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human mip 3α  (Elabscience Biotechnology)


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    Structured Review

    Elabscience Biotechnology human mip 3α
    Human Mip 3α, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+mip+3%CE%B1/pmc13081452-230-31-105?v=Elabscience+Biotechnology
    Average 91 stars, based on 5 article reviews
    human mip 3α - by Bioz Stars, 2026-08
    91/100 stars

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    Correlations between LL-37 and citLL-37-mediated increase in the mRNA abundance of COX-2 and chemokines. HBEC-3KT cells were stimulated with either (⬤) LL-37 or (🞅) citLL-37 (0.50 µM each). mRNA abundance of COX-2, IL-8, GROα <t>and</t> <t>MIP-3α</t> were examined in cell lysates using qRT-PCR after 4 h. Relative fold changes were calculated compared to unstimulated cells normalized to 1, using the ΔΔCt method after normalization with 18s RNA expression. Pearson’s correlation analysis was performed to determine the correlation between COX-2 and ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α mRNA abundance (fold changes compared to unstimulated cells)
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    (A) Heatmap of gene expression changes after overexpression of BNC1. (B) Venn diagram showing the screening of target genes of BNC1. Genes showing decreased expression after overexpression of BNC1 and highly expressed genes in gastric cancer from the TCGA database. (C) Downstream target genes of BNC1 were screened by transcriptome sequencing in AGS stable cell lines overexpressing BNC1 and control cells (log 2 fold change [FC] > 1.5 or < −1.5). (D–H) mRNA levels of PTPRC, SERPINB9, RAC2, BAKN1, and CCL20 in MKN-28, AGS and GES-1 cell lines. (I) KEGG analysis of genes showing decreased expression after overexpression of BNC1. (J) mRNA levels of CCL20 in MKN-28 and AGS stable cell lines overexpressing BNC1 and in control cells. (K) <t>ELISA</t> shows the protein levels of CCL20 in MKN-28 and AGS cell lines after overexpression of BNC1. (L) AlphaFold3 prediction of BNC1 binding to the CCL20 promoter region. (M) Dual luciferase results for BNC1 and CCL20.
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    R&D Systems recombinant human rh ccl20 mip 3α protein
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    R&D Systems human mip 3α ccl20 quantikine elisa kit
    (A) Heatmap of gene expression changes after overexpression of BNC1. (B) Venn diagram showing the screening of target genes of BNC1. Genes showing decreased expression after overexpression of BNC1 and highly expressed genes in gastric cancer from the TCGA database. (C) Downstream target genes of BNC1 were screened by transcriptome sequencing in AGS stable cell lines overexpressing BNC1 and control cells (log 2 fold change [FC] > 1.5 or < −1.5). (D–H) mRNA levels of PTPRC, SERPINB9, RAC2, BAKN1, and CCL20 in MKN-28, AGS and GES-1 cell lines. (I) KEGG analysis of genes showing decreased expression after overexpression of BNC1. (J) mRNA levels of CCL20 in MKN-28 and AGS stable cell lines overexpressing BNC1 and in control cells. (K) <t>ELISA</t> shows the protein levels of CCL20 in MKN-28 and AGS cell lines after overexpression of BNC1. (L) AlphaFold3 prediction of BNC1 binding to the CCL20 promoter region. (M) Dual luciferase results for BNC1 and CCL20.
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    Image Search Results


    Correlations between LL-37 and citLL-37-mediated increase in the mRNA abundance of COX-2 and chemokines. HBEC-3KT cells were stimulated with either (⬤) LL-37 or (🞅) citLL-37 (0.50 µM each). mRNA abundance of COX-2, IL-8, GROα and MIP-3α were examined in cell lysates using qRT-PCR after 4 h. Relative fold changes were calculated compared to unstimulated cells normalized to 1, using the ΔΔCt method after normalization with 18s RNA expression. Pearson’s correlation analysis was performed to determine the correlation between COX-2 and ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α mRNA abundance (fold changes compared to unstimulated cells)

