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rat basophilic leukemia cell line  (ATCC)


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    ATCC rat basophilic leukemia cell line
    Rat Basophilic Leukemia Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 859 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+lines+rbl+2h3+cells/RBL-2H3/pm42269830-98-4-23
    Average 97 stars, based on 859 article reviews
    rat basophilic leukemia cell line - by Bioz Stars, 2026-09
    97/100 stars

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    Related Articles

    other:

    Article Title: The Functional Basis for Hemophagocytic Lymphohistiocytosis in a Patient with Co-inherited Missense Mutations in the Perforin ( PFN1 ) Gene
    Article Snippet: The cell lines RBL-2H3 cells (rat basophil leukemia; American Type Culture Collection), which will be referred to in the text as RBL, and 293T (human embryonic kidney) were maintained in DMEM medium supplemented with 10% FCS, 2 mM glutamine, and 100 μg/ml each of streptomycin and penicillin in a humidified incubator at 37°C.



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    ( A–D ) In vitro antioxidant capacity of E-CME evaluated by ( A ) DPPH radical scavenging activity, ( B ) hydrogen peroxide (H 2 O 2 ) scavenging activity, ( C ) ferrous ion (Fe 2+ ) chelating activity, and ( D ) ferric reducing antioxidant power (FRAP) assays at concentrations of 0.125, 0.25, 0.5, and 1 mg/ml. Data are presented as mean ± SD (n = 3). Statistical comparisons were performed using one-way ANOVA with Tukey’s post hoc test; groups not sharing the same letter (a–c) are significantly different ( p < 0.05). ( E–F ) Effects of E-CME on TNF-α mRNA expression in HaCaT keratinocytes ( E ) <t>and</t> <t>RBL-2H3</t> mast cells ( F ). Cells were treated with various concentrations of E-CME, and TNF-α gene expression was analyzed by reverse transcription PCR using glyceradehyde 3-phospate dehydrogenase (GAPDH) as internal control. E-CME treatment downregulated TNF-α expression in a concentration dependent manner. Data represents SD from three independent experiments. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05). ( G ) Cell viability of HaCaT and RBL-2H3 cells following 24-h exposure to E-CME (62.5–1,000 μg/ml) determined by MTT assay. Viability remained above 80% at concentrations ≤125 μg/ml but declined significantly at higher concentrations. ( H ) Inhibitory effect of E-CME on β-hexosaminidase release in IgE-sensitized RBL-2H3 cells. Cells were presensitized with anti-dinitrophenyl (DNP) IgE and stimulated with DNP-bovine serum albumin (BSA). E-CME significantly suppressed β-hexosaminidase release in a dose-dependent manner, indicating inhibition of mast cell degranulation. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05).
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    ( A–D ) In vitro antioxidant capacity of E-CME evaluated by ( A ) DPPH radical scavenging activity, ( B ) hydrogen peroxide (H 2 O 2 ) scavenging activity, ( C ) ferrous ion (Fe 2+ ) chelating activity, and ( D ) ferric reducing antioxidant power (FRAP) assays at concentrations of 0.125, 0.25, 0.5, and 1 mg/ml. Data are presented as mean ± SD (n = 3). Statistical comparisons were performed using one-way ANOVA with Tukey’s post hoc test; groups not sharing the same letter (a–c) are significantly different ( p < 0.05). ( E–F ) Effects of E-CME on TNF-α mRNA expression in HaCaT keratinocytes ( E ) <t>and</t> <t>RBL-2H3</t> mast cells ( F ). Cells were treated with various concentrations of E-CME, and TNF-α gene expression was analyzed by reverse transcription PCR using glyceradehyde 3-phospate dehydrogenase (GAPDH) as internal control. E-CME treatment downregulated TNF-α expression in a concentration dependent manner. Data represents SD from three independent experiments. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05). ( G ) Cell viability of HaCaT and RBL-2H3 cells following 24-h exposure to E-CME (62.5–1,000 μg/ml) determined by MTT assay. Viability remained above 80% at concentrations ≤125 μg/ml but declined significantly at higher concentrations. ( H ) Inhibitory effect of E-CME on β-hexosaminidase release in IgE-sensitized RBL-2H3 cells. Cells were presensitized with anti-dinitrophenyl (DNP) IgE and stimulated with DNP-bovine serum albumin (BSA). E-CME significantly suppressed β-hexosaminidase release in a dose-dependent manner, indicating inhibition of mast cell degranulation. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05).
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    ( A–D ) In vitro antioxidant capacity of E-CME evaluated by ( A ) DPPH radical scavenging activity, ( B ) hydrogen peroxide (H 2 O 2 ) scavenging activity, ( C ) ferrous ion (Fe 2+ ) chelating activity, and ( D ) ferric reducing antioxidant power (FRAP) assays at concentrations of 0.125, 0.25, 0.5, and 1 mg/ml. Data are presented as mean ± SD (n = 3). Statistical comparisons were performed using one-way ANOVA with Tukey’s post hoc test; groups not sharing the same letter (a–c) are significantly different ( p < 0.05). ( E–F ) Effects of E-CME on TNF-α mRNA expression in HaCaT keratinocytes ( E ) and RBL-2H3 mast cells ( F ). Cells were treated with various concentrations of E-CME, and TNF-α gene expression was analyzed by reverse transcription PCR using glyceradehyde 3-phospate dehydrogenase (GAPDH) as internal control. E-CME treatment downregulated TNF-α expression in a concentration dependent manner. Data represents SD from three independent experiments. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05). ( G ) Cell viability of HaCaT and RBL-2H3 cells following 24-h exposure to E-CME (62.5–1,000 μg/ml) determined by MTT assay. Viability remained above 80% at concentrations ≤125 μg/ml but declined significantly at higher concentrations. ( H ) Inhibitory effect of E-CME on β-hexosaminidase release in IgE-sensitized RBL-2H3 cells. Cells were presensitized with anti-dinitrophenyl (DNP) IgE and stimulated with DNP-bovine serum albumin (BSA). E-CME significantly suppressed β-hexosaminidase release in a dose-dependent manner, indicating inhibition of mast cell degranulation. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05).

