Schwann cells are a type of glial cell found in the peripheral nervous system (PNS). These cells are essential for the myelination of peripheral axons. There are two main types of Schwann cells: myelinating and non-myelinating.​

​Myelinating Schwann cells wrap around a single axon to form a myelin sheath, while non-myelinating Schwann cells support multiple small-diameter axons without forming myelin. In addition to their insulating role, Schwann cells are active participants in nerve development, maintenance, and repair. ​

​In pathological conditions such as peripheral neuropathies and Charcot-Marie-Tooth disease, Schwann cell dysfunction contributes to disease progression, making them a target of interest for therapeutic intervention. Moreover, their regenerative potential is being explored in biomedical applications, including nerve grafts and tissue engineering.

Product Details

The post Schwann Cells (iPSC-derived, Normal) appeared first on iXCells.

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disease of the motor system, characterized by selective and progressive loss of motor neurons, eventually leading to paralysis and death within 2–5 years ^[1]. iPSC-derived motor neurons are valuable tools for biochemical analysis, disease modelling and clinical application of this disease. Cytoplasmic accumulation and nuclear loss of the RNA binding protein transactive response DNA-binding protein 43 (TDP-43) from affected neurons in most instances of ALS ^[2-3]. Over 40 dominantly inherited mutations in the gene encoding TDP-43 have subsequently been identified in familial ALS patients ^[4], implicating TDP-43 dysfunction in the vast majority of ALS cases.

Human Motor Neurons (iPSC-derived, TDP-43 mutation, N352S) is derived from a genetically modified normal iPSC line carrying the heterozygous or homozygous N352S mutation in the TDP-43 gene (Figure 1). iXCells hiPSC-derived motor neurons express typical markers of motor neurons, e.g. HB9 (MNX1), ISL1, CHAT, (Figure 2), with the purity higher than 85%. iXCells motor neurons are available in both cryopreserved vials and fresh plate formats (12, 24, 48, and 96-well plate). Most of the cells will express high level of HB9 and ISL-1 after thawing in the Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML). And after cultured in the medium for 5-7 days, these cells will express high levels of CHAT and MAP2.

Figure 1. Heterozygous and homozygous N352S mutation (highlighted) has been introduced to TDP-43 gene using CRISPR/Cas9 based genome editing technology. The targeted site is verified by genomic PCR/Sanger sequencing.

Figure 2. Immunofluorescence staining showing HB9 and ChAT positive cells on day 2 and 7 in culture respectively.

Product Details

Organism	Homo Sapiens, Human
Cell Type	Brain Cell
Disease	ALS
Package Size	1 x 106 cells/vial and 2 x 106 cells/vial
Passage Number	P0
Growth Properties	Adherent
Shipped	Cryopreserved
Storage	Liquid Nitrogen
Associated Media	iXCells Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML)

References

[1] Taylor, J. P., Brown, R. H. Jr & Cleveland, D. W. Decoding ALS: from genes to mechanism. Nature 539, 197–206 (2016).

[2] Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).

[3] Ling, S. C., Polymenidou, M. & Cleveland, D. W. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron 79, 416–438 (2013).

[4] Lagier-Tourenne, C., Polymenidou, M. & Cleveland, D. W. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. Hum. Mol. Genet. 19, R46–R64 (2010).

Datasheet & Culture Protocol

The post Human Motor Neurons (iPSC-derived, TDP-43 mutation, N352S, ISO) appeared first on iXCells.

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disease of the motor system, characterized by selective and progressive loss of motor neurons, eventually leading to paralysis and death within 2–5 years ^[1]. iPSC-derived motor neurons are valuable tools for biochemical analysis, disease modelling and clinical application of this disease. Cytoplasmic accumulation and nuclear loss of the RNA binding protein transactive response DNA-binding protein 43 (TDP-43) from affected neurons in most instances of ALS ^[2-3]. Over 40 dominantly inherited mutations in the gene encoding TDP-43 have subsequently been identified in familial ALS patients ^[4], implicating TDP-43 dysfunction in the vast majority of ALS cases.

