Iscove's Modified Dulbecco's Medium

Iscove's Modified Dulbecco's Medium (IMDM) with 25 mM HEPES

Iscove's Modified Dulbecco's Medium

Iscove's Modified Dulbecco's Medium (IMDM) with 25 mM HEPES

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Iscove's Modified Dulbecco's Medium (IMDM) with 25 mM HEPES
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Overview

Iscove's Modified Dulbecco's Medium (IMDM) with 25 mM HEPES is recommended for a wide variety of cell culture applications. Selection of suitable nutrient medium is dependent on the type of cell, conditions of culture, and degree of chemical definition required for the cell culture application.
Subtype
Basal Media
Cell Type
Other
Species
Human, Mouse, Non-Human Primate, Other, Rat
Application
Cell Culture

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
Catalog #
36150
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
36150
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (1)

SHIP represses Th2 skewing by inhibiting IL-4 production from basophils. E. Kuroda et al. Journal of immunology (Baltimore, Md. : 1950) 2011 JAN

Abstract

We report that SHIP(-/-) mice, compared to SHIP(+/+) mice, are Th2 skewed with elevated serum IgE and twice as many splenic CD4(+) Th2 cells that, when stimulated with anti-CD3, produce more IL-4 and less IFN-$\gamma$. Exploring the reason for this Th2 skewing, we found that freshly isolated SHIP(-/-) splenic and bone marrow basophils are present in elevated numbers and secrete far more IL-4 in response to IL-3 or to Fc$\epsilon$RI stimulation than do WT basophils. These SHIP(-/-) basophils markedly skew wild-type macrophage colony stimulating factor-derived macrophages toward an M2 phenotype, stimulate OT-II CD4(+) Th cells to differentiate into Th2 cells, and trigger SHIP(+/+) B cells to become IgE-producing cells. All these effects are completely abrogated with neutralizing anti-IL-4 Ab. Exploring the cell signaling pathways responsible for hyperproduction of IL-4 by SHIP(-/-) basophils, we found that IL-3-induced activation of the PI3K pathway is significantly enhanced and that PI3K inhibitors, especially a p110$\alpha$ inhibitor, dramatically suppresses IL-4 production from these cells. In vivo studies, in which basophils were depleted from mast cell-deficient SHIP(+/+) and SHIP(-/-) mice, confirmed the central role that basophils play in the Th2 skewing of naive SHIP-deficient mice. Taken together, these studies demonstrate that SHIP is a potent negative regulator of IL-4 production from basophils and thus may be a novel therapeutic target for Th1- and Th2-related diseases.