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human spinal cord total rna  (TaKaRa)


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    TaKaRa human spinal cord total rna
    Human Spinal Cord Total Rna, supplied by TaKaRa, used in various techniques. Bioz Stars score: 94/100, based on 47 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human spinal cord total rna/product/TaKaRa
    Average 94 stars, based on 47 article reviews
    human spinal cord total rna - by Bioz Stars, 2026-04
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    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Human Astrocytes-Spinal Cord , ScienCell , 1820.

    Techniques: Recombinant, Control, Protease Inhibitor, Western Blot, Electron Microscopy, Amplification, Reverse Transcription, SYBR Green Assay, Bicinchoninic Acid Protein Assay, RNA Sequencing, Software, Real-time Polymerase Chain Reaction

    (A) PCA of RNA sequencing demonstrating distinct gene expression patterns of human spinal cord astrocytes treated with 10 ng/mL IFNγ, TNF-α, IL-1β, IL-17, GM-CSF, and media for 24 h. (B) Heatmap of top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent log2 fold change compared to media from 3 independent samples. (C) Top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent the log2 fold change compared to media from 3 independent samples. (D) BATF2 transcript levels of human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 0–48 h. ** p < 0.01 and *** p < 0.001 compared to media-treated samples by one-way ANOVA. Data points represent mean ± SEM ( n = 3). (E) BATF2 transcript levels of human spinal cord astrocytes treated with 10 ng/mL of various inflammatory stimuli for 24 h. **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n = 4). (F) Representative western blot of whole-cell BATF2 protein levels in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h. (G) Quantification of whole-cell BATF2 protein levels in primary human spinal cord astrocytes shown in (F), normalized to β-actin expression. * p < 0.05 compared to media-treated samples by one-way ANOVA. Bars represent mean ± SEM ( n = 3).

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: (A) PCA of RNA sequencing demonstrating distinct gene expression patterns of human spinal cord astrocytes treated with 10 ng/mL IFNγ, TNF-α, IL-1β, IL-17, GM-CSF, and media for 24 h. (B) Heatmap of top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent log2 fold change compared to media from 3 independent samples. (C) Top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent the log2 fold change compared to media from 3 independent samples. (D) BATF2 transcript levels of human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 0–48 h. ** p < 0.01 and *** p < 0.001 compared to media-treated samples by one-way ANOVA. Data points represent mean ± SEM ( n = 3). (E) BATF2 transcript levels of human spinal cord astrocytes treated with 10 ng/mL of various inflammatory stimuli for 24 h. **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n = 4). (F) Representative western blot of whole-cell BATF2 protein levels in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h. (G) Quantification of whole-cell BATF2 protein levels in primary human spinal cord astrocytes shown in (F), normalized to β-actin expression. * p < 0.05 compared to media-treated samples by one-way ANOVA. Bars represent mean ± SEM ( n = 3).

    Article Snippet: Total RNA was collected from human primary spinal cord astrocytes (ScienCell) treated with recombinant human IFNγ, TNFα, IL-1β, IL-17, GMCSF, or media (Peprotech) for 24h using an RNeasy Mini Kit (Qiagen) according to the manufacturer’s instructions and quantified using a NanoDrop One spectrophotometer (Thermofisher).

    Techniques: RNA Sequencing, Gene Expression, Western Blot, Expressing

    (A) Merged peak region heatmap of BATF2 binding in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. Scale bar indicates BATF2 binding events per merged region. (B) Peak tag numbers of BATF2 binding events in 1,289 merged peak regions of human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. (C) Peak location of BATF2 binding events in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. hg38 binding events were used as an internal control. Data are the average peak locations between two independent samples per treatment. (D and E) Top BATF2 binding motifs of media- and IFNγ-treated human spinal cord astrocytes. Data shown in (A)–(E) are representative of two independent samples per treatment.

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: (A) Merged peak region heatmap of BATF2 binding in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. Scale bar indicates BATF2 binding events per merged region. (B) Peak tag numbers of BATF2 binding events in 1,289 merged peak regions of human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. (C) Peak location of BATF2 binding events in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. hg38 binding events were used as an internal control. Data are the average peak locations between two independent samples per treatment. (D and E) Top BATF2 binding motifs of media- and IFNγ-treated human spinal cord astrocytes. Data shown in (A)–(E) are representative of two independent samples per treatment.

    Article Snippet: Total RNA was collected from human primary spinal cord astrocytes (ScienCell) treated with recombinant human IFNγ, TNFα, IL-1β, IL-17, GMCSF, or media (Peprotech) for 24h using an RNeasy Mini Kit (Qiagen) according to the manufacturer’s instructions and quantified using a NanoDrop One spectrophotometer (Thermofisher).

