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microglial cell medium kit  (AcceGen Biotechnology)


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    AcceGen Biotechnology microglial cell medium kit
    (a) Differential expression analyses confirm significant up- or downregulated genes under various stimulation conditions (FDR < 0.05, DESeq2). (b) Gene set enrichment analyses of resting and stimulated THP-1 macrophages reveal immune-related shifts (IFN-β, IFN-γ, LPS+IFN-γ) that mirror ATAC-seq changes in . (FDR < 0.05, fast gene set enrichment analysis). (c) PCA of RNA-seq data shows distinct transcriptomic clusters for each state, reflecting diverse immune states. (d) <t>Microglial</t> and macrophage markers were expressed in all conditions. (e) Differential expression of microglial-state marker genes (Sun et al. ) in stimulated THP-1 macrophages versus non-marker genes (two-sided Mann-Whitney U, Benjamini- Hochberg correction). Significance codes, Benjamini-Hochberg FDR: **** < 1 × 10⁻⁴; *** < 1 × 10⁻³; ** < 1 × 10⁻²; * < 0.05; NS, not significant. (f) Transcriptomic concordance between LPS + IFN-γ-stimulated THP-1 macrophages and amyloid-fibril-treated iPSC-microglia. Pearson’s r is calculated on the expression levels of genes that are differentially expressed in the amyloid-fibril model (Sun et al. ).
    Microglial Cell Medium Kit, supplied by AcceGen Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/microglial+cell+medium+kit/Microglial+Cell+Medium+Kit/bio_rxiv__2025__07__11__659973-271-8-12
    Average 93 stars, based on 2 article reviews
    microglial cell medium kit - by Bioz Stars, 2026-10
    93/100 stars

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    1) Product Images from "Context-dependent regulatory variants in Alzheimer’s disease"

    Article Title: Context-dependent regulatory variants in Alzheimer’s disease

    Journal: bioRxiv

    doi: 10.1101/2025.07.11.659973

    (a) Differential expression analyses confirm significant up- or downregulated genes under various stimulation conditions (FDR < 0.05, DESeq2). (b) Gene set enrichment analyses of resting and stimulated THP-1 macrophages reveal immune-related shifts (IFN-β, IFN-γ, LPS+IFN-γ) that mirror ATAC-seq changes in . (FDR < 0.05, fast gene set enrichment analysis). (c) PCA of RNA-seq data shows distinct transcriptomic clusters for each state, reflecting diverse immune states. (d) Microglial and macrophage markers were expressed in all conditions. (e) Differential expression of microglial-state marker genes (Sun et al. ) in stimulated THP-1 macrophages versus non-marker genes (two-sided Mann-Whitney U, Benjamini- Hochberg correction). Significance codes, Benjamini-Hochberg FDR: **** < 1 × 10⁻⁴; *** < 1 × 10⁻³; ** < 1 × 10⁻²; * < 0.05; NS, not significant. (f) Transcriptomic concordance between LPS + IFN-γ-stimulated THP-1 macrophages and amyloid-fibril-treated iPSC-microglia. Pearson’s r is calculated on the expression levels of genes that are differentially expressed in the amyloid-fibril model (Sun et al. ).
    Figure Legend Snippet: (a) Differential expression analyses confirm significant up- or downregulated genes under various stimulation conditions (FDR < 0.05, DESeq2). (b) Gene set enrichment analyses of resting and stimulated THP-1 macrophages reveal immune-related shifts (IFN-β, IFN-γ, LPS+IFN-γ) that mirror ATAC-seq changes in . (FDR < 0.05, fast gene set enrichment analysis). (c) PCA of RNA-seq data shows distinct transcriptomic clusters for each state, reflecting diverse immune states. (d) Microglial and macrophage markers were expressed in all conditions. (e) Differential expression of microglial-state marker genes (Sun et al. ) in stimulated THP-1 macrophages versus non-marker genes (two-sided Mann-Whitney U, Benjamini- Hochberg correction). Significance codes, Benjamini-Hochberg FDR: **** < 1 × 10⁻⁴; *** < 1 × 10⁻³; ** < 1 × 10⁻²; * < 0.05; NS, not significant. (f) Transcriptomic concordance between LPS + IFN-γ-stimulated THP-1 macrophages and amyloid-fibril-treated iPSC-microglia. Pearson’s r is calculated on the expression levels of genes that are differentially expressed in the amyloid-fibril model (Sun et al. ).