Human Motor Neurons (iPSC-derived, TDP-43 mutation, N352S) is derived from a genetically modified normal iPSC line carrying the heterozygous or homozygous N352S mutation in the TDP-43 gene (Figure 1). iXCells hiPSC-derived motor neurons express typical markers of motor neurons, e.g. HB9 (MNX1), ISL1, CHAT, (Figure 2), with the purity higher than 85%. iXCells motor neurons are available in both cryopreserved vials and fresh plate formats (12, 24, 48, and 96-well plate). Most of the cells will express high level of HB9 and ISL-1 after thawing in the Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML). And after cultured in the medium for 5-7 days, these cells will express high levels of CHAT and MAP2.

Figure 1. Heterozygous and homozygous N352S mutation (highlighted) has been introduced to TDP-43 gene using CRISPR/Cas9 based genome editing technology. The targeted site is verified by genomic PCR/Sanger sequencing.

Figure 2. Immunofluorescence staining showing HB9 and ChAT positive cells on day 2 and 7 in culture respectively.

Product Details

Organism	Homo Sapiens, Human
Cell Type	Brain Cell
Disease	ALS
Package Size	1 x 106 cells/vial and 2 x 106 cells/vial
Passage Number	P0
Growth Properties	Adherent
Shipped	Cryopreserved
Storage	Liquid Nitrogen
Associated Media	iXCells Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML)

References

[1] Taylor, J. P., Brown, R. H. Jr & Cleveland, D. W. Decoding ALS: from genes to mechanism. Nature 539, 197–206 (2016).

[2] Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).

[3] Ling, S. C., Polymenidou, M. & Cleveland, D. W. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron 79, 416–438 (2013).

[4] Lagier-Tourenne, C., Polymenidou, M. & Cleveland, D. W. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. Hum. Mol. Genet. 19, R46–R64 (2010).

Datasheet & Culture Protocol

The post Human Motor Neurons (iPSC-derived, TDP-43 mutation, N352S, HOM) appeared first on iXCells.

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disease of the motor system, characterized by selective and progressive loss of motor neurons, eventually leading to paralysis and death within 2–5 years ^[1].  iPSC-derived motor neurons are valuable tools for biochemical analysis, disease modelling and clinical application of this disease.  Cytoplasmic accumulation and nuclear loss of the RNA binding protein transactive response DNA-binding protein 43 (TDP-43) from affected neurons in most instances of ALS ^[2-3]. Over 40 dominantly inherited mutations in the gene encoding TDP-43 have subsequently been identified in familial ALS patients ^[4], implicating TDP-43 dysfunction in the vast majority of ALS cases.

Human Motor Neurons (iPSC-derived, TDP-43 mutation, Q331K) is derived from a genetically modified normal iPSC line carrying the heterozygous or homozygous Q331K mutation in the TDP-43 gene (Figure 1). iXCells hiPSC-derived motor neurons express typical markers of motor neurons, e.g. HB9 (MNX1), ISL1, CHAT, (Figure 2), with the purity higher than 85%. iXCells motor neurons are available in both cryopreserved vials and fresh plate formats (12, 24, 48, and 96-well plate). Most of the cells will express high level of HB9 and ISL-1 after thawing in the Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML). After culturing in the medium for 5-7 days, these cells will express high levels of CHAT and MAP2.

Figure 1.Heterozygous and homozygous Q331K mutation (highlighted) has been introduced to TDP-43 gene using CRISPR/Cas9 based genome editing technology. The targeted site is verified by genomic PCR/Sanger .sequencing.

Figure 2.Immunofluorescence staining showing HB9 and ChAT positive cells on day 2 and 7 in culture respectively.

Product Details

Tissue Origin	Homo Sapiens, Human
Cell Type	Brain Cell
Disease	ALS
Package Size	1.0 million cells/vial; 2.0 million cells/vial
Passage Number	P0
Growth Properties	Adherent
Shipped	Cryopreserved
Storage	Liquid Nitrogen
Media	iXCells Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML)

References

[1] Taylor, J. P., Brown, R. H. Jr & Cleveland, D. W. Decoding ALS: from genes to mechanism. Nature 539, 197–206 (2016).

[2] Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).

[3] Ling, S. C., Polymenidou, M. & Cleveland, D. W. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron 79, 416–438 (2013).

[4] Lagier-Tourenne, C., Polymenidou, M. & Cleveland, D. W. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. Hum. Mol. Genet. 19, R46–R64 (2010).

