M0518
Medio esencial mínimo Eagle
Joklik Modification, with L-glutamine, without calcium chloride and sodium bicarbonate, suitable for cell culture
Sinónimos:
Joklik Modified MEM, MEM
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NACRES:
NA.75
UNSPSC Code:
12352207
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Permítanos ayudarleform
powder
technique(s)
cell culture | mammalian: suitable
components
HEPES: no
sodium pyruvate: no
L-glutamine: yes
NaHCO3: no
phenol red: yes
shipped in
ambient
storage temp.
2-8°C
Quality Level
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Application
Recommended for suspension cultures.
Preparation Note
Formulated to contain 11.0 grams of powder per liter of medium.
Supplement with 2.0 g/L sodium bicarbonate.
Clase de almacenamiento
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Population-based studies identified an association between a prior pregnancy complicated by gestational diabetes mellitus (GDM) and cardiac hypertrophy and dysfunction later in life. It is however unclear whether GDM initiates this phenotype and what are the underlying mechanisms. We addressed
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Despite their important role in metastatic disease, no general method to detect circulating stromal cells (CStCs) exists. Here, we present the Metabolic Assay-Chip (MA-Chip) as a label-free, droplet-based microfluidic approach allowing single-cell extracellular pH measurement for the detection and isolation
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Activating transcription factor-6 α (ATF6) is one of the three main sensors and effectors of the endoplasmic reticulum (ER) stress response and, as such, it is critical for protecting the heart and other tissues from a variety of environmental insults
Christopher A Drummond et al.
Physiological genomics, 48(3), 220-229 (2015-12-25)
Chronic kidney disease (CKD) is accompanied by cardiac fibrosis, hypertrophy, and dysfunction, which are commonly referred to as uremic cardiomyopathy. Our previous studies found that Na/K-ATPase ligands or 5/6th partial nephrectomy (PNx) induces cardiac fibrosis in rats and mice. The
Giulia Elisa Cambi et al.
Molecular bioSystems, 8(9), 2351-2359 (2012-06-28)
Although angiotensin (Ang)II-induced Janus-activated kinase (JAK)2 phosphorylation was reported to be enhanced in failing human cardiomyocytes, the downstream balance between cardio-protective (signal transducer and activator of transcription-STAT3) and the pro-inflammatory (STAT2 and STAT5) response remains unexplored. Therefore STATs phosphorylation and
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