产品号 #07152_C
用于小鼠和人胚胎干细胞和iPS细胞的神经和胰腺分化
总览
N2 添加物-A 富含铁人源转铁蛋白，专为小鼠或人胚胎干细胞（ES）及诱导多能干细胞（iPS）在体外分化为神经及类胰腺细胞类型而开发。在将人 ES/iPS 细胞分化得到的神经祖细胞接种于 BrainPhys™ 神经元培养基（产品号 #05790）并补充 N2 添加物-A、NeuroCult™ SM1 神经元添加物（产品号 #05711）及其他因子后，可进一步诱导形成不同亚型的神经元细胞。
N2 添加物-A 以 100 倍浓缩液形式提供，可单独购买，也可作为 BrainPhys™ 神经元培养基 N2-A & SM1 试剂盒（产品号 #05793）的组分购买。
包含
• Recombinant human insulin
• Human holo-transferrin (iron-saturated)
• Sodium selenite
• Putrescine
• Progesterone
• Other ingredients
亚型
添加剂
细胞类型
内胚层，PSC衍生，神经细胞，PSC衍生，神经干/祖细胞，胰腺细胞，多能干细胞
种属
人，小鼠
应用
细胞培养，分化
研究领域
疾病建模，神经科学，干细胞生物学
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
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 (6)
Publications (7)
Modelling Lyssavirus Infections in Human Stem Cell-Derived Neural Cultures. Viruses 2020 mar
Abstract
Rabies is a zoonotic neurological infection caused by lyssavirus that continues to result in devastating loss of human life. Many aspects of rabies pathogenesis in human neurons are not well understood. Lack of appropriate ex-vivo models for studying rabies infection in human neurons has contributed to this knowledge gap. In this study, we utilize advances in stem cell technology to characterize rabies infection in human stem cell-derived neurons. We show key cellular features of rabies infection in our human neural cultures, including upregulation of inflammatory chemokines, lack of neuronal apoptosis, and axonal transmission of viruses in neuronal networks. In addition, we highlight specific differences in cellular pathogenesis between laboratory-adapted and field strain lyssavirus. This study therefore defines the first stem cell-derived ex-vivo model system to study rabies pathogenesis in human neurons. This new model system demonstrates the potential for enabling an increased understanding of molecular mechanisms in human rabies, which could lead to improved control methods.
Maturation of Human Pluripotent Stem Cell-Derived Cerebellar Neurons in the Absence of Co-culture. Frontiers in bioengineering and biotechnology 2020
Abstract
The cerebellum plays a critical role in all vertebrates, and many neurological disorders are associated with cerebellum dysfunction. A major limitation in cerebellar research has been the lack of adequate disease models. As an alternative to animal models, cerebellar neurons differentiated from pluripotent stem cells have been used. However, previous studies only produced limited amounts of Purkinje cells. Moreover, in vitro generation of Purkinje cells required co-culture systems, which may introduce unknown components to the system. Here we describe a novel differentiation strategy that uses defined medium to generate Purkinje cells, granule cells, interneurons, and deep cerebellar nuclei projection neurons, that self-formed and differentiated into electrically active cells. Using a defined basal medium optimized for neuronal cell culture, we successfully promoted the differentiation of cerebellar precursors without the need for co-culturing. We anticipate that our findings may help developing better models for the study of cerebellar dysfunctions, while providing an advance toward the development of autologous replacement strategies for treating cerebellar degenerative diseases.
Mutations in ACTL6B Cause Neurodevelopmental Deficits and Epilepsy and Lead to Loss of Dendrites in Human Neurons. American journal of human genetics 2019
Abstract
We identified individuals with variations in ACTL6B, a component of the chromatin remodeling machinery including the BAF complex. Ten individuals harbored bi-allelic mutations and presented with global developmental delay, epileptic encephalopathy, and spasticity, and ten individuals with de novo heterozygous mutations displayed intellectual disability, ambulation deficits, severe language impairment, hypotonia, Rett-like stereotypies, and minor facial dysmorphisms (wide mouth, diastema, bulbous nose). Nine of these ten unrelated individuals had the identical de novo c.1027G{\textgreater}A (p.Gly343Arg) mutation. Human-derived neurons were generated that recaptured ACTL6B expression patterns in development from progenitor cell to post-mitotic neuron, validating the use of this model. Engineered knock-out of ACTL6B in wild-type human neurons resulted in profound deficits in dendrite development, a result recapitulated in two individuals with different bi-allelic mutations, and reversed on clonal genetic repair or exogenous expression of ACTL6B. Whole-transcriptome analyses and whole-genomic profiling of the BAF complex in wild-type and bi-allelic mutant ACTL6B neural progenitor cells and neurons revealed increased genomic binding of the BAF complex in ACTL6B mutants, with corresponding transcriptional changes in several genes including TPPP and FSCN1, suggesting that altered regulation of some cytoskeletal genes contribute to altered dendrite development. Assessment of bi-alleic and heterozygous ACTL6B mutations on an ACTL6B knock-out human background demonstrated that bi-allelic mutations mimic engineered deletion deficits while heterozygous mutations do not, suggesting that the former are loss of function and the latter are gain of function. These results reveal a role for ACTL6B in neurodevelopment and implicate another component of chromatin remodeling machinery in brain disease.
更多信息
| Species | Human, Mouse |
|---|---|
| Contains | • Recombinant human insulin • Human holo-transferrin (iron-saturated) • Sodium selenite • Putrescine • Progesterone • Other ingredients |
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N2 添加物-B用于小鼠和人胚胎干细胞和iPS细胞的神经分化
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 STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE. Safety Statement: CA WARNING: This product can expose you to Progesterone which is known to the State of California to cause cancer. For more information go to www.P65Warnings.ca.gov