Datasheet & Culture Protocol

The post Human Motor Neurons (iPSC-derived, TDP-43 mutation, Q331K, ISO) appeared first on iXCells.

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disease of the motor system, characterized by selective and progressive loss of motor neurons, eventually leading to paralysis and death within 2–5 years ^[1].  iPSC-derived motor neurons are valuable tools for biochemical analysis, disease modelling and clinical application of this disease.  Cytoplasmic accumulation and nuclear loss of the RNA binding protein transactive response DNA-binding protein 43 (TDP-43) from affected neurons in most instances of ALS ^[2-3]. Over 40 dominantly inherited mutations in the gene encoding TDP-43 have subsequently been identified in familial ALS patients ^[4], implicating TDP-43 dysfunction in the vast majority of ALS cases.

Human Motor Neurons (iPSC-derived, TDP-43 mutation, Q331K) is derived from a genetically modified normal iPSC line carrying the heterozygous or homozygous Q331K mutation in the TDP-43 gene (Figure 1). iXCells hiPSC-derived motor neurons express typical markers of motor neurons, e.g. HB9 (MNX1), ISL1, CHAT, (Figure 2), with the purity higher than 85%. iXCells motor neurons are available in both cryopreserved vials and fresh plate formats (12, 24, 48, and 96-well plate). Most of the cells will express high level of HB9 and ISL-1 after thawing in the Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML). After culturing in the medium for 5-7 days, these cells will express high levels of CHAT and MAP2.

Figure 1.Heterozygous and homozygous Q331K mutation (highlighted) has been introduced to TDP-43 gene using CRISPR/Cas9 based genome editing technology. The targeted site is verified by genomic PCR/Sanger .sequencing.

Figure 2.Immunofluorescence staining showing HB9 and ChAT positive cells on day 2 and 7 in culture respectively.

Product Details

Tissue Origin	Homo Sapiens, Human
Cell Type	Brain Cell
Disease	ALS
Package Size	1.0 million cells/vial; 2.0 million cells/vial
Passage Number	P0
Growth Properties	Adherent
Shipped	Cryopreserved
Storage	Liquid Nitrogen
Media	iXCells Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML)

References

[1] Taylor, J. P., Brown, R. H. Jr & Cleveland, D. W. Decoding ALS: from genes to mechanism. Nature 539, 197–206 (2016).

[2] Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).

[3] Ling, S. C., Polymenidou, M. & Cleveland, D. W. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron 79, 416–438 (2013).

[4] Lagier-Tourenne, C., Polymenidou, M. & Cleveland, D. W. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. Hum. Mol. Genet. 19, R46–R64 (2010).

Datasheet & Culture Protocol

The post Human Motor Neurons (iPSC-derived, TDP-43 mutation, Q331K, HOM) appeared first on iXCells.

iPSC-derived skeletal muscle myoblasts are valuable tools for biochemical analysis, disease modelling.

iXCells Biotechnologies is proud to provide ready-to-use human iPSC-derived skeletal muscle myoblasts for differentiation into functional myotubes. iXCells hiPSC-derived myoblasts express typical markers, e.g. MyoD and Desmin (Figure 1) and rapidly differentiate into functional myotubes expressing markers including MHC, Dystrophin and MyoG (Figure 2), with the purity higher than 85%. Functional validation of iPSC-derived myotubes can be observed by their spontaneous twitching in the well (Conci). iXCells human iPSC-derived skeletal muscle myoblasts are available in a kit format containing both cryopreserved vials (1 or 3 million cells/vial) along with the necessary media components to expand, differentiate and maintain the myotubes in culture for at least 4-6 weeks. Longevity of the myotubes in culture can be extended with a bi-weekly 24-hr pulse of Myoblast Expansion Medium (Cat# MD-0102A) followed by replacement with Myoblast Differentiation Medium (Cat# MD-0102B).

iXCells also provide customized differentiation service with your own iPS cell lines. Please contact us at orders@ixcellsbiotech.com for more details.

Figure 1. MyoD and Desmin staining of human iPSC-derived myoblasts upon recovery in the Myoblast Expansion Medium (Cat# MD-0102A).

Figure 2. Formation of myotubes were observed after 4 days of differentiation of human iPSC-derived myoblasts in the Myoblast Differentiation Medium (Cat# MD-0102B). MHC staining of myotubes were shown by immunofluorescence staining (red).

