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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). <t>(G)</t> <t>ELISA</t> quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and <t>IFN-γ)</t> in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.
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MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). (G) ELISA quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and IFN-γ) in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.

Journal: iScience

Article Title: Maimendong decoction suppresses non-small cell lung cancer growth by promoting dendritic cell maturation via the SIRT1/p65 acetylation pathway

doi: 10.1016/j.isci.2026.114774

Figure Lengend Snippet: MMDD suppresses tumor growth via SIRT1 downregulation and enhanced p65 acetylation (A and C) Western blot analysis of SIRT1 and acetyl-p65 protein levels in tumor tissues from vehicle control (sterile deionized water), L-MMDD, M-MMDD, and H-MMDD groups. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in tumor tissues using ImageJ software ( n = 3). (E) Representative immunofluorescence images of SIRT1 (red) and acetyl-p65 (green) in tumor sections. Nuclei were counterstained with DAPI (blue) (scale bar, 50 μm). (F) Quantification of mean fluorescence intensity for SIRT1 and acetyl-p65 ( n = 3). (G) ELISA quantification of cytokine levels (IL-1β, IL-6, IL-12, TNF-α, and IFN-γ) in tumor homogenates ( n = 6). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.

Article Snippet: ELISA Kits (IL-1β, IL-6, IL-12, TNF-α, IFN-γ) , LiankeBio , Cat# EK201B; EK206; EK2183; EK282; EK280.

Techniques: Western Blot, Control, Sterility, Expressing, Software, Immunofluorescence, Fluorescence, Enzyme-linked Immunosorbent Assay, Comparison

MMDD-containing serum-treated DCs enhance the migration, invasion, and activation of CD8 + T cells (A) Representative transwell assay images show the migration and invasion capacities of CD8 + T cells co-cultured with DCs pretreated with control (drug-free serum from vehicle-treated rats), low-, medium-, or high-dose MMDD-containing serum (scale bar, 50 μm). (B) Quantification of migrated and invaded CD8 + T cells ( n = 3). (C) Flow cytometry analysis of IFN-γ expression in CD8 + T cells co-cultured with supernatant of MMDD-treated DCs. (D) Quantification of the proportion of IFN-γ + cells among CD8 + T cells ( n = 3). Data are represented as mean ± SD. One-way ANOVA (D) and two-way ANOVA (B) are used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.

Journal: iScience

Article Title: Maimendong decoction suppresses non-small cell lung cancer growth by promoting dendritic cell maturation via the SIRT1/p65 acetylation pathway

doi: 10.1016/j.isci.2026.114774

Figure Lengend Snippet: MMDD-containing serum-treated DCs enhance the migration, invasion, and activation of CD8 + T cells (A) Representative transwell assay images show the migration and invasion capacities of CD8 + T cells co-cultured with DCs pretreated with control (drug-free serum from vehicle-treated rats), low-, medium-, or high-dose MMDD-containing serum (scale bar, 50 μm). (B) Quantification of migrated and invaded CD8 + T cells ( n = 3). (C) Flow cytometry analysis of IFN-γ expression in CD8 + T cells co-cultured with supernatant of MMDD-treated DCs. (D) Quantification of the proportion of IFN-γ + cells among CD8 + T cells ( n = 3). Data are represented as mean ± SD. One-way ANOVA (D) and two-way ANOVA (B) are used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01.

Article Snippet: ELISA Kits (IL-1β, IL-6, IL-12, TNF-α, IFN-γ) , LiankeBio , Cat# EK201B; EK206; EK2183; EK282; EK280.

