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mTeSR™1

cGMP, feeder-free maintenance medium for human ES and iPS Cells

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cGMP, feeder-free maintenance medium for human ES and iPS Cells
From: 279 USD

Overview

mTeSR™1, now manufactured under cGMP, is the most widely published feeder-free cell culture medium for human embryonic stem cells (ES cells) and induced pluripotent stem cells (iPS cells), with established protocols for applications ranging from derivation to differentiation. It has been used to successfully maintain thousands of ES and iPS cell lines in over 50 countries, and has supported top pluripotent stem cell publications and researchers. mTeSR™1 is a highly specialized, serum-free and complete cell culture medium. With pre-screened raw materials that ensure batch-to-batch consistency and robust feeder-free protocols for ES and iPS cell culture, mTeSR™1 provides more consistent cultures with homogeneous, undifferentiated phenotypes.

mTeSR™1 is manufactured under a cGMP quality management system compliant to 21 CFR 820, ensuring the highest quality and consistency for reproducible results.
Components:
  • mTeSR™1 Complete Kit (Catalog #85850)
    • mTeSR™1 Basal Medium, 400 mL (Catalog #85851)
    • mTeSR™1 5X Supplement, 100 mL (Catalog #85852)
  • mTeSR™1 Complete Kit, 1 L (Catalog #85857)
    • mTeSR™1 Basal Medium, 800 mL (Catalog #85871)
    • mTeSR™1 5X Supplement, 100 mL, 2 Bottles
  • mTeSR™1 Complete Kit, 10 Pack (Catalog #85870)
    • mTeSR™1 Basal Medium, 400 mL, 10 Bottles
    • mTeSR™1 5X Supplement, 100 mL, 10 Bottles
  • mTeSR™1 Complete Kit, 25 Pack (Catalog #85875)
    • mTeSR™1 Basal Medium, 400 mL, 25 Bottles
    • mTeSR™1 5X Supplement, 100 mL, 25 Bottles
Subtype:
Specialized Media
Cell Type:
Pluripotent Stem Cells
Species:
Human
Application:
Cell Culture; Expansion; Maintenance
Brand:
TeSR
Area of Interest:
Stem Cell Biology
Formulation:
Serum-Free; Defined

Scientific Resources

Product Documentation

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Educational Materials

(23)
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Product 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.

Data and Publications

Data

Figure 1. Normal hES and hiPS Cell Morphology is Observed in cGMP mTeSR™1 Cultures

Undifferentiated (A) H1 human embryonic stem (hES) and (B) WLS-1C human induced pluripotent stem (hiPS) cells cultured on Corning® Matrigel® Matrix in cGMP mTeSR™1 retain the prominent nucleoli and high nuclear-to-cytoplasmic ratio characteristic of this cell type after 10 passages. Densely packed cells and multi-layering are prominent when cells are ready to be passaged.

Figure 2. High Expansion Rates are Observed in cGMP mTeSR™1 Cultures

Graph shows the average fold expansion per passage +/- SEM obtained for hES (H1 and H9) and hiPS (WLS-1C) cells cultured in cGMP mTeSR­™1 (red) or non-cGMP mTeSR™1 (gray) on Corning® Matrigel® Matrix over 10 passages. Expansion was determined by enumerating the cell aggregates obtained at harvest and dividing by the number of cell aggregates seeded. Note that this data is representative of cultures passaged after 6-7 days in culture, lower expansion should be expected if using shorter culture times.

Figure 3. Cells Cultured in cGMP mTeSR™1 Medium Express Undifferentiated Cell Markers

Histogram analysis for hES (H1 and H9) and hiPS (WLS-1C) cells characterized using FACS for undifferentiated cell markers, OCT4 (OCT3) (Catalog #60093) and TRA-1-60 (Catalog #60064), after 8 - 10 passages in cGMP mTeSR™1 (filled = sample, blank = isotype control).

Figure 4. hPSCs Maintained in cGMP mTeSR™1 Display a Normal Karyotype

Karyograms of (A) H1 hES and (B) WLS-1C hiPS cells cultured in cGMP mTeSR™1 for 11 passages shows that a normal karyotype is retained.

Publications

(1554)
eLife 2018 MAY

A homozygous loss-of-function CAMK2A mutation causes growth delay, frequent seizures and severe intellectual disability.

P. H. Chia et al.

Abstract

Calcium/calmodulin-dependent protein kinase II (CAMK2) plays fundamental roles in synaptic plasticity that underlies learning and memory. Here, we describe a new recessive neurodevelopmental syndrome with global developmental delay, seizures and intellectual disability. Using linkage analysis and exome sequencing, we found that this disease maps to chromosome 5q31.1-q34 and is caused by a biallelic germline mutation in CAMK2A. The missense mutation, p.His477Tyr is located in the CAMK2A association domain that is critical for its function and localization. Biochemically, the p.His477Tyr mutant is defective in self-oligomerization and unable to assemble into the multimeric holoenzyme.In vivo, CAMK2AH477Y failed to rescue neuronal defects in C. elegans lacking unc-43, the ortholog of human CAMK2A. In vitro, neurons derived from patient iPSCs displayed profound synaptic defects. Together, our data demonstrate that a recessive germline mutation in CAMK2A leads to neurodevelopmental defects in humans and suggest that dysfunctional CAMK2 paralogs may contribute to other neurological disorders.
Stem cell reports 2018 MAY

Inflammatory Responses and Barrier Function of Endothelial Cells Derived from Human Induced Pluripotent Stem Cells.