    Journal: Respiratory Research

    Article Title: LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells

    doi: 10.1186/s12931-026-03493-w

    Figure Lengend Snippet: Correlations between LL-37 and citLL-37-mediated increase in the mRNA abundance of COX-2 and chemokines. HBEC-3KT cells were stimulated with either (⬤) LL-37 or (🞅) citLL-37 (0.50 µM each). mRNA abundance of COX-2, IL-8, GROα and MIP-3α were examined in cell lysates using qRT-PCR after 4 h. Relative fold changes were calculated compared to unstimulated cells normalized to 1, using the ΔΔCt method after normalization with 18s RNA expression. Pearson’s correlation analysis was performed to determine the correlation between COX-2 and ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α mRNA abundance (fold changes compared to unstimulated cells)

    Article Snippet: The abundance of IL-8 (Cat# DY208), GROα (Cat# DY275) and MIP-3α (Cat# DY360) were examined in TC supernatants using ELISA kits obtained from R&D Systems, according to the manufacturer’s instructions.

    Techniques: Quantitative RT-PCR, RNA Expression

    Inhibition of COX-2 suppresses LL-37-mediated chemokine production. HBEC-3KT cells were pre-treated with COX-2 inhibitor Rofecoxib (20 nM) for 1 h, followed by stimulation with either LL-37, citLL-37 or sLL-37 (0.50 µM each) for 24 h (n = 5). TC supernatants were examined for the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α by ELISA. Chemokine levels shown in pg/mL after background subtraction of levels in unstimulated cells. Each dot represents an independent experiment (n = 5), the bars show IQR with the median line and the whiskers represent the min-max range. Statistical significance was measured using Two-Way ANOVA, and # represents statistical significance compared to unstimulated cells ( ** p < 0.005, *** p < 0.0005, #### or **** p < 0.0001)

    Journal: Respiratory Research

    Article Title: LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells

    doi: 10.1186/s12931-026-03493-w

    Figure Lengend Snippet: Inhibition of COX-2 suppresses LL-37-mediated chemokine production. HBEC-3KT cells were pre-treated with COX-2 inhibitor Rofecoxib (20 nM) for 1 h, followed by stimulation with either LL-37, citLL-37 or sLL-37 (0.50 µM each) for 24 h (n = 5). TC supernatants were examined for the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α by ELISA. Chemokine levels shown in pg/mL after background subtraction of levels in unstimulated cells. Each dot represents an independent experiment (n = 5), the bars show IQR with the median line and the whiskers represent the min-max range. Statistical significance was measured using Two-Way ANOVA, and # represents statistical significance compared to unstimulated cells ( ** p < 0.005, *** p < 0.0005, #### or **** p < 0.0001)

    Article Snippet: The abundance of IL-8 (Cat# DY208), GROα (Cat# DY275) and MIP-3α (Cat# DY360) were examined in TC supernatants using ELISA kits obtained from R&D Systems, according to the manufacturer’s instructions.

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay

    Inhibition of PGE2 receptors (EP1-4) suppresses LL-37-mediated enhancement of chemokines. HBEC-3KT cells were pre-treated with specific inhibitors for PGE2 receptors, EP1 (SC-19220; 20 nM), EP2 (PF-044EP2; 25 nM), EP3 (L-798,106; 20 nM), or EP4 (MF498; 10 nM), 1 h prior to stimulation with either LL-37or sLL-37 (0.50 μM). Tissue culture (TC) supernatants were collected after 24 h and the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α were measured by ELISA. Each dot represents an independent experiment (n=4), the bars show IQR with the median line and the whiskers represent the min-max range. Results shown are after subtracting baseline values obtained from unstimulated cells in each independent experiment. Statistical significance was determined using Two-Way ANOVA (** p < 0.001 and **** p < 0.0001)