Product Details

Datasheet & Culture Protocol

The post Human Skeletal Muscle Myoblasts (iPSC-derived, SOD1 mutant, A4V, HOM) appeared first on iXCells.

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disease of the motor system, characterized by selective and progressive loss of motor neurons, eventually leading to paralysis and death within 2–5 years ^[1].  iPSC-derived motor neurons are valuable tools for biochemical analysis, disease modelling and clinical application of this disease.  Cytoplasmic accumulation and nuclear loss of the RNA binding protein transactive response DNA-binding protein 43 (TDP-43) from affected neurons in most instances of ALS ^[2-3]. Over 40 dominantly inherited mutations in the gene encoding TDP-43 have subsequently been identified in familial ALS patients ^[4], implicating TDP-43 dysfunction in the vast majority of ALS cases.

Human Motor Neurons (iPSC-derived, TDP-43 mutation, M337V) is derived from a genetically modified normal iPSC line carrying the heterozygous or homozygous M337V mutation in the TDP-43 gene (Figure 1). iXCells hiPSC-derived motor neurons express typical markers of motor neurons, e.g. HB9 (MNX1), ISL1, CHAT, (Figure 2), with the purity higher than 85%. iXCells motor neurons are available in both cryopreserved vials and fresh plate formats (12, 24, 48, and 96-well plate). Most of the cells will express high level of HB9 and ISL-1 after thawing in the Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML). After culturing in the medium for 5-7 days, these cells will express high levels of CHAT and MAP2.

Figure 1. Heterozygous and homozygous M337V mutation (highlighted) has been introduced to TDP-43 gene using CRISPR/Cas9 based genome editing technology. The targeted site is verified by genomic PCR/Sanger sequencing.

Figure 2. Immunofluorescence staining showing HB9 and ChAT positive cells on day 2 and 7 in culture respectively.

Product Details

Tissue Origin	Homo Sapiens, Human
Cell Type	Brain Cell
Disease	ALS
Package Size	1.0 million cells/vial; 2.0 million cells/vial
Passage Number	P0
Growth Properties	Adherent
Shipped	Cryopreserved
Storage	Liquid Nitrogen
Media	iXCells Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML)

References

[1] Taylor, J. P., Brown, R. H. Jr & Cleveland, D. W. Decoding ALS: from genes to mechanism. Nature 539, 197–206 (2016).

[2] Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).

[3] Ling, S. C., Polymenidou, M. & Cleveland, D. W. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron 79, 416–438 (2013).

[4] Lagier-Tourenne, C., Polymenidou, M. & Cleveland, D. W. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. Hum. Mol. Genet. 19, R46–R64 (2010).

Datasheet & Culture Protocol

The post Human Motor Neurons (iPSC-derived, TDP-43 mutation, M337V, HET) appeared first on iXCells.

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disease of the motor system, characterized by selective and progressive loss of motor neurons, eventually leading to paralysis and death within 2–5 years ^[1].  iPSC-derived motor neurons are valuable tools for biochemical analysis, disease modelling and clinical application of this disease.  Cytoplasmic accumulation and nuclear loss of the RNA binding protein transactive response DNA-binding protein 43 (TDP-43) from affected neurons in most instances of ALS ^[2-3]. Over 40 dominantly inherited mutations in the gene encoding TDP-43 have subsequently been identified in familial ALS patients ^[4], implicating TDP-43 dysfunction in the vast majority of ALS cases.

Human Motor Neurons (iPSC-derived, TDP-43 mutation, M337V) is derived from a genetically modified normal iPSC line carrying the heterozygous or homozygous M337V mutation in the TDP-43 gene (Figure 1). iXCells hiPSC-derived motor neurons express typical markers of motor neurons, e.g. HB9 (MNX1), ISL1, CHAT, (Figure 2), with the purity higher than 85%. iXCells motor neurons are available in both cryopreserved vials and fresh plate formats (12, 24, 48, and 96-well plate). Most of the cells will express high level of HB9 and ISL-1 after thawing in the Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML). After culturing in the medium for 5-7 days, these cells will express high levels of CHAT and MAP2.