O. V. Halaidych et al.

Abstract

Several studies have reported endothelial cell (EC) derivation from human induced pluripotent stem cells (hiPSCs). However, few have explored their functional properties in depth with respect to line-to-line and batch-to-batch variability and how they relate to primary ECs. We therefore carried out accurate characterization of hiPSC-derived ECs (hiPSC-ECs) from multiple (non-integrating) hiPSC lines and compared them with primary ECs in various functional assays, which included barrier function using real-time impedance spectroscopy with an integrated assay of electric wound healing, endothelia-leukocyte interaction under physiological flow to mimic inflammation and angiogenic responses in in vitro and in vivo assays. Overall, we found many similarities but also some important differences between hiPSC-derived and primary ECs. Assessment of vasculogenic responses in vivo showed little difference between primary ECs and hiPSC-ECs with regard to functional blood vessel formation, which may be important in future regenerative medicine applications requiring vascularization.
Journal of molecular and cellular cardiology 2018 MAY

Afterload promotes maturation of human induced pluripotent stem cell derived cardiomyocytes in engineered heart tissues.

A. Leonard et al.

Abstract

Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM) grown in engineered heart tissue (EHT) can be used for drug screening, disease modeling, and heart repair. However, the immaturity of hiPSC-CMs currently limits their use. Because mechanical loading increases during development and facilitates cardiac maturation, we hypothesized that afterload would promote maturation of EHTs. To test this we developed a system in which EHTs are suspended between a rigid post and a flexible one, whose resistance to contraction can be modulated by applying braces of varying length. These braces allow us to adjust afterload conditions over two orders of magnitude by increasing the flexible post resistance from 0.09 up to 9.2 mu$N/mu$m. After three weeks in culture, optical tracking of post deflections revealed that auxotonic twitch forces increased in correlation with the degree of afterload, whereas twitch velocities decreased with afterload. Consequently, the power and work of the EHTs were maximal under intermediate afterloads. When studied isometrically, the inotropy of EHTs increased with afterload up to an intermediate resistance (0.45 mu$N/mu$m) and then plateaued. Applied afterload increased sarcomere length, cardiomyocyte area and elongation, which are hallmarks of maturation. Furthermore, progressively increasing the level of afterload led to improved calcium handling, increased expression of several key markers of cardiac maturation, including a shift from fetal to adult ventricular myosin heavy chain isoforms. However, at the highest afterload condition, markers of pathological hypertrophy and fibrosis were also upregulated, although the bulk tissue stiffness remained the same for all levels of applied afterload tested. Together, our results indicate that application of moderate afterloads can substantially improve the maturation of hiPSC-CMs in EHTs, while high afterload conditions may mimic certain aspects of human cardiac pathology resulting from elevated mechanical overload.
Biomaterials 2018 JUN

Substrate stiffness modulates the multipotency of human neural crest derived ectomesenchymal stem cells via CD44 mediated PDGFR signaling.

A. Srinivasan et al.

Abstract

Mesenchymal stem cells (MSCs) have been isolated from various mesodermal and ectodermal tissues. While the phenotypic and functional heterogeneity of MSCs stemming from their developmental origins has been acknowledged, the genetic and environmental factors underpinning these differences are not well-understood. Here, we investigated whether substrate stiffness mediated mechanical cues can directly modulate the development of ectodermal MSCs (eMSCs) from a precursor human neural crest stem cell (NCSC) population. We showed that NCSC-derived eMSCs were transcriptionally and functionally distinct from mesodermal bone marrow MSCs. eMSCs derived on lower substrate stiffness specifically increased their expression of the MSC marker, CD44 in a Rho-ROCK signaling dependent manner, which resulted in a concomitant increase in the eMSCs' adipogenic and chondrogenic differentiation potential. This mechanically-induced effect can only be maintained for short-term upon switching back to a stiff substrate but can be sustained for longer-term when the eMSCs were exclusively maintained on soft substrates. We also discovered that CD44 expression modulated eMSC self-renewal and multipotency via the downregulation of downstream platelet-derived growth factor receptor beta (PDGFRbeta$) signaling. This is the first instance demonstrating that substrate stiffness not only influences the differentiation trajectories of MSCs but also their derivation from upstream progenitors, such as NCSCs.
Stem cell reports 2018 JUL

Disruption of GRIN2B Impairs Differentiation in Human Neurons.

S. Bell et al.

Abstract

Heterozygous loss-of-function mutations in GRIN2B, a subunit of the NMDA receptor, cause intellectual disability and language impairment. We developed clonal models of GRIN2B deletion and loss-of-function mutations in a region coding for the glutamate binding domain in human cells and generated neurons from a patient harboring a missense mutation in the same domain. Transcriptome analysis revealed extensive increases in genes associated with cell proliferation and decreases in genes associated with neuron differentiation, a result supported by extensive protein analyses. Using electrophysiology and calcium imaging, we demonstrate that NMDA receptors are present on neural progenitor cells and that human mutations in GRIN2B can impair calcium influx and membrane depolarization even in a presumed undifferentiated cell state, highlighting an important role for non-synaptic NMDA receptors. It may be this function, in part, which underlies the neurological disease observed in patients with GRIN2B mutations.