AV37192
Anti-SP1 (AB1) antibody produced in rabbit
IgG fraction of antiserum
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About This Item
NACRES:
NA.41
UNSPSC Code:
12352203
Product Name
Anti-SP1 (AB1) antibody produced in rabbit, IgG fraction of antiserum
biological source
rabbit
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
51 kDa
species reactivity
human, mouse, rat
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
target post-translational modification
unmodified
Quality Level
Gene Information
mouse ... SP1(20683)
Biochem/physiol Actions
SP1 is a transcription factor binds to GC box
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 middle region of human SP1
Other Notes
Synthetic peptide located within the following region: GSSGTSSQGQTPQRVGGLQGSDSLNIQQNQTSGGSLQGSQQKEGEQSQQT
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
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wgk
WGK 1
Storage Class
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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Hemanth N Banavath et al.
Journal of the American Heart Association, 8(24), e012919-e012919 (2019-12-06)
Background Translocation of miR-181c into cardiac mitochondria downregulates the mitochondrial gene, mt-COX1. miR-181c/d-/- hearts experience less oxidative stress during ischemia/reperfusion (I/R) and are protected against I/R injury. Additionally, miR-181c overexpression can increase mitochondrial matrix Ca2+ ([Ca2+]m), but the mechanism by
Barbara Roman et al.
Journal of molecular and cellular cardiology, 144, 87-96 (2020-05-23)
In cardiomyocytes, there is microRNA (miR) in the mitochondria that originates from the nuclear genome and matures in the cytoplasm before translocating into the mitochondria. Overexpression of one such miR, miR-181c, can lead to heart failure by stimulating reactive oxygen
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