Figure 1. Heterozygous and homozygous M337V mutation (highlighted) has been introduced to TDP-43 gene using CRISPR/Cas9 based genome editing technology. The targeted site is verified by genomic PCR/Sanger sequencing.

Figure 2. Immunofluorescence staining showing HB9 and ChAT positive cells on day 2 and 7 in culture respectively.

Product Details

Tissue Origin	Homo Sapiens, Human
Cell Type	Neuronal Cells
Disease	ALS
Package Size	1.0 million cells/vial; 2.0 million cells/vial
Passage Number	P0
Growth Properties	Adherent
Shipped	Cryopreserved
Storage	Liquid Nitrogen
Media	iXCells Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML)

References

[1] Taylor, J. P., Brown, R. H. Jr & Cleveland, D. W. Decoding ALS: from genes to mechanism. Nature 539, 197–206 (2016).

[2] Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).

[3] Ling, S. C., Polymenidou, M. & Cleveland, D. W. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron 79, 416–438 (2013).

[4] Lagier-Tourenne, C., Polymenidou, M. & Cleveland, D. W. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. Hum. Mol. Genet. 19, R46–R64 (2010).

Datasheet & Culture Protocol

The post Human Motor Neurons (iPSC-derived, TDP-43 mutation, M337V, HOM) appeared first on iXCells.

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disease of the motor system, characterized by selective and progressive loss of motor neurons, eventually leading to paralysis and death within 2–5 years ^[1].  iPSC-derived motor neurons are valuable tools for biochemical analysis, disease modelling and clinical application of this disease.  Cytoplasmic accumulation and nuclear loss of the RNA binding protein transactive response DNA-binding protein 43 (TDP-43) from affected neurons in most instances of ALS ^[2-3]. Over 40 dominantly inherited mutations in the gene encoding TDP-43 have subsequently been identified in familial ALS patients ^[4], implicating TDP-43 dysfunction in the vast majority of ALS cases.

Human Motor Neurons (iPSC-derived, TDP-43 mutation, M337V) is derived from a genetically modified normal iPSC line carrying the heterozygous or homozygous M337V mutation in the TDP-43 gene (Figure 1). iXCells hiPSC-derived motor neurons express typical markers of motor neurons, e.g. HB9 (MNX1), ISL1, CHAT, (Figure 2), with the purity higher than 85%. iXCells motor neurons are available in both cryopreserved vials and fresh plate formats (12, 24, 48, and 96-well plate). Most of the cells will express high level of HB9 and ISL-1 after thawing in the Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML). After culturing in the medium for 5-7 days, these cells will express high levels of CHAT and MAP2.

Figure 1. Heterozygous and homozygous M337V mutation (highlighted) has been introduced to TDP-43 gene using CRISPR/Cas9 based genome editing technology. The targeted site is verified by genomic PCR/Sanger sequencing.

Figure 2. Immunofluorescence staining showing HB9 and ChAT positive cells on day 2 and 7 in culture respectively.

Product Details

Tissue Origin	Homo Sapiens, Human
Cell Type	Neuronal Cells
Disease	ALS
Package Size	1.0 million cells/vial; 2.0 million cells/vial
Passage Number	P0
Growth Properties	Adherent
Shipped	Cryopreserved
Storage	Liquid Nitrogen
Media	iXCells Motor Neuron Culture Medium Kit (Cat# MD-0022-100ML)

References

[1] Taylor, J. P., Brown, R. H. Jr & Cleveland, D. W. Decoding ALS: from genes to mechanism. Nature 539, 197–206 (2016).

[2] Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006).

[3] Ling, S. C., Polymenidou, M. & Cleveland, D. W. Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron 79, 416–438 (2013).

[4] Lagier-Tourenne, C., Polymenidou, M. & Cleveland, D. W. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. Hum. Mol. Genet. 19, R46–R64 (2010).

Datasheet & Culture Protocol

The post Human Motor Neurons (iPSC-derived, TDP-43 mutation, M337V, ISO) appeared first on iXCells.

