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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

Sinónimos:

DME, DMEM

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About This Item

UNSPSC Code:
12352207
NACRES:
NA.75

Quality Level

500

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.

Other Notes

2024 CiteAb Award Winner for Supplier Succeeding in Parkinson′s Research

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pictograms

Exclamation mark
GHS07

signalword

Warning

hcodes

H319

Hazard Classifications

Eye Irrit. 2

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Elija entre una de las versiones más recientes:

Certificados de análisis (COA)

Lot/Batch Number
SLCL8142
SLCG2659
SLBW2010
SLBW1406
SLBS0115V

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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
Xiulan Yang et al.
Journal of molecular and cellular cardiology, 72, 296-304 (2014-04-17)
Cardiomyocytes derived from human induced pluripotent stem cells (hiPSC-CMs) have great potential as a cell source for therapeutic applications such as regenerative medicine, disease modeling, drug screening, and toxicity testing. This potential is limited, however, by the immature state of
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-
Zhongjie Fu et al.
EMBO molecular medicine, 10(1), 76-90 (2017-11-29)
The neural cells and factors determining normal vascular growth are not well defined even though vision-threatening neovessel growth, a major cause of blindness in retinopathy of prematurity (ROP) (and diabetic retinopathy), is driven by delayed normal vascular growth. We here
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