    Journal: Journal of Microbiology and Biotechnology

    Article Title: Chaga Mushroom ( Inonotus obliquus ) Attenuates DNCB-Induced Atopic Dermatitis by Modulating Oxidative Stress and Cytokine Expression

    doi: 10.4014/jmb.2510.10032

    Figure Lengend Snippet: ( A–D ) In vitro antioxidant capacity of E-CME evaluated by ( A ) DPPH radical scavenging activity, ( B ) hydrogen peroxide (H 2 O 2 ) scavenging activity, ( C ) ferrous ion (Fe 2+ ) chelating activity, and ( D ) ferric reducing antioxidant power (FRAP) assays at concentrations of 0.125, 0.25, 0.5, and 1 mg/ml. Data are presented as mean ± SD (n = 3). Statistical comparisons were performed using one-way ANOVA with Tukey’s post hoc test; groups not sharing the same letter (a–c) are significantly different ( p < 0.05). ( E–F ) Effects of E-CME on TNF-α mRNA expression in HaCaT keratinocytes ( E ) and RBL-2H3 mast cells ( F ). Cells were treated with various concentrations of E-CME, and TNF-α gene expression was analyzed by reverse transcription PCR using glyceradehyde 3-phospate dehydrogenase (GAPDH) as internal control. E-CME treatment downregulated TNF-α expression in a concentration dependent manner. Data represents SD from three independent experiments. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05). ( G ) Cell viability of HaCaT and RBL-2H3 cells following 24-h exposure to E-CME (62.5–1,000 μg/ml) determined by MTT assay. Viability remained above 80% at concentrations ≤125 μg/ml but declined significantly at higher concentrations. ( H ) Inhibitory effect of E-CME on β-hexosaminidase release in IgE-sensitized RBL-2H3 cells. Cells were presensitized with anti-dinitrophenyl (DNP) IgE and stimulated with DNP-bovine serum albumin (BSA). E-CME significantly suppressed β-hexosaminidase release in a dose-dependent manner, indicating inhibition of mast cell degranulation. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05).

    Article Snippet: HaCaT and RBL-2H3 cell lines were obtained from the Korean Cell Line Bank (Republic of Korea).

    Techniques: In Vitro, Activity Assay, Expressing, Gene Expression, Reverse Transcription, Control, Concentration Assay, MTT Assay, Inhibition