The rapid and highly reproducible generation of mature and functioning neurons from human pluripotent stem cells (hPSCs), neural progenitors, or fibroblasts has been made possible through the utilization of transcription factors. These factors have played a pivotal role in facilitating investigations related to neurodevelopment, disease modeling, drug screening, and neuronal replacement therapies. By employing various combinations of transcription factors along with specific small molecules, researchers have successfully generated populations of glutamatergic neurons^[1,2] .This significant breakthrough has provided valuable insights into neural processes and offered potential avenues for therapeutic advancements. This significant breakthrough has provided valuable insights into neural processes and offered potential avenues for therapeutic advancements.iXCells Biotechnologies takes pride in offering fully differentiated and functional human iPSC-derived glutamatergic neurons that exhibit typical neuronal morphology and express key markers associated with glutamatergic identity, such as VGLUT2, MAP2, and TUJ1 (Figure 1A, B). These neurons not only display robust neural activity but also show an increase in activity over time, indicating progressive maturation (Figure 1C, D). When cultured in the Human Glutamatergic Neuron Maturation Media (Cat# MD-0116), our neurons provide a reliable model for studying neuronal function and responses (Figure 2). Additionally, our iPSC-derived neurons can be co-cultured with glial cells, enabling the development of comprehensive drug screening platforms to evaluate drug efficacy, neurotoxicity, and other neural responses.

iXCells Biotechnologies takes pride in offering fully differentiated and functional human iPSC-derived glutamatergic neurons that exhibit typical neuronal morphology and express key markers associated with glutamatergic identity, such as VGLUT2, MAP2, and TUJ1 (Figure 1A, B). These neurons not only display robust neural activity but also show an increase in activity over time, indicating progressive maturation (Figure 1C, D). When cultured in the Human Glutamatergic Neuron Maturation Media (Cat# MD-0116), our neurons provide a reliable model for studying neuronal function and responses (Figure 2). Additionally, our iPSC-derived neurons can be co-cultured with glial cells, enabling the development of comprehensive drug screening platforms to evaluate drug efficacy, neurotoxicity, and other neural responses.

Figure 1. Human iPSCs-derived glutamatergic neurons show expression of characteristic biological markers. (A) Immunostaining shows the expression of neuronal makers MAP2 and Tuj1 at 5 days post-thawing. (B) Immunostaining shows expression of glutamatergic marker VGLUT2, 25 days post-thawing Scale bar 30μm. (C) Glutamatergic neurons were differentiated as a monolayer on a MEA plate and co-cultured with iPSC-derived Astrocytes (40HU-008) and subsequently neuronal activity was measured. (D) The electrical parameters were measured in the MEA over time and the results are graphed as mean ± SEM for mean firing rate and number of spikes..

Figure 2. (A) An image of the cells during the experiment. The patch pipette is visible on the left. (B) The Sodium/potassium currents were recorded in voltage clamp mode with test potentials of -100 mV to 90 mV. (C) Excitatory postsynaptic currents (EPSCs) were recorded in voltage clamp mode while clamping the cell at -60 mV. (D) Evoked action potentials were recorded in current clamp mode starting with a current injection 12 pA below what is needed to hold the neuron at – 60 mV and with 3pA current steps. (E) Spontaneous activity was recorded in current clamp mode with a current injection needed for a membrane potential of -45 mV.

Product Details

References

[1] Yingsha Zhang, Changhui Pak, Yan Han, Henrik Ahlenius, Zhenjie Zhang, Soham Chanda, Samuele Marro, Christopher Patzke, Claudio Acuna, Jason Covy, Wei Xu, Nan Yang, Tamas Danko, Lu Chen, Marius Wernig, Thomas C Südhof (2013) “Rapid single-step induction of functional neurons from human pluripotent stem cells’’. Neuron, 78,785-798

[2] Ralda Nehme, Emanuela Zuccaro, Sulagna Dia Ghosh, Chenchen Li, John L Sherwood, Olli Pietilainen, Lindy E Barrett, Francesco Limone, Kathleen A Worringer, Sravya Kommineni, Ying Zang, Davide Cacchiarelli, Alex Meissner, Rolf Adolfsson, Stephen Haggarty, Jon Madison, Matthias Muller, Paola Arlotta, Zhanyan Fu, Guoping Feng, Kevin Eggan. (2018) “Combining NGN2 programming with developmental patterning generates human excitatory neurons with NMDAR-mediated synaptic transmission”. Cell Rep., 23, 2509-2523.

Datasheet & Culture Protocol

The post Human Glutamatergic Neurons (iPSC-derived, GFP-labeled, Normal) appeared first on iXCells.