    Techniques: Binding Assay, Control

    (A) Ingenuity pathway analysis of top regulated pathways by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (B) Graphical summary of predicated targets regulated by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (C) Adapted ingenuity pathway analysis: IFNγ signaling pathway from (A). (D) Adapted ingenuity pathway analysis: multiple sclerosis signaling pathway from (A). (E) Peak region counts of BATF2 binding events upstream of the IRF1 gene locus and at CpG islands in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h (green) or media (gray). (F–K) Quantification of Irf1 and target gene transcript expression in Batf2 +/+ and Batf2 −/− primary murine spinal cord astrocytes stimulated with media or 10 ng/mL IFNγ for 48 h. Data are representative of 2 independent experiments. Individual data points were normalized to the media average and are representative of individual mice. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n =7). Data shown in (A)–(E) are representative of two independent samples per treatment.

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: (A) Ingenuity pathway analysis of top regulated pathways by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (B) Graphical summary of predicated targets regulated by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (C) Adapted ingenuity pathway analysis: IFNγ signaling pathway from (A). (D) Adapted ingenuity pathway analysis: multiple sclerosis signaling pathway from (A). (E) Peak region counts of BATF2 binding events upstream of the IRF1 gene locus and at CpG islands in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h (green) or media (gray). (F–K) Quantification of Irf1 and target gene transcript expression in Batf2 +/+ and Batf2 −/− primary murine spinal cord astrocytes stimulated with media or 10 ng/mL IFNγ for 48 h. Data are representative of 2 independent experiments. Individual data points were normalized to the media average and are representative of individual mice. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n =7). Data shown in (A)–(E) are representative of two independent samples per treatment.

    Article Snippet: Total RNA was collected from human primary spinal cord astrocytes (ScienCell) treated with recombinant human IFNγ, TNFα, IL-1β, IL-17, GMCSF, or media (Peprotech) for 24h using an RNeasy Mini Kit (Qiagen) according to the manufacturer’s instructions and quantified using a NanoDrop One spectrophotometer (Thermofisher).

    Techniques: Binding Assay, Expressing

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Total RNA was collected from human primary spinal cord astrocytes (ScienCell) treated with recombinant human IFNγ, TNFα, IL-1β, IL-17, GMCSF, or media (Peprotech) for 24h using an RNeasy Mini Kit (Qiagen) according to the manufacturer’s instructions and quantified using a NanoDrop One spectrophotometer (Thermofisher).

    Techniques: Recombinant, Control, Protease Inhibitor, Western Blot, Electron Microscopy, Amplification, Reverse Transcription, SYBR Green Assay, Bicinchoninic Acid Protein Assay, RNA Sequencing, Software, Real-time Polymerase Chain Reaction

    (A) PCA of RNA sequencing demonstrating distinct gene expression patterns of human spinal cord astrocytes treated with 10 ng/mL IFNγ, TNF-α, IL-1β, IL-17, GM-CSF, and media for 24 h. (B) Heatmap of top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent log2 fold change compared to media from 3 independent samples. (C) Top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent the log2 fold change compared to media from 3 independent samples. (D) BATF2 transcript levels of human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 0–48 h. ** p < 0.01 and *** p < 0.001 compared to media-treated samples by one-way ANOVA. Data points represent mean ± SEM ( n = 3). (E) BATF2 transcript levels of human spinal cord astrocytes treated with 10 ng/mL of various inflammatory stimuli for 24 h. **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n = 4). (F) Representative western blot of whole-cell BATF2 protein levels in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h. (G) Quantification of whole-cell BATF2 protein levels in primary human spinal cord astrocytes shown in (F), normalized to β-actin expression. * p < 0.05 compared to media-treated samples by one-way ANOVA. Bars represent mean ± SEM ( n = 3).

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: (A) PCA of RNA sequencing demonstrating distinct gene expression patterns of human spinal cord astrocytes treated with 10 ng/mL IFNγ, TNF-α, IL-1β, IL-17, GM-CSF, and media for 24 h. (B) Heatmap of top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent log2 fold change compared to media from 3 independent samples. (C) Top upregulated genes in human spinal cord astrocytes treated with 10 ng/mL IFNγ for 24 h compared to TNF-α and IL-1β treatments. Data represent the log2 fold change compared to media from 3 independent samples. (D) BATF2 transcript levels of human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 0–48 h. ** p < 0.01 and *** p < 0.001 compared to media-treated samples by one-way ANOVA. Data points represent mean ± SEM ( n = 3). (E) BATF2 transcript levels of human spinal cord astrocytes treated with 10 ng/mL of various inflammatory stimuli for 24 h. **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n = 4). (F) Representative western blot of whole-cell BATF2 protein levels in human spinal cord astrocytes treated with 10 ng/mL of IFNγ for 24 h. (G) Quantification of whole-cell BATF2 protein levels in primary human spinal cord astrocytes shown in (F), normalized to β-actin expression. * p < 0.05 compared to media-treated samples by one-way ANOVA. Bars represent mean ± SEM ( n = 3).

