MABE343-AF647
Anti-Puromycin, clone 12D10, Alexa Fluor™ 647 Conjugate Antibody
clone 12D10, 0.5 mg/mL, from mouse
Synonym(s):
Alexa Fluor 647 Anti-Puromycin, Clone 12D10 Anti-Puromycin, Puromycin Detection Antibody
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
conjugate
ALEXA FLUOR™ 647
antibody form
purified antibody
antibody product type
primary antibodies
clone
12D10, monoclonal
species reactivity
human
concentration
0.5 mg/mL
technique(s)
immunocytochemistry: suitable
shipped in
wet ice
target post-translational modification
unmodified
General description
Puromycin is an aminonucleoside antibiotic, derived from the Streptomyces alboniger bacterium, that functions as a protein synthesis inhibitor that blocks translation through premature chain termination in the ribosome. Monoclonal antibodies to puromycin may be used with standard immunochemical methods to directly monitor translation, a method known as surface sensing of translation (SUnSET). Part of the molecule resembles the 3′ end of the aminoacylated tRNA, making it useful for protein translation analysis. Puromycin induces DNA fragmentation in thymocytes and in human HL-60 leukemia cells.
This Anti-Puromycin, clone 12D10 is validated for use in Immunocytochemistry for the detection of Puromycin.
Specificity
Predicted to react with cells from all species when pre-incubated with puromycin.
Quality
Evaluated by Immunocytochemistry Analysis untreated and puromycin treated HeLa cells.
Immunocytochemistry Analysis: A 1:2,500 dilution of this antibody detected puromycin-incorporated neosynthesized proteins in puromycin treated HeLa cells.
Alexa Fluor™ is a registered trademark of Life Technologies.
Immunocytochemistry Analysis: A 1:2,500 dilution of this antibody detected puromycin-incorporated neosynthesized proteins in puromycin treated HeLa cells.
Alexa Fluor™ is a registered trademark of Life Technologies.
Target description
Refer to Cat. No. MABE343 for observed molecular weight information.
Legal Information
ALEXA FLUOR is a trademark of Life Technologies
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Noga Ron-Harel et al.
Cell reports, 28(12), 3011-3021 (2019-09-19)
T cell stimulation is metabolically demanding. To exit quiescence, T cells rely on environmental nutrients, including glucose and the amino acids glutamine, leucine, serine, and arginine. The expression of transporters for these nutrients is tightly regulated and required for T cell activation.
Hongcheng Cheng et al.
Nature metabolism, 5(2), 314-330 (2023-01-31)
The accumulation of acidic metabolic waste products within the tumor microenvironment inhibits effector functions of tumor-infiltrating lymphocytes (TILs). However, it remains unclear how an acidic environment affects T cell metabolism and differentiation. Here we show that prolonged exposure to acid
Li Wang et al.
The British journal of nutrition, 1-11 (2023-05-29)
Se deficiency causes impaired growth of fish skeletal muscle due to the retarded hypertrophy of muscle fibres. However, the inner mechanisms remain unclear. According to our previous researches, we infer this phenomenon is associated with Se deficiency-induced high concentration of
Noémie Mazaré et al.
Cell reports, 32(8), 108076-108076 (2020-08-28)
Local translation is a conserved mechanism conferring cells the ability to quickly respond to local stimuli. In the brain, it has been recently reported in astrocytes, whose fine processes contact blood vessels and synapses. Yet the specificity and regulation of
Domnica Luca et al.
Science advances, 10(9), eadk0820-eadk0820 (2024-03-01)
Chronic and aberrant nucleic acid sensing causes type I IFN-driven autoimmune diseases, designated type I interferonopathies. We found a significant reduction of regulatory T cells (Tregs) in patients with type I interferonopathies caused by mutations in ADAR1 or IFIH1 (encoding
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