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D5030

Sigma-Aldrich

Dulbecco′s Modified Eagle′s Medium

Without glucose, L-glutamine, phenol red, sodium pyruvate and sodium bicarbonate, powder, suitable for cell culture

Synonym(s):

DME, DMEM

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About This Item

UNSPSC Code:
12352207
NACRES:
NA.75

Quality Level

form

powder

technique(s)

cell culture | mammalian: suitable

components

phenol red: no
NaHCO3: no
L-glutamine: no
HEPES: no
glucose: no
sodium pyruvate: no

shipped in

ambient

storage temp.

2-8°C

General description

Dulbecco′s Modified Eagle′s Medium (DME) is a modification of Basal Medium Eagle (BME) that has been formulated with a 4-fold higher concentration of amino acids and vitamins. It includes additional supplementary components. The DME formula, first reported for culturing embryonic mouse cells, contained 1,000 mg/L of glucose. Modifying the medium with 4,500 mg/L glucose is optimal for culturing certain cell types.
The most basic formulation offered. This formulation is used by investigators who want to start with the essential components of DME, and have the flexibility to optimize the formula for their own application.

Application

Dulbecco′s Modified Eagle′s Medium has been used:
  • to culture the isolated flexor digitorum brevis (FDB) fibers to measure exogenous fatty acid (FA) utilization as part of oxygen consumption rate (OCR) measurements
  • to culture the isolated tibialis anterior (TA) muscle fibers for lactate measurements
  • to culture the human bone marrow mesenchymal stem cells for osteogenic differentiation to prepare a low-glucose medium to culture human hepatocellular carcinoma HepG2 cells

Quantity

Formulated to contain 8.3 grams of powder per liter of medium.

Reconstitution

Supplement with 1.0 g/L glucose, 0.584 g/L L-glutamine, 3.7 g/L sodium bicarbonate.

Pictograms

Exclamation mark

Signal Word

Warning

Hazard Statements

Hazard Classifications

Eye Irrit. 2

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Nataly Stylianou et al.
Oncogene, 38(7), 913-934 (2018-09-09)
The propensity of cancer cells to transition between epithelial and mesenchymal phenotypic states via the epithelial-mesenchymal transition (EMT) program can regulate metastatic processes, cancer progression, and treatment resistance. Transcriptional investigations using reversible models of EMT, revealed the mesenchymal-to-epithelial reverting transition
Eunyong Ahn et al.
Molecular systems biology, 13(11), 953-953 (2017-11-08)
Cellular metabolic demands change throughout the cell cycle. Nevertheless, a characterization of how metabolic fluxes adapt to the changing demands throughout the cell cycle is lacking. Here, we developed a temporal-fluxomics approach to derive a comprehensive and quantitative view of
Abhinav Joshi et al.
BMC biology, 18(1), 10-10 (2020-01-29)
The molecular chaperone TRAP1, the mitochondrial isoform of cytosolic HSP90, remains poorly understood with respect to its pivotal role in the regulation of mitochondrial metabolism. Most studies have found it to be an inhibitor of mitochondrial oxidative phosphorylation (OXPHOS) and
Anna Vysochan et al.
Proceedings of the National Academy of Sciences of the United States of America, 114(8), E1528-E1535 (2017-02-09)
Recent studies have shown that human cytomegalovirus (HCMV) can induce a robust increase in lipid synthesis which is critical for the success of infection. In mammalian cells the central precursor for lipid biosynthesis, cytosolic acetyl CoA (Ac-CoA), is produced by
Charlotte Petersen et al.
Scientific reports, 7(1), 13101-13101 (2017-10-14)
Adipose tissue takes up glucose and releases lactate, thereby contributing significantly to systemic glucose and lactate homeostasis. This implies the necessity of upregulation of net acid and lactate flux capacity during adipocyte differentiation and function. However, the regulation of lactate-

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