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cGMP, 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 mTeSRâ„¢ Plus.
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What Our Scientist Says
It makes me proud knowing that my work is critical to keeping thousands of hPSC lines reliably healthy and consistent around the world.
Arwen HunterAssociate Director, Stem Cell Biology
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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 (40)
Publications (1903)
Consequences of the Novel ALS-Associated KIF5A Variant c.2993-6C > A for Exon 27 Splicing and Axonal Transport of SFPQ
Neurology: Genetics 2026 Mar
Abstract
Background and Objectives: Recent studies have identified variants in the kinesin family member 5A (KIF5A) gene that predispose to amyotrophic lateral sclerosis (ALS). These ALS-linked KIF5A variants lead to the exclusion of exon 27, resulting in the production of a mutated protein with an altered C-terminal region (KIF5A ΔExon27). Through whole genome sequencing, we identified a novel KIF5A intronic variant, rs1057522322 (c.2993-6C > A; chr12:57582596C > A, GRCh38.p14), in a family segregating ALS. Our goal is to investigate the effect of this variant on exon 27 splicing and to assess its functional consequences on KIF5A-mediated cargo transport. Methods: Induced pluripotent stem cells (iPSCs) were generated from siblings with and without the c.2993-6C > A variant. RT-PCR was performed on RNA extracted from iPSC-derived neurons to assess exon 27 splicing. Functional studies were conducted on iPSC-derived motor neurons (MNs). Results: RT-PCR confirmed that the c.2993-6C > A variant induced exon 27 skipping in KIF5A. Immunofluorescent staining showed that KIF5A ΔExon27 abolished the axonal interaction with splicing factor proline- and glutamine-rich, a cargo specifically transported by KIF5A. Under stress conditions, MNs carrying the c.2993-6C > A variant exhibited TDP-43 proteinopathy. Discussion: KIF5A intronic variant c.2993-6C > A could be a risk factor for ALS. KIF5A ΔExon27 impairs KIF5A-mediated cargo transport and contributes to ALS pathogenesis in a TDP-43–dependent manner.
Predicting metabolic dysfunction–associated steatotic liver disease risk using patient-derived induced pluripotent stem cells
Stem Cells Translational Medicine 2026 Jan
Abstract
Metabolic dysfunction–associated steatotic liver disease (MASLD) is reversible at early stages, making early identification critical. We previously demonstrated that patient-derived induced pluripotent stem cells (iPSCs) carrying MASLD-associated genetic risk variants exhibit greater oleate-induced intracellular lipid accumulation than those without these variants. This study aimed to develop an iPSC-based MASLD risk predictor using functional lipid accumulation assessments. We quantified oleate-induced lipid accumulation in iPSCs from three cohorts: (1) CIRM (22 cases, 20 controls), (2) POST (18 cases, 16 controls), and (3) UCSF (4 cases, 8 controls). Data from the CIRM cohort was used to define an iPSC-based MASLD risk score, which was subsequently validated in the POST and UCSF cohorts. Lipid accumulation was consistently higher in MASLD iPSCs across cohorts. The risk score achieved 44% sensitivity/75% specificity in POST and 75%/100% in UCSF. These findings suggest that oleate-induced lipid accumulation in iPSCs may be a predictor of MASLD risk. Larger studies incorporating additional cellular phenotypes, clinical, and genetic data could enhance predictive accuracy for MASLD surveillance and prevention.
The serotonin receptor 2b (5-HT2B) modulates heart remodeling following myocardial infarction via regulation of Hippo pathway
iScience 2026 Jan
Abstract
Myocardial infarction (MI) is a leading cause of death globally. Following MI, the heart undergoes remodeling leading to heart failure. The Hippo pathway is a major regulator of cell growth and survival in cardiomyocytes. Here, we show that serotonin receptor 2B (5-HT2B) regulates the Hippo pathway in cardiomyocytes and modulates heart remodeling following MI. 5-HT2B expression significantly enhanced the Hippo pathway effector Yes-associated protein (YAP) activity resulting in increased cardiomyocyte proliferation and decreased apoptosis. However, transgenic mice overexpressing 5-HT2B in cardiomyocytes had a lower survival rate post-MI. Conversely, modified mRNA (modRNA)-mediated transient 5-HT2B expression in the heart was sufficient to inhibit post-MI remodeling. Pharmacological screening of serotonergic compounds identified SB204741 as a modulator of the Hippo/YAP pathway in cardiomyocytes. SB204741 has been shown to protect the heart from adverse remodeling post-MI. Our findings identify 5-HT2B as a regulator of the Hippo pathway that can be targeted to improve cardiac phenotype following MI. Highlights•Serotonin receptor 2B (5HT2B) regulates the Hippo pathway and activates YAP in cardiomyocytes•5HT2B promotes cardiomyocyte proliferation and survival in vitro•Transgenic overexpression of 5HT2B exacerbates hypertrophic remodeling following MI•modRNA delivery of exogenous 5HT2B was partially protective against MI-induced remodeling Biochemical mechanism; Human metabolism; Molecular network
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This product was developed under license to intellectual property owned by WiCellâ„¢ 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 WiCellâ„¢ 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 º£½ÇÆƽâ°æ, REFER TO WWW.º£½ÇÆƽâ°æ.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 º£½ÇÆƽâ°æ, REFER TO WWW.º£½ÇÆƽâ°æ.COM/COMPLIANCE.