    Article Snippet: Primary human spinal cord astrocytes were obtained commercially from ScienCell Laboratories and grown according to provided protocols in complete ScienCell Astrocyte Medium.

    Techniques: RNA Sequencing, Gene Expression, Western Blot, Expressing

    (A) Merged peak region heatmap of BATF2 binding in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. Scale bar indicates BATF2 binding events per merged region. (B) Peak tag numbers of BATF2 binding events in 1,289 merged peak regions of human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. (C) Peak location of BATF2 binding events in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. hg38 binding events were used as an internal control. Data are the average peak locations between two independent samples per treatment. (D and E) Top BATF2 binding motifs of media- and IFNγ-treated human spinal cord astrocytes. Data shown in (A)–(E) are representative of two independent samples per treatment.

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: (A) Merged peak region heatmap of BATF2 binding in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. Scale bar indicates BATF2 binding events per merged region. (B) Peak tag numbers of BATF2 binding events in 1,289 merged peak regions of human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. (C) Peak location of BATF2 binding events in human spinal cord astrocytes treated with 10 ng/mL IFNγ or media for 24 h. hg38 binding events were used as an internal control. Data are the average peak locations between two independent samples per treatment. (D and E) Top BATF2 binding motifs of media- and IFNγ-treated human spinal cord astrocytes. Data shown in (A)–(E) are representative of two independent samples per treatment.

    Article Snippet: Primary human spinal cord astrocytes were obtained commercially from ScienCell Laboratories and grown according to provided protocols in complete ScienCell Astrocyte Medium.

    Techniques: Binding Assay, Control

    (A) Ingenuity pathway analysis of top regulated pathways by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (B) Graphical summary of predicated targets regulated by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (C) Adapted ingenuity pathway analysis: IFNγ signaling pathway from (A). (D) Adapted ingenuity pathway analysis: multiple sclerosis signaling pathway from (A). (E) Peak region counts of BATF2 binding events upstream of the IRF1 gene locus and at CpG islands in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h (green) or media (gray). (F–K) Quantification of Irf1 and target gene transcript expression in Batf2 +/+ and Batf2 −/− primary murine spinal cord astrocytes stimulated with media or 10 ng/mL IFNγ for 48 h. Data are representative of 2 independent experiments. Individual data points were normalized to the media average and are representative of individual mice. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n =7). Data shown in (A)–(E) are representative of two independent samples per treatment.

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: (A) Ingenuity pathway analysis of top regulated pathways by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (B) Graphical summary of predicated targets regulated by BATF2 in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h. (C) Adapted ingenuity pathway analysis: IFNγ signaling pathway from (A). (D) Adapted ingenuity pathway analysis: multiple sclerosis signaling pathway from (A). (E) Peak region counts of BATF2 binding events upstream of the IRF1 gene locus and at CpG islands in human spinal cord astrocytes stimulated with 10 ng/mL IFNγ for 24 h (green) or media (gray). (F–K) Quantification of Irf1 and target gene transcript expression in Batf2 +/+ and Batf2 −/− primary murine spinal cord astrocytes stimulated with media or 10 ng/mL IFNγ for 48 h. Data are representative of 2 independent experiments. Individual data points were normalized to the media average and are representative of individual mice. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 compared to media-treated samples by two-way ANOVA. Bars represent mean ± SEM ( n =7). Data shown in (A)–(E) are representative of two independent samples per treatment.

    Article Snippet: Primary human spinal cord astrocytes were obtained commercially from ScienCell Laboratories and grown according to provided protocols in complete ScienCell Astrocyte Medium.

    Techniques: Binding Assay, Expressing

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation

    doi: 10.1016/j.celrep.2025.115393

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Primary human spinal cord astrocytes were obtained commercially from ScienCell Laboratories and grown according to provided protocols in complete ScienCell Astrocyte Medium.

    Techniques: Recombinant, Control, Protease Inhibitor, Western Blot, Electron Microscopy, Amplification, Reverse Transcription, SYBR Green Assay, Bicinchoninic Acid Protein Assay, RNA Sequencing, Software, Real-time Polymerase Chain Reaction

    Journal: Cell Reports Medicine

    Article Title: Long-term clinical and safety outcomes from a single-site phase 1 study of neural stem cell transplantation for chronic thoracic spinal cord injury

    doi: 10.1016/j.xcrm.2024.101841

    Figure Lengend Snippet:

    Article Snippet: Human fetal spinal cord-derived neural precursor line , Neuralstem Inc. , NSI-566.

    Techniques: