.
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