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MABE343-AF647

Sigma-Aldrich

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

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.

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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WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


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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
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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.
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Reversible phase separation underpins the role of FUS in ribonucleoprotein granules and other membrane-free organelles and is, in part, driven by the intrinsically disordered low-complexity (LC) domain of FUS. Here, we report that cooperative cation-π interactions between tyrosines in the
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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
Eric J Allenspach et al.
The Journal of experimental medicine, 218(5) (2021-03-17)
SAMD9L is an interferon-induced tumor suppressor implicated in a spectrum of multisystem disorders, including risk for myeloid malignancies and immune deficiency. We identified a heterozygous de novo frameshift variant in SAMD9L in an infant with B cell aplasia and clinical

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