    Journal: Respiratory Research

    Article Title: LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells

    doi: 10.1186/s12931-026-03493-w

    Figure Lengend Snippet: Inhibition of PGE2 receptors (EP1-4) suppresses LL-37-mediated enhancement of chemokines. HBEC-3KT cells were pre-treated with specific inhibitors for PGE2 receptors, EP1 (SC-19220; 20 nM), EP2 (PF-044EP2; 25 nM), EP3 (L-798,106; 20 nM), or EP4 (MF498; 10 nM), 1 h prior to stimulation with either LL-37or sLL-37 (0.50 μM). Tissue culture (TC) supernatants were collected after 24 h and the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α were measured by ELISA. Each dot represents an independent experiment (n=4), the bars show IQR with the median line and the whiskers represent the min-max range. Results shown are after subtracting baseline values obtained from unstimulated cells in each independent experiment. Statistical significance was determined using Two-Way ANOVA (** p < 0.001 and **** p < 0.0001)

    Article Snippet: The abundance of IL-8 (Cat# DY208), GROα (Cat# DY275) and MIP-3α (Cat# DY360) were examined in TC supernatants using ELISA kits obtained from R&D Systems, according to the manufacturer’s instructions.

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay

    (A) Heatmap of gene expression changes after overexpression of BNC1. (B) Venn diagram showing the screening of target genes of BNC1. Genes showing decreased expression after overexpression of BNC1 and highly expressed genes in gastric cancer from the TCGA database. (C) Downstream target genes of BNC1 were screened by transcriptome sequencing in AGS stable cell lines overexpressing BNC1 and control cells (log 2 fold change [FC] > 1.5 or < −1.5). (D–H) mRNA levels of PTPRC, SERPINB9, RAC2, BAKN1, and CCL20 in MKN-28, AGS and GES-1 cell lines. (I) KEGG analysis of genes showing decreased expression after overexpression of BNC1. (J) mRNA levels of CCL20 in MKN-28 and AGS stable cell lines overexpressing BNC1 and in control cells. (K) ELISA shows the protein levels of CCL20 in MKN-28 and AGS cell lines after overexpression of BNC1. (L) AlphaFold3 prediction of BNC1 binding to the CCL20 promoter region. (M) Dual luciferase results for BNC1 and CCL20.

    Journal: PeerJ

    Article Title: BNC1 inhibits the development and progression of gastric cancer by regulating the CCL20/JAK-STAT axis

    doi: 10.7717/peerj.19477

    Figure Lengend Snippet: (A) Heatmap of gene expression changes after overexpression of BNC1. (B) Venn diagram showing the screening of target genes of BNC1. Genes showing decreased expression after overexpression of BNC1 and highly expressed genes in gastric cancer from the TCGA database. (C) Downstream target genes of BNC1 were screened by transcriptome sequencing in AGS stable cell lines overexpressing BNC1 and control cells (log 2 fold change [FC] > 1.5 or < −1.5). (D–H) mRNA levels of PTPRC, SERPINB9, RAC2, BAKN1, and CCL20 in MKN-28, AGS and GES-1 cell lines. (I) KEGG analysis of genes showing decreased expression after overexpression of BNC1. (J) mRNA levels of CCL20 in MKN-28 and AGS stable cell lines overexpressing BNC1 and in control cells. (K) ELISA shows the protein levels of CCL20 in MKN-28 and AGS cell lines after overexpression of BNC1. (L) AlphaFold3 prediction of BNC1 binding to the CCL20 promoter region. (M) Dual luciferase results for BNC1 and CCL20.

    Article Snippet: The stable BNC1-overexpressing MKN-28 and AGS cell lines were used to perform the ELISA analysis using the Human MIP-3α/CCL20 (C-C motif chemokine ligand 20) QuickTest ELISA Kit (QT-EH0231; Wuhan Fine Biotech Co., Ltd).

    Techniques: Gene Expression, Over Expression, Expressing, Sequencing, Stable Transfection, Control, Enzyme-linked Immunosorbent Assay, Binding Assay, Luciferase