STEMdiff™ 神经诱导培养基

用于人 ES 和 iPS 细胞神经诱导的成分明确的无血清培养基

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产品号 #05835_C

用于人 ES 和 iPS 细胞神经诱导的成分明确的无血清培养基

产品优势

成分明确，无血清
快速高效的神经诱导
兼容拟胚体和单层培养方案
可重复分化多种在mTeSR™ Plus、mTeSR™ 1或TeSR™-AOF中维持的ES细胞和iPS细胞系
方便、便捷、用户友好的格式和操作流程

产品组分包括

STEMdiff™ 神经诱导培养基，250 mL（产品号 #05835）
STEMdiff™ 神经诱导培养基，2 x 250 mL（产品号 #05839）

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总览

STEMdiff™ 神经诱导培养基是一种成分明确的无血清培养基，用于诱导人类胚胎干细胞 (ES) 和诱导性多能干细胞 (iPS) 的神经分化。该培养基能够通过基于胚状体或单层培养的方案高效生成神经祖细胞。

您可以在我们的按需神经诱导课程中学习如何从人类多能干细胞 (hPSC) 生成神经祖细胞，并浏览我们关于使用胚状体法或单层法进行 hPSC 神经诱导的技术技巧。

产品说明书及文档

请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。

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Document Type

Product Information Sheet

Product Name

STEMdiff™ Neural Induction Medium

Catalog #

05839, 05835

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All

Language

English

Document Type

Technical Manual

Product Name

STEMdiff™ Neural Induction Medium

Catalog #

05835

Lot #

All

Language

English

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Safety Data Sheet

Product Name

STEMdiff™ Neural Induction Medium

Catalog #

05839, 05835

Lot #

All

Language

English

文献 (52)

Lithium partially rescues gene expression and enhancer activity from heterozygous knockout of AKAP11 while inducing novel differential changes N. Farhangdoost et al. Scientific Reports 2025 Oct

Abstract

Bipolar disorder (BD) is a complex psychiatric condition usually requiring long-term treatment. Lithium (Li) remains the most effective mood stabilizer for BD, yet it benefits only a subset of patients, and its precise mechanism of action remains elusive. Exome sequencing has identified AKAP11 (A-kinase anchoring protein 11) as a shared risk gene for BD and schizophrenia (SCZ). Given that both the AKAP11-Protein Kinase A (PKA) complex and Li target and inhibit Glycogen Synthase Kinase-3 beta (GSK3β), we hypothesize that Li may partially normalize the transcriptomic and/or epigenomic alterations observed in heterozygous AKAP11-knockout (Het-AKAP11-KO) iPSC-derived neurons. In this study, we employed genome-wide approaches to assess the effects of Li on the transcriptome and epigenome of human iPSC-derived Het-AKAP11-KO neuronal culture. We show that chronic Li treatment in this cellular model upregulates key pathways that were initially downregulated by Het-AKAP11-KO, several of which have also been reported as downregulated in synapses of BD and SCZ post-mortem brain tissues. Moreover, we demonstrated that Li treatment partially rescues certain transcriptomic alterations resulting from Het-AKAP11-KO, bringing them closer to the WT state. We suggest two possible mechanisms underlying these transcriptomic effects: (1) Li modulates histone H3K27ac levels at intergenic and intronic enhancers, influencing enhancer activity and transcription factor binding, and (2) Li enhances GSK3β serine 9 phosphorylation, impacting WNT/β-catenin signaling and downstream transcription. These findings underscore Li’s potential as a therapeutic agent for BD and SCZ patients carrying AKAP11 loss-of-function variants or exhibiting similar pathway alterations to those observed in Het-AKAP11-KO models.

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Antiretroviral drug therapy does not reduce neuroinflammation in an HIV-1 infection brain organoid model Journal of Neuroinflammation 2025 Mar

Abstract

BackgroundHIV-1-associated neurocognitive impairment (HIV-1-NCI) is marked by ongoing and chronic neuroinflammation with loss and decline in neuronal function even when antiretroviral drug therapy (ART) successfully suppresses viral replication. Microglia, the primary reservoirs of HIV-1 in the central nervous system (CNS), play a significant role in maintaining this neuroinflammatory state. However, understanding how chronic neuroinflammation is generated and sustained by HIV-1, or impacted by ART, is difficult due to limited access to human CNS tissue.MethodsWe generated an in vitro model of admixed hematopoietic progenitor cell (HPC) derived microglia embedded into embryonic stem cell (ESC) derived Brain Organoids (BO). Microglia were infected with HIV-1 prior to co-culture. Infected microglia were co-cultured with brain organoids BOs to infiltrate the BOs and establish a model for HIV-1 infection, “HIV-1 M-BO”. HIV-1 M-BOs were treated with ART for variable directions. HIV-1 infection was monitored with p24 ELISA and by digital droplet PCR (ddPCR). Inflammation was measured by cytokine or p-NF-kB levels using multiplex ELISA, flow cytometry and confocal microscopy.ResultsHIV-1 infected microglia could be co-cultured with BOs to create a model for “brain” HIV-1 infection. Although HIV-1 infected microglia were the initial source of pro-inflammatory cytokines, astrocytes, neurons and neural stem cells also had increased p-NF-kB levels, along with elevated CCL2 levels in the supernatant of HIV-1 M-BOs compared to Uninfected M-BOs. ART suppressed the virus to levels below the limit of detection but did not decrease neuroinflammation.ConclusionsThese findings indicate that HIV-1 infected microglia are pro-inflammatory. Although ART significantly suppressed HIV-1 levels, neuronal inflammation persisted in ART-treated HIV-1 M-BOs. Together, these findings indicate that HIV-1 infection of microglia infiltrated into BOs provides a robust in vitro model to understand the impact of HIV-1 and ART on neuroinflammation.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12974-025-03375-w.

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CACNA1A loss-of-function affects neurogenesis in human iPSC-derived neural models I. Musante et al. Cellular and Molecular Life Sciences: CMLS 2025 Jun

Abstract

CACNA1A encodes the pore-forming α 1A subunit of the Ca V 2.1 calcium channel, whose altered function is associated with various neurological disorders, including forms of ataxia, epilepsy, and migraine. In this study, we generated isogenic iPSC-derived neural cultures carrying CACNA1A loss-of-function mutations differently affecting Ca V 2.1 splice isoforms. Morphological, molecular, and functional analyses revealed an essential role of CACNA1A in neurodevelopmental processes. We found that different CACNA1A loss-of-function mutations produce distinct neurodevelopmental deficits. The F1491S mutation, which is located in a constitutive domain of the channel and therefore causes a complete loss-of-function, impaired neural induction at very early stages, as demonstrated by changes in single-cell transcriptomic signatures of neural progenitors, and by defective polarization of neurons. By contrast, cells carrying the Y1854X mutation, which selectively impacts the synaptically-expressed Ca V 2.1[EFa] isoform, behaved normally in terms of neural induction but showed altered neuronal network composition and lack of synchronized activity. Our findings reveal previously unrecognized roles of CACNA1A in the mechanisms underlying neural induction and neural network dynamics and highlight the differential contribution of the divergent variants Ca V 2.1[EFa] and Ca V 2.1[EFb] in the development of human neuronal cells. The online version contains supplementary material available at 10.1007/s00018-025-05740-7.

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物种	人类
配方	无血清

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STEMdiff™ 神经诱导培养基

产品号 #05839

产品号 #05835

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产品号 #05835_C

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STEMdiff™ 神经诱导培养基

产品号 #05839

产品号 #05835

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产品号 #05835_C

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文献 (52)

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