Ionomycin

Calcium ionophore

Ionomycin

Calcium ionophore

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Calcium ionophore
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Overview

Ionomycin is a potent and selective calcium ionophore derived from Streptomyces conglobatus (Liu et al.). It is used as a research tool to rapidly raise the intracellular level of calcium, and to study calcium transport across biological membranes by inducing the release of cytosolic calcium stores (Morgan & Jacob; Yoshida & Plant). Ionomycin is a more effective Ca++ ionophore than A23187, but less effective at binding and carrying Mg++ (Liu & Hermann). Ionomycin is able to activate and prime the polymorphonuclear neutrophil (PMN) oxidase (Elzi et al.), and is used in conjunction with Phorbol 12-myristate 13-acetate (PMA; Catalog #74042) for the activation of T cells (IC₅₀ = 5.8 nM; Caraher et al.; Zhang et al.). This product is supplied as a 10 mg/mL solution in ethanol.

IMMUNOLOGY
· Activates T cells from human, mouse, or rat sources, in combination with PMA, to express cytokines including IL-17, IL-4, IL-10, and IL-2 (Caraher et al.; Harrington et al.; Parrish-Novak et al.).
Cell Type
T Cells
Species
Human, Mouse, Non-Human Primate, Other, Rat
Application
Activation
Area of Interest
Immunology
CAS Number
56092-81-0; 64-17-5
Chemical Formula
C₄₁H₇₂O₉
Purity
≥ 98%
Pathway
Calcium Signaling
Target
Calcium

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Product Name
Ionomycin
Catalog #
73722, 73724
Lot #
Lot BX29711 or lower
Language
English
Product Name
Ionomycin
Catalog #
73722, 73724
Lot #
Lot BX29879 or higher
Language
English
Document Type
Safety Data Sheet
Product Name
Ionomycin
Catalog #
73722, 73724
Lot #
All
Language
English

Resources and Publications

Publications (9)

Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Harrington LE et al. Nature immunology 2005 NOV

Abstract

CD4(+) T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (T(H)1) or T(H)2 lineages and instead favor the idea of a distinct effector lineage we call 'T(H)-17'. The development of T(H)-17 cells from naive precursor cells was potently inhibited by interferon-gamma (IFN-gamma) and IL-4, whereas committed T(H)-17 cells were resistant to suppression by T(H)1 or T(H)2 cytokines. In the absence of IFN-gamma and IL-4, IL-23 induced naive precursor cells to differentiate into T(H)-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-gamma signaling enhances development of pathogenic T(H)-17 effector cells that can exacerbate autoimmunity.
Ionomycin causes activation of p38 and p42/44 mitogen-activated protein kinases in human neutrophils. Elzi DJ et al. American journal of physiology. Cell physiology 2001 JUL

Abstract

Many receptor-linked agents that prime or activate the NADPH oxidase in polymorphonuclear neutrophils (PMNs) elicit changes in cytosolic Ca2+ concentration and activate mitogen-activated protein (MAP) kinases. To investigate the role of Ca2+ in the activation of p38 and p42/44 MAP kinases, we examined the effects of the Ca2+-selective ionophore ionomycin on priming and activation of the PMN oxidase. Ionomycin caused a rapid rise in cytosolic Ca2+ that was due to both a release of cytosolic Ca2+ stores and Ca2+ influx. Ionomycin also activated (2 microM) and primed (20-200 nM) the PMN oxidase. Dual phosphorylation of p38 MAP kinase and phosphorylation of its substrate activating transcription factor-2 were detected at ionomycin concentrations that prime or activate the PMN oxidase, while dual phosphorylation of p42/44 MAP kinase and phosphorylation of its substrate Elk-1 were elicited at 0.2-2 microM. SB-203580, a p38 MAP kinase antagonist, inhibited ionomycin-induced activation of the oxidase (68 +/- 8%, P textless 0.05) and tyrosine phosphorylation of 105- and 72-kDa proteins; conversely, PD-98059, an inhibitor of MAP/extracellular signal-related kinase 1, had no effect. Treatment of PMNs with thapsigargin resulted in priming of the oxidase and activation of p38 MAP kinase. Chelation of cytosolic but not extracellular Ca2+ completely inhibited ionomycin activation of p38 MAP kinase, whereas chelation of extracellular Ca2+ abrogated activation of p42/44 MAP kinase. These results demonstrate the importance of changes in cytosolic Ca2+ for MAP kinase activation in PMNs.
Flow cytometric analysis of intracellular IFN-gamma, IL-4 and IL-10 in CD3(+)4(+) T-cells from rat spleen. Caraher EM et al. Journal of immunological methods 2000 OCT

Abstract

The application of multi-parameter flow cytometry for the assessment of T-cell and cytokine functioning has been used by several groups for studying human and mouse samples, although little has been reported for the rat. Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3(+)4(+) T-cells that produce IFN-gamma, IL-4 and IL-10. In vitro stimulation of IFN-gamma production required incubation of splenocytes with PMA and ionomycin in the presence of the protein transport inhibitor brefeldin A for 6 h. Three stimulation protocols for IL-4 and IL-10 production were evaluated. In vitro priming of splenic T-cells with antibodies against CD3 and CD28 and recombinant cytokines (IL-2 and IL-4) for 5 days followed by restimulation with PMA and ionomycin was required to stimulate cells to produce either IL-4 or IL-10. Brefeldin A was found to be a more suitable protein transport inhibitor than monensin. This method will be useful for analysing the nature of individual rat cytokine-producing cells in a variety of experimental model systems.