Techniques: Migration, Activation Assay, Transwell Assay, Cell Culture, Control, Flow Cytometry, Expressing, Comparison

MMDD exerts antitumor activity by modulating the SIRT1/acetyl-p65 axis in DCs (A and C) Western blot analysis of SIRT1, acetyl-p65, and p65 expression in DCs treated with control (drug-free serum from vehicle-treated rats), low-, medium-, or high-dose MMDD-containing serum. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in DCs using ImageJ software ( n = 3). (E) ELISA quantification of pro-inflammatory cytokines (IL-1β, IL-6, IL-12, and TNF-α) and IFN-γ in supernatants of MMDD-treated DCs ( n = 6). (F) Western blot analysis of SIRT1 expression in control, negative control (NC), and AAV-SIRT1-transduced (OE-SIRT1) BMDCs. (G) Quantification of SIRT1 expression levels in DCs ( n = 3). (H) Western blot analysis of SIRT1, acetyl-p65, and p65 in DCs from the control, high-dose MMDD-containing serum, OE-SIRT1, or OE-SIRT1+high-dose MMDD-containing serum groups. (I and J) Quantification of relative SIRT1, acetyl-p65/p65 levels in DCs ( n = 3). (K) ELISA analysis of pro-inflammatory cytokines (IL-1β, IL-6, IL-12, and TNF-α) and IFN-γ in DC supernatants ( n = 6). (L) Flow cytometry profiles of DCs maturation markers (CD40, CD80, CD83, and MHC-II) across groups. (M) Quantitative analysis of CD40 + , CD80 + , CD83 + , and MHC-II + DC proportions ( n = 3). (N) Flow cytometry analysis of IFN-γ expression in CD8 + T cells treated with DC-conditioned supernatant from different groups. (O) Quantification of the proportion of IFN-γ + cells among CD8 + T cells ( n = 3). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01. See also .

Journal: iScience

Article Title: Maimendong decoction suppresses non-small cell lung cancer growth by promoting dendritic cell maturation via the SIRT1/p65 acetylation pathway

doi: 10.1016/j.isci.2026.114774

Figure Lengend Snippet: MMDD exerts antitumor activity by modulating the SIRT1/acetyl-p65 axis in DCs (A and C) Western blot analysis of SIRT1, acetyl-p65, and p65 expression in DCs treated with control (drug-free serum from vehicle-treated rats), low-, medium-, or high-dose MMDD-containing serum. GAPDH served as the internal loading control for SIRT1, acetyl-p65, and p65. (B and D) Quantitative analysis of relative SIRT1 and acetyl-p65/p65 expression levels in DCs using ImageJ software ( n = 3). (E) ELISA quantification of pro-inflammatory cytokines (IL-1β, IL-6, IL-12, and TNF-α) and IFN-γ in supernatants of MMDD-treated DCs ( n = 6). (F) Western blot analysis of SIRT1 expression in control, negative control (NC), and AAV-SIRT1-transduced (OE-SIRT1) BMDCs. (G) Quantification of SIRT1 expression levels in DCs ( n = 3). (H) Western blot analysis of SIRT1, acetyl-p65, and p65 in DCs from the control, high-dose MMDD-containing serum, OE-SIRT1, or OE-SIRT1+high-dose MMDD-containing serum groups. (I and J) Quantification of relative SIRT1, acetyl-p65/p65 levels in DCs ( n = 3). (K) ELISA analysis of pro-inflammatory cytokines (IL-1β, IL-6, IL-12, and TNF-α) and IFN-γ in DC supernatants ( n = 6). (L) Flow cytometry profiles of DCs maturation markers (CD40, CD80, CD83, and MHC-II) across groups. (M) Quantitative analysis of CD40 + , CD80 + , CD83 + , and MHC-II + DC proportions ( n = 3). (N) Flow cytometry analysis of IFN-γ expression in CD8 + T cells treated with DC-conditioned supernatant from different groups. (O) Quantification of the proportion of IFN-γ + cells among CD8 + T cells ( n = 3). Data are represented as mean ± SD. One-way ANOVA was used for comparison among multiple groups.∗ p < 0.05 and ∗∗ p < 0.01. See also .

Article Snippet: ELISA Kits (IL-1β, IL-6, IL-12, TNF-α, IFN-γ) , LiankeBio , Cat# EK201B; EK206; EK2183; EK282; EK280.

Techniques: Activity Assay, Western Blot, Expressing, Control, Software, Enzyme-linked Immunosorbent Assay, Negative Control, Flow Cytometry, Comparison