mTeSR™ Plus
cGMP, stabilized feeder-free maintenance medium for human ES and iPS cells
Need a high-quality cell source? Choose from our hiPSC healthy control lines, manufactured with mTeSR™ Plus.
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What Our Scientist Says
Innovation is a core value at ƽ. The evolution to mTeSR™ Plus reflects that and our desire to serve the next generation of pluripotent stem cell researchers.
Matthew WongScientist
Overview
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Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
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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
Educational Materials (56)
Publications (216)
AEOL-induced NRF2 activation and DWORF overexpression mitigate myocardial I/R injury
Molecular Medicine 2025 May
Abstract
BackgroundThe causal relationship between the activation of nuclear factor erythroid 2-related factor 2 (NRF2) and the preservation of SERCA2a function in mitigating myocardial ischemia–reperfusion (mI/R) injury, along with the associated regulatory mechanisms, remains incompletely understood. This study aims to unravel how NRF2 directly or indirectly influences SERCA2a function and its regulators, phospholamban (PLN) and Dwarf Open Reading Frame (DWORF), by testing the pharmacological repositioning of AEOL-10150 (AEOL) in the context of mI/R injury.MethodsC57BL6/J, Nrf2 knockout (Nrf2?/?), and wild-type (Nrf2+/+) mice, as well as human induced pluripotent stem cell-derived cardiomyocytes (hiPSCMs) were subjected to I/R injury. Gain/loss of function techniques, RT-qPCR, western blotting, LC/MS/MS, and fluorescence spectroscopy were utilized. Cardiac dimensions and function were assessed by echocardiography.ResultsIn the early stages of mI/R injury, AEOL administration reduced mitochondrial ROS production, decreased myocardial infarct size, and improved cardiac function. These effects were due to NRF2 activation, leading to the overexpression of the micro-peptide DWORF, consequently enhancing SERCA2a activity. The cardioprotective effect induced by AEOL was diminished in Nrf2?/? mice and in Nrf2/Dworf knockdown models in hiPSCMs subjected to simulated I/R injury. Our data show that AEOL-induced NRF2-mediated upregulation of DWORF disrupts the phospholamban-SERCA2a interaction, leading to enhanced SERCA2a activation and improved cardiac function.ConclusionsTaken together, our study reveals that AEOL-induced NRF2-mediated overexpression of DWORF enhances myocardial function through the activation of the SERCA2a offering promising therapeutic avenues for mI/R injury.Supplementary InformationThe online version contains supplementary material available at 10.1186/s10020-025-01242-1. Highlights• Novel AEOL-10150 therapeutic potential. AEOL-10150 demonstrates promise in activating NRF2 and mitigating myocardial ischemia-reperfusion injury.• DWORF overexpression breakthrough. Overexpression of DWORF significantly contributes to preserving cardiac function and reducing myocardial injury through the NRF2-DWORF pathway.• Enhanced cardiac protection mechanisms. The study highlights the dual role of AEOL-10150 and DWORF in enhancing cardiac protection and preventing heart failure.• Future research directions. Additional studies are required to validate the long-term efficacy of AEOL-10150 and the regulatory effects of NRF2-DWORF axis in clinical applications.Supplementary InformationThe online version contains supplementary material available at 10.1186/s10020-025-01242-1.
Creatine mitigates neurogenesis impairment caused by defective DcpS decapping
Scientific Reports 2025 May
Abstract
Biallelic mutations in the DCPS gene disrupting the decapping activity of the scavenger decapping protein DcpS, leads to neurodevelopmental deficiencies and intellectual disability. However, the molecular basis for the neurogenesis defects in these individuals remains unknown. Here we show that cells derived from individuals with a DCPS mutation harbor a creatine deficiency and a corresponding elevation of the creatine precursor, guanidinoacetate (GAA). The altered metabolite levels are a consequence of a reduction in both the mRNA and protein levels for the enzyme that converts GAA into creatine, guanidinoacetate methyltransferase. Importantly, the compromised neurogenesis and neurite outgrowth phenotypes observed during the differentiation of DcpS mutant patient derived induced pluripotent stem cells into neurons was reversed upon supplementation of creatine monohydrate. These findings suggest creatine deficiency as an underlying factor for the neurogenetic defect detected in DcpS mutant cells and a potential driver of the neurological deficiencies in affected individuals.
Single-cell RNA-sequencing reveals early mitochondrial dysfunction unique to motor neurons shared across FUS- and TARDBP-ALS
Nature Communications 2025 May
Abstract
Mutations in FUS and TARDBP cause amyotrophic lateral sclerosis (ALS), but the precise mechanisms of selective motor neuron degeneration remain unresolved. To address if pathomechanisms are shared across mutations and related to either gain- or loss-of-function, we performed single-cell RNA sequencing across isogenic induced pluripotent stem cell-derived neuron types, harbouring FUS P525L, FUS R495X, TARDBP M337V mutations or FUS knockout. Transcriptional changes were far more pronounced in motor neurons than interneurons. About 20% of uniquely dysregulated motor neuron transcripts were shared across FUS mutations, half from gain-of-function. Most indicated mitochondrial impairments, with attenuated pathways shared with mutant TARDBP M337V as well as C9orf72-ALS patient motor neurons. Mitochondrial motility was impaired in ALS motor axons, even with nuclear localized FUS mutants, demonstrating shared toxic gain-of-function mechanisms across FUS- and TARDBP-ALS, uncoupled from protein mislocalization. These early mitochondrial dysfunctions unique to motor neurons may affect survival and represent therapeutic targets in ALS. In this study, the authors performed single-cell RNA-sequencing across various isogenic mutant FUS and TDP43 neurons. Mitochondrial dysfunction emerged as pathway unique to motor neurons demonstrating shared toxic gain of-function mechanisms, uncoupled from protein mislocalization.
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Legal Statement:
This product was developed under license to intellectual property owned by WiCell™ Research Institute. This product is sold for research use only (whether the buyer is an academic or for-profit entity) under a non-transferable, limited-use license. Purchase of this product does not include the right to sell, use or otherwise transfer this product for commercial purposes (i.e., any activity undertaken for consideration, such as use of this product for manufacturing, or resale of this product or any materials made using this product, or use of this product or any materials made using this product to provide services) or clinical use (i.e., administration of this product or any material using this product to humans) or the right to implant any material made using this product into an animal by, or in collaboration with, a for-profit entity, for purposes other than basic pre-clinical research applications (including without limitation teratoma assays) to validate the function of the cells. Purchasers who do not agree to the terms and conditions set forth above should return the product in acceptable conditions to the seller for a refund.
This product was developed under license to intellectual property owned by WiCell™ Research Institute. This product is sold for research use only (whether the buyer is an academic or for-profit entity) under a non-transferable, limited-use license. Purchase of this product does not include the right to sell, use or otherwise transfer this product for commercial purposes (i.e., any activity undertaken for consideration, such as use of this product for manufacturing, or resale of this product or any materials made using this product, or use of this product or any materials made using this product to provide services) or clinical use (i.e., administration of this product or any material using this product to humans) or the right to implant any material made using this product into an animal by, or in collaboration with, a for-profit entity, for purposes other than basic pre-clinical research applications (including without limitation teratoma assays) to validate the function of the cells. Purchasers who do not agree to the terms and conditions set forth above should return the product in acceptable conditions to the seller for a refund.
Quality Statement:
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT ƽ, REFER TO WWW.ƽ.COM/COMPLIANCE.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT ƽ, REFER TO WWW.ƽ.COM/COMPLIANCE.