    Techniques Used: Quantitative Proteomics, RNA Sequencing, Marker, MANN-WHITNEY, Expressing

    (a) Hi-C in THP-1 macrophages (<5-kb resolution) places the enhancer (black bar) in the same contact domain as the SEC63 promoter and shows a looping interaction with the OSTM1 promoter and a CTCF anchor in the intronic regions of AFG1L (b) Three-dimensional chromatin model of the SEC63-OSTM1 enhancer and nearby genes. (c) SEC63 , the enhancer, and OSTM1 knockdown in hyperinflammatory (LPS + IFN-γ- treated) THP-1 macrophages. (d) CRISPRi knockdown of the SEC63 and OSTM1 promoters perturbs distinct transcriptional pathways in resting and hyperinflammatory (LPS + IFN-γ-treated) THP-1 macrophages (fgsea, FDR<0.05). (e) Expression of the microglial-state marker genes defined by Sun et al. after CRISPRi. Silencing SEC63 shifts multiple microglial programs, and these shifts are amplified under LPS + IFN-γ-highlighting a central role for SEC63 in state transitions and immune responses.
    Figure Legend Snippet: (a) Hi-C in THP-1 macrophages (<5-kb resolution) places the enhancer (black bar) in the same contact domain as the SEC63 promoter and shows a looping interaction with the OSTM1 promoter and a CTCF anchor in the intronic regions of AFG1L (b) Three-dimensional chromatin model of the SEC63-OSTM1 enhancer and nearby genes. (c) SEC63 , the enhancer, and OSTM1 knockdown in hyperinflammatory (LPS + IFN-γ- treated) THP-1 macrophages. (d) CRISPRi knockdown of the SEC63 and OSTM1 promoters perturbs distinct transcriptional pathways in resting and hyperinflammatory (LPS + IFN-γ-treated) THP-1 macrophages (fgsea, FDR<0.05). (e) Expression of the microglial-state marker genes defined by Sun et al. after CRISPRi. Silencing SEC63 shifts multiple microglial programs, and these shifts are amplified under LPS + IFN-γ-highlighting a central role for SEC63 in state transitions and immune responses.

    Techniques Used: Hi-C, Knockdown, Expressing, Marker, Amplification

    Related Articles

    other:

    Article Title: Context-dependent regulatory variants in Alzheimer’s disease
    Article Snippet: Differentiation into macrophages was induced by treating cells with 100 nM phorbol 12-myristate 13-acetate (PMA, Sigma-Aldrich) for 72 h, followed by a 24 h resting period in PMA-free medium.

    Derivative Assay:

    Article Title: Examining Epigenetic Variation in The Brain in Mental Illness
    Article Snippet: .. 4.5.4.1 Growth ofS V40 immortalised primary human microglia Human microglia derived from Primary Human Microglia Cells (>99% purity) (Accegen Biotech, Cat.No ABI-TC4171) immortalised used the Lenti-SV40 Lentjvirus (SV40 cell line) was acquired and grown indefinitely in cell culture using the microglial Cell Medium Kit (AcceGen Biotech, Cat. No ABI-TM009). .. After growing and plating (30,000 cells per coverslip) the coverslips coated with SV40 immortalised microglia were imagined before staining using the EVOS XL Core Configured Microscope (Invitrogen, Carlsbad, CA) to confirm presence and identity of microglia (Figure 4.17).

    Cell Culture:

    Article Title: Examining Epigenetic Variation in The Brain in Mental Illness
    Article Snippet: .. 4.5.4.1 Growth ofS V40 immortalised primary human microglia Human microglia derived from Primary Human Microglia Cells (>99% purity) (Accegen Biotech, Cat.No ABI-TC4171) immortalised used the Lenti-SV40 Lentjvirus (SV40 cell line) was acquired and grown indefinitely in cell culture using the microglial Cell Medium Kit (AcceGen Biotech, Cat. No ABI-TM009). .. After growing and plating (30,000 cells per coverslip) the coverslips coated with SV40 immortalised microglia were imagined before staining using the EVOS XL Core Configured Microscope (Invitrogen, Carlsbad, CA) to confirm presence and identity of microglia (Figure 4.17).



