A toxin used in GPCR and EAE research
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Pertussis Toxin (islet-activating protein)

Item No. 19546

Product Insert (PDF)Safety Data Sheet (SDS) (PDF)
Technical Information
CAS Number
70323-44-3
Purity
≥95% estimated by SDS-PAGE
Formulation (Request formulation change)
Each vial, when reconstituted to 500 μl with water, contains 50 μg of pertussis toxin in in 0.01 M sodium phosphate, 0.05 M sodium chloride, pH 7.0
Solubility(Learn about Variance in Solubility)
Water: soluble
Shipping & Storage Information
Storage
2°C to 8°C
Shipping
Room temperature in continental US; may vary elsewhere
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    50 µg

    $527

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    Product Description

    Pertussis toxin (islet-activating protein) is a toxin, first isolated from B. pertussis, that is used to study G protein-coupled receptor signaling in cells and experimental autoimmune encephalomyelitis (EAE) in animals. Pertussis toxin catalyzes the transfer of the ADP-ribose moiety of NAD to the α subunits of heterotrimeric Gi/o proteins, resulting in the receptors being uncoupled from Gi/o proteins.1,2 Pertussis toxin is also used as an adjuvant, given with specific antigens, to immunize animals and induce EAE, an animal model of multiple sclerosis.3,4 Pertussis toxin was first described as an islet-activating protein because it caused a sustained potentiation of the secretory response of pancreatic islet cells to various stimuli that stimulate Gi-linked α-adrenergic receptors.5,6

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Kaslow, H.R., and Burns, D.L. Pertussis toxin and target eukaryotic cells: Binding, entry, and activation. The FASEB Journal 6(9), 2684-2690 (1992).

    2. Ui, M. Islet-activating protein, pertussis toxin: A probe for functions of the inhibitory guanine nucleotide regulatory component of adenylate cyclase. Trends Pharmacol. Sci. 5, 277-279 (1984).

    3. Hofstetter, H.H., Shive, C.L., and Forsthuber, T.G. Pertussis toxin modulates the immune response to neuroantigens injected in incomplete Freund’s adjuvant: Induction of Th1 cells and experimental autoimmune encephalomyelitis in the presence of high frequencies of Th2 cells. J. Immunol. 169(1), 117-125 (2002).

    4. Ronchi, F., Basso, C., Preite, S., et al. Experimental priming of encephalitogenic Th1/Th17 cells requires pertussis toxin-driven IL-1β production by myeloid cells. Nat. Commun. 7:11541, (2016).

    5. Heyworth, C.M., Grey, A.M., Wilson, S.R., et al. The action of islet activating protein (pertussis toxin) on insulin’s ability to inhibit adenylate cyclase and activate cyclic AMP phosphodiesterases in hepatocytes. Biochem. J. 235(1), 145-149 (1986).

    6. Katada, T., and Michio, U. Slow interaction of islet-activating protein with pancreatic islets during primary culture to cause reversal of α-adrenergic inhibition of insulin secretion. The Journal of Biological Chemisty 255(20), 9580-9588 (1980).

    Product Citations

    Biliktu, M., Senol, S.P., Temiz-Resitoglu, M., et al. Pharmacological inhibition of soluble epoxide hydrolase attenuates chronic experimental autoimmune encephalomyelitis by modulating inflammatory and anti-inflammatory pathways in an inflammasome-dependent and -independent manner. Inflammopharmacology 28(6), 1509-1524 (2020).

    Ning, X., Wang, Y., Jing, M., et al. Apoptotic caspases suppress type I interferon production via the cleavage of cGAS, MAVS, and IRF3. Mol. Cell 74(1), 19-31 (2019).