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Submit ReviewPertussis Toxin is a bacterial toxin that catalyzes ADP-ribosylation of G-proteins Gi, Go and Gt. Impairs G protein heterotrimer interaction with receptors, blocking receptor coupling. Pertussis Toxin protects against ischemic stroke in a mouse model of permanent middle cerebral artery occlusion. Pertussis Toxin inhibits microglia migration to the spinal cord and prevents dissemination of disease in an experimental autoimmune encephalomyelitis mouse model.
Storage | Store at +4°C |
CAS Number | 70323-44-3 |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Bokoch et al (1983) Indentification of the predominant substrate for ADP-ribosylation by islet activating protein. J.Biol.Chem. 258 2072 PMID: 6296122
Barbieri and Cortina (1988) ADP-ribosyltransferase mutations in the catalytic S-1 subunit of pertussis toxin. Infect.Immun. 56 1934 PMID: 3135265
Casey et al (1989) G protein βγ subunits from bovine brain and retina: equivalent catalytic support of ADP-ribosylation of a subunits by pertussis toxin but differential interactions with Gsa. Biochemistry 28 611 PMID: 2496748
Tang et al (2015) Pertussis toxin reduces calcium influx to protect ischemic stroke in a middle cerebral artery occlusion model. J.Neurochem. 135 998 PMID: 26365274
Yin et al (2010) Centrally administered pertussis toxin inhibits microglia migration to the spinal cord and prevents dissemination of disease in an EAE mouse model. PLoS One 5 e12400 PMID: 20811645
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Keywords: Pertussis Toxin, Pertussis Toxin supplier, Catalyzes, ADP-ribosylation, G-Protein, Heterotrimeric, Gi, Go, Gt, toxin, G-protein, GTPases, 3097, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for Pertussis Toxin include:
Li et al (2017) Follicular Stimulating Hormone Accelerates Atherogenesis by Increasing Endothelial VCAM-1 Expression. Theranostics 7 4671 PMID: 29187895
Schutsky et al (2011) Stress and glucocorticoids impair memory retrieval via β2-adrenergic, Gi/o-coupled suppression of cAMP signaling. J Neurosci 31 14172 PMID: 21976502
Rimmerman et al (2013) Direct modulation of the outer mitochondrial membrane channel, voltage-dependent anion channel 1 (VDAC1) by cannabidiol: a novel mechanism for cannabinoid-induced cell death. Cell Death Dis 4 e949 PMID: 24309936
Wydeven et al (2012) Structural elements in the Girk1 subunit that potentiate G protein-gated potassium channel activity. Proc Natl Acad Sci U S A 109 21492 PMID: 23236146
O'Neill & Sylantyev (2018) Selective modulation of tonically active GABAA receptor functional subgroups by G-proteins and protein kinase C. Exp Biol Med (Maywood) 243 1046 PMID: 30205722
Cheng et al (2012) Cytoskeletal role in protection of the failing heart by β-adrenergic blockade. Proc Natl Acad Sci U S A 302 H675 PMID: 22081703
Hu et al (2022) Epigenetic drug screen identified IOX1 as an inhibitor of Th17-mediated inflammation through targeting TET2. EBioMedicine 86 104333 PMID: 36335665
Wyant et al (2022) Mitochondrial remodeling and ischemic protection by G protein–coupled receptor 35 agonists. Science 377 621 PMID: 35926043
Yuan et al (2016) Ciliary IFT80 balances canonical versus non-canonical hedgehog signalling for osteoblast differentiation. Am J Physiol Heart Circ Physiol 7 11024 PMID: 26996322
Stott et al (2015) G-protein βγ subunits are positive regulators of Kv7.4 and native vascular Kv7 channel activity. Dis Model Mech 112 6497 PMID: 25941381
Sim et al (2015) A simple method for in vivo labelling of infiltrating leukocytes in the mouse retina using indocy. green dye. Int J Cancer 8 1479 PMID: 26398933
Choi et al (2015) SDF-1α stiffens myeloma bone marrow mesenchymal stromal cells through the activation of RhoA-ROCK-Myosin II. J Neurosci 136 E219 PMID: 25137150
Boldison et al (2014) Tissue-resident exhausted effector memory CD8+ T cells accumulate in the retina during chronic experimental autoimmune uveoretinitis. J Immunol 192 4541 PMID: 24740509
Butschkau et al (2014) Protein z exerts pro-angiogenic effects and upregulates CXCR4. PLoS One 9 e113554 PMID: 25474349
Nepomuceno et al (2018) Re-evaluation of Adrenocorticotropic Hormone and Melanocyte Stimulating Hormone Activation of GPR139 in Vitro. Front Pharmacol 9 157 PMID: 29599718
Zhao et al (2018) Ethanolic Extract of Folium Sennae Mediates the Glucose Uptake of L6 Cells by GLUT4 and Ca2. Molecules 23 PMID: 30424024
Park et al (2011) Resolvin D2 is a potent endogenous inhibitor for transient receptor potential subtype V1/A1, inflammatory pain, and spinal cord synaptic plasticity in mice: distinct roles of resolvin D1, D2, and E1. Neuron 31 18433 PMID: 22171045
Crawford et al (2015) The role of lipoprotein-associated phospholipase A2 in a murine model of experimental autoimmune uveoretinitis. PLoS One 10 e0122093 PMID: 25874928
Jones et al (2015) Pathogenic aquaporin-4 reactive T cells are sufficient to induce mouse model of neuromyelitis optica. Acta Neuropathol Commun 3 28 PMID: 25990016
Meitzen et al (2011) β1-Adrenergic receptors activate two distinct signaling pathways in striatal neurons. J Neurochem 116 984 PMID: 21143600
Nagaraja et al (1999) Treatment with inverse agonists enhances baseline atrial contractility in transgenic mice with chronic β2-adrenoceptor activation. Nat Commun 127 1099 PMID: 10455254
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Pertussis toxin (PeTX) was used to compare effects of PKA and G-protein signalling on root mean square noise (RMS) produced by GABA-A receptors in electrophysiological recording. We found that after block of G-protein signalling with PeTX GABA-A receptor antagonists SR 95531 and Picrotoxin generate smaller impact on RMS noise than after block of PKA with PKI.
MG-63 cells were treated with LPA (10 µM) alone or in combination with C3 (20 µM), PTX (Pertussis Toxin, 400 ng/ml) or H2L 5765834 (20 µM) for 3 h to follow COX-2 expression using Western blot. Pertussis Toxin inhibited COX-2 expression induced by LPA.