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    microglial cell medium kit  (AcceGen Biotechnology)
    93
    AcceGen Biotechnology microglial cell medium kit
    (a) Differential expression analyses confirm significant up- or downregulated genes under various stimulation conditions (FDR < 0.05, DESeq2). (b) Gene set enrichment analyses of resting and stimulated THP-1 macrophages reveal immune-related shifts (IFN-β, IFN-γ, LPS+IFN-γ) that mirror ATAC-seq changes in . (FDR < 0.05, fast gene set enrichment analysis). (c) PCA of RNA-seq data shows distinct transcriptomic clusters for each state, reflecting diverse immune states. (d) <t>Microglial</t> and macrophage markers were expressed in all conditions. (e) Differential expression of microglial-state marker genes (Sun et al. ) in stimulated THP-1 macrophages versus non-marker genes (two-sided Mann-Whitney U, Benjamini- Hochberg correction). Significance codes, Benjamini-Hochberg FDR: **** < 1 × 10⁻⁴; *** < 1 × 10⁻³; ** < 1 × 10⁻²; * < 0.05; NS, not significant. (f) Transcriptomic concordance between LPS + IFN-γ-stimulated THP-1 macrophages and amyloid-fibril-treated iPSC-microglia. Pearson’s r is calculated on the expression levels of genes that are differentially expressed in the amyloid-fibril model (Sun et al. ).
    Microglial Cell Medium Kit, supplied by AcceGen Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/microglial+cell+medium+kit/Microglial+Cell+Medium+Kit/bio_rxiv__2025__07__11__659973-271-8-12
    Average 93 stars, based on 1 article reviews
    microglial cell medium kit - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier
    microglial cell medium  (AcceGen Biotechnology)
    93
    AcceGen Biotechnology microglial cell medium
    (a) Differential expression analyses confirm significant up- or downregulated genes under various stimulation conditions (FDR < 0.05, DESeq2). (b) Gene set enrichment analyses of resting and stimulated THP-1 macrophages reveal immune-related shifts (IFN-β, IFN-γ, LPS+IFN-γ) that mirror ATAC-seq changes in . (FDR < 0.05, fast gene set enrichment analysis). (c) PCA of RNA-seq data shows distinct transcriptomic clusters for each state, reflecting diverse immune states. (d) <t>Microglial</t> and macrophage markers were expressed in all conditions. (e) Differential expression of microglial-state marker genes (Sun et al. ) in stimulated THP-1 macrophages versus non-marker genes (two-sided Mann-Whitney U, Benjamini- Hochberg correction). Significance codes, Benjamini-Hochberg FDR: **** < 1 × 10⁻⁴; *** < 1 × 10⁻³; ** < 1 × 10⁻²; * < 0.05; NS, not significant. (f) Transcriptomic concordance between LPS + IFN-γ-stimulated THP-1 macrophages and amyloid-fibril-treated iPSC-microglia. Pearson’s r is calculated on the expression levels of genes that are differentially expressed in the amyloid-fibril model (Sun et al. ).
    Microglial Cell Medium, supplied by AcceGen Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/microglial+cell+medium+kit/Microglial+Cell+Medium+Kit/policicchio_stefania__2020__examining_epigenetic_variation_in_the_brain_in_mental_illness-8389-30-33
    Average 93 stars, based on 1 article reviews
    microglial cell medium - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier

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    (a) Differential expression analyses confirm significant up- or downregulated genes under various stimulation conditions (FDR < 0.05, DESeq2). (b) Gene set enrichment analyses of resting and stimulated THP-1 macrophages reveal immune-related shifts (IFN-β, IFN-γ, LPS+IFN-γ) that mirror ATAC-seq changes in . (FDR < 0.05, fast gene set enrichment analysis). (c) PCA of RNA-seq data shows distinct transcriptomic clusters for each state, reflecting diverse immune states. (d) Microglial and macrophage markers were expressed in all conditions. (e) Differential expression of microglial-state marker genes (Sun et al. ) in stimulated THP-1 macrophages versus non-marker genes (two-sided Mann-Whitney U, Benjamini- Hochberg correction). Significance codes, Benjamini-Hochberg FDR: **** < 1 × 10⁻⁴; *** < 1 × 10⁻³; ** < 1 × 10⁻²; * < 0.05; NS, not significant. (f) Transcriptomic concordance between LPS + IFN-γ-stimulated THP-1 macrophages and amyloid-fibril-treated iPSC-microglia. Pearson’s r is calculated on the expression levels of genes that are differentially expressed in the amyloid-fibril model (Sun et al. ).

