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vaca knockout mutant strain 26 695  (ATCC)


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    ATCC vaca knockout mutant strain 26 695
    H. pylori transcriptionally increased gastric epithelial NFIL3 expression via ERK-SP1 pathway. ( A ) AGS cells were subjected to infection with H. pylori 11,637 or 26,695 (MOI = 100, 24 h) either in the same (lower) chamber or in a separate (upper) chamber of a Transwell apparatus. The expression levels of NFIL3 were assessed using qRT-PCR ( n = 3) and WB. ( B ) The expression of NFIL3 in AGS cells infected with H. pylori TN2GF4 or its virulence mutant strains was evaluated through the GEO database ( GSE60661 ). ( C ) NFIL3 expression was further examined in AGS cells infected with H. pylori 11,637 or the Δ cagA mutant, utilizing qRT-PCR ( n = 3) and WB. ( D ) The expression of NFIL3 was also analyzed in AGS cells infected with H. pylori 26,695 or the Δ <t>vacA</t> mutant through qRT-PCR ( n = 3) and WB. ( E ) The expression levels of NR1D1 were investigated in AGS cells infected with H. pylori TN2GF4 or virulence mutant strains utilizing the GEO database ( GSE60661 ). ( F ) Potential transcription factor binding sites were predicted via the PROMO website, focusing on a 2000 bp segment of the NFIL3 promoter. ( G ) A conserved sequence of putative SP1 binding sites (red line) was identified in both human and mouse models. ( H ) WB and qRT-PCR ( n = 3) analyses of NFIL3 were conducted in AGS cells post-treatment with H. pylori 11,637, U0126, and Mithramycin A (MMA). ( I ) Following a 24-hour transfection with SP1 siRNA, AGS cells were subsequently infected with H. pylori 11,637 for an additional 24 h. The expression levels of NFIL3 and SP1 were analyzed using qRT-PCR ( n = 3) and WB. ( J ) NFIL3 promoter luciferase reporter assays were conducted in AGS cell lines treated with H. pylori 11,637, U0126, Mithramycin A (MMA), and the Δ cagA mutant. ( K ) Luciferase reporter assay for NFIL3-Luc and mutant-Luc. n.s. P > 0.05, ** P < 0.01, and *** P < 0.001
    Vaca Knockout Mutant Strain 26 695, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1029 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/vaca+knockout+mutant+strain+26+695/pmc12168321-38-19-38?v=ATCC
    Average 96 stars, based on 1029 article reviews
    vaca knockout mutant strain 26 695 - by Bioz Stars, 2026-08
    96/100 stars

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    1) Product Images from "Disruption of the biorhythm in gastric epithelial cell triggers inflammation in Helicobacter pylori -associated gastritis by aberrantly regulating NFIL3 via CagA activated ERK-SP1 pathway"

    Article Title: Disruption of the biorhythm in gastric epithelial cell triggers inflammation in Helicobacter pylori -associated gastritis by aberrantly regulating NFIL3 via CagA activated ERK-SP1 pathway