    Journal: bioRxiv

    Article Title: Context-dependent regulatory variants in Alzheimer’s disease

    doi: 10.1101/2025.07.11.659973

    Figure Lengend Snippet: (a) Differential expression analyses confirm significant up- or downregulated genes under various stimulation conditions (FDR < 0.05, DESeq2). (b) Gene set enrichment analyses of resting and stimulated THP-1 macrophages reveal immune-related shifts (IFN-β, IFN-γ, LPS+IFN-γ) that mirror ATAC-seq changes in . (FDR < 0.05, fast gene set enrichment analysis). (c) PCA of RNA-seq data shows distinct transcriptomic clusters for each state, reflecting diverse immune states. (d) Microglial and macrophage markers were expressed in all conditions. (e) Differential expression of microglial-state marker genes (Sun et al. ) in stimulated THP-1 macrophages versus non-marker genes (two-sided Mann-Whitney U, Benjamini- Hochberg correction). Significance codes, Benjamini-Hochberg FDR: **** < 1 × 10⁻⁴; *** < 1 × 10⁻³; ** < 1 × 10⁻²; * < 0.05; NS, not significant. (f) Transcriptomic concordance between LPS + IFN-γ-stimulated THP-1 macrophages and amyloid-fibril-treated iPSC-microglia. Pearson’s r is calculated on the expression levels of genes that are differentially expressed in the amyloid-fibril model (Sun et al. ).

    Article Snippet: HMC3 microglia-like cells (ATCC CRL-3304) were cultured in Microglial Cell Medium Kit (Accegen, ABI-TM009) and maintained at 37°C with 5% CO2.

    Techniques: Quantitative Proteomics, RNA Sequencing, Marker, MANN-WHITNEY, Expressing

    (a) Hi-C in THP-1 macrophages (<5-kb resolution) places the enhancer (black bar) in the same contact domain as the SEC63 promoter and shows a looping interaction with the OSTM1 promoter and a CTCF anchor in the intronic regions of AFG1L (b) Three-dimensional chromatin model of the SEC63-OSTM1 enhancer and nearby genes. (c) SEC63 , the enhancer, and OSTM1 knockdown in hyperinflammatory (LPS + IFN-γ- treated) THP-1 macrophages. (d) CRISPRi knockdown of the SEC63 and OSTM1 promoters perturbs distinct transcriptional pathways in resting and hyperinflammatory (LPS + IFN-γ-treated) THP-1 macrophages (fgsea, FDR<0.05). (e) Expression of the microglial-state marker genes defined by Sun et al. after CRISPRi. Silencing SEC63 shifts multiple microglial programs, and these shifts are amplified under LPS + IFN-γ-highlighting a central role for SEC63 in state transitions and immune responses.

    Journal: bioRxiv

    Article Title: Context-dependent regulatory variants in Alzheimer’s disease

    doi: 10.1101/2025.07.11.659973

    Figure Lengend Snippet: (a) Hi-C in THP-1 macrophages (<5-kb resolution) places the enhancer (black bar) in the same contact domain as the SEC63 promoter and shows a looping interaction with the OSTM1 promoter and a CTCF anchor in the intronic regions of AFG1L (b) Three-dimensional chromatin model of the SEC63-OSTM1 enhancer and nearby genes. (c) SEC63 , the enhancer, and OSTM1 knockdown in hyperinflammatory (LPS + IFN-γ- treated) THP-1 macrophages. (d) CRISPRi knockdown of the SEC63 and OSTM1 promoters perturbs distinct transcriptional pathways in resting and hyperinflammatory (LPS + IFN-γ-treated) THP-1 macrophages (fgsea, FDR<0.05). (e) Expression of the microglial-state marker genes defined by Sun et al. after CRISPRi. Silencing SEC63 shifts multiple microglial programs, and these shifts are amplified under LPS + IFN-γ-highlighting a central role for SEC63 in state transitions and immune responses.

    Article Snippet: HMC3 microglia-like cells (ATCC CRL-3304) were cultured in Microglial Cell Medium Kit (Accegen, ABI-TM009) and maintained at 37°C with 5% CO2.

    Techniques: Hi-C, Knockdown, Expressing, Marker, Amplification