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-025-02302-z

    H. pylori transcriptionally increased gastric epithelial NFIL3 expression via ERK-SP1 pathway. ( A ) AGS cells were subjected to infection with H. pylori 11,637 or 26,695 (MOI = 100, 24 h) either in the same (lower) chamber or in a separate (upper) chamber of a Transwell apparatus. The expression levels of NFIL3 were assessed using qRT-PCR ( n = 3) and WB. ( B ) The expression of NFIL3 in AGS cells infected with H. pylori TN2GF4 or its virulence mutant strains was evaluated through the GEO database ( GSE60661 ). ( C ) NFIL3 expression was further examined in AGS cells infected with H. pylori 11,637 or the Δ cagA mutant, utilizing qRT-PCR ( n = 3) and WB. ( D ) The expression of NFIL3 was also analyzed in AGS cells infected with H. pylori 26,695 or the Δ vacA mutant through qRT-PCR ( n = 3) and WB. ( E ) The expression levels of NR1D1 were investigated in AGS cells infected with H. pylori TN2GF4 or virulence mutant strains utilizing the GEO database ( GSE60661 ). ( F ) Potential transcription factor binding sites were predicted via the PROMO website, focusing on a 2000 bp segment of the NFIL3 promoter. ( G ) A conserved sequence of putative SP1 binding sites (red line) was identified in both human and mouse models. ( H ) WB and qRT-PCR ( n = 3) analyses of NFIL3 were conducted in AGS cells post-treatment with H. pylori 11,637, U0126, and Mithramycin A (MMA). ( I ) Following a 24-hour transfection with SP1 siRNA, AGS cells were subsequently infected with H. pylori 11,637 for an additional 24 h. The expression levels of NFIL3 and SP1 were analyzed using qRT-PCR ( n = 3) and WB. ( J ) NFIL3 promoter luciferase reporter assays were conducted in AGS cell lines treated with H. pylori 11,637, U0126, Mithramycin A (MMA), and the Δ cagA mutant. ( K ) Luciferase reporter assay for NFIL3-Luc and mutant-Luc. n.s. P > 0.05, ** P < 0.01, and *** P < 0.001
    Figure Legend Snippet: H. pylori transcriptionally increased gastric epithelial NFIL3 expression via ERK-SP1 pathway. ( A ) AGS cells were subjected to infection with H. pylori 11,637 or 26,695 (MOI = 100, 24 h) either in the same (lower) chamber or in a separate (upper) chamber of a Transwell apparatus. The expression levels of NFIL3 were assessed using qRT-PCR ( n = 3) and WB. ( B ) The expression of NFIL3 in AGS cells infected with H. pylori TN2GF4 or its virulence mutant strains was evaluated through the GEO database ( GSE60661 ). ( C ) NFIL3 expression was further examined in AGS cells infected with H. pylori 11,637 or the Δ cagA mutant, utilizing qRT-PCR ( n = 3) and WB. ( D ) The expression of NFIL3 was also analyzed in AGS cells infected with H. pylori 26,695 or the Δ vacA mutant through qRT-PCR ( n = 3) and WB. ( E ) The expression levels of NR1D1 were investigated in AGS cells infected with H. pylori TN2GF4 or virulence mutant strains utilizing the GEO database ( GSE60661 ). ( F ) Potential transcription factor binding sites were predicted via the PROMO website, focusing on a 2000 bp segment of the NFIL3 promoter. ( G ) A conserved sequence of putative SP1 binding sites (red line) was identified in both human and mouse models. ( H ) WB and qRT-PCR ( n = 3) analyses of NFIL3 were conducted in AGS cells post-treatment with H. pylori 11,637, U0126, and Mithramycin A (MMA). ( I ) Following a 24-hour transfection with SP1 siRNA, AGS cells were subsequently infected with H. pylori 11,637 for an additional 24 h. The expression levels of NFIL3 and SP1 were analyzed using qRT-PCR ( n = 3) and WB. ( J ) NFIL3 promoter luciferase reporter assays were conducted in AGS cell lines treated with H. pylori 11,637, U0126, Mithramycin A (MMA), and the Δ cagA mutant. ( K ) Luciferase reporter assay for NFIL3-Luc and mutant-Luc. n.s. P > 0.05, ** P < 0.01, and *** P < 0.001

    Techniques Used: Expressing, Infection, Quantitative RT-PCR, Mutagenesis, Binding Assay, Sequencing, Transfection, Luciferase, Reporter Assay



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    vaca knockout mutant strain 26 695  (ATCC)
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    ATCC vaca knockout mutant strain 26 695
    H. pylori transcriptionally increased gastric epithelial NFIL3 expression via ERK-SP1 pathway. ( A ) AGS cells were subjected to infection with H. pylori 11,637 or 26,695 (MOI = 100, 24 h) either in the same (lower) chamber or in a separate (upper) chamber of a Transwell apparatus. The expression levels of NFIL3 were assessed using qRT-PCR ( n = 3) and WB. ( B ) The expression of NFIL3 in AGS cells infected with H. pylori TN2GF4 or its virulence mutant strains was evaluated through the GEO database ( GSE60661 ). ( C ) NFIL3 expression was further examined in AGS cells infected with H. pylori 11,637 or the Δ cagA mutant, utilizing qRT-PCR ( n = 3) and WB. ( D ) The expression of NFIL3 was also analyzed in AGS cells infected with H. pylori 26,695 or the Δ <t>vacA</t> mutant through qRT-PCR ( n = 3) and WB. ( E ) The expression levels of NR1D1 were investigated in AGS cells infected with H. pylori TN2GF4 or virulence mutant strains utilizing the GEO database ( GSE60661 ). ( F ) Potential transcription factor binding sites were predicted via the PROMO website, focusing on a 2000 bp segment of the NFIL3 promoter. ( G ) A conserved sequence of putative SP1 binding sites (red line) was identified in both human and mouse models. ( H ) WB and qRT-PCR ( n = 3) analyses of NFIL3 were conducted in AGS cells post-treatment with H. pylori 11,637, U0126, and Mithramycin A (MMA). ( I ) Following a 24-hour transfection with SP1 siRNA, AGS cells were subsequently infected with H. pylori 11,637 for an additional 24 h. The expression levels of NFIL3 and SP1 were analyzed using qRT-PCR ( n = 3) and WB. ( J ) NFIL3 promoter luciferase reporter assays were conducted in AGS cell lines treated with H. pylori 11,637, U0126, Mithramycin A (MMA), and the Δ cagA mutant. ( K ) Luciferase reporter assay for NFIL3-Luc and mutant-Luc. n.s. P > 0.05, ** P < 0.01, and *** P < 0.001
    Vaca Knockout Mutant Strain 26 695, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/vaca+knockout+mutant+strain+26+695/pmc12168321-38-19-38?v=ATCC
    Average 96 stars, based on 1 article reviews
    vaca knockout mutant strain 26 695 - by Bioz Stars, 2026-08
    96/100 stars
    		  Buy from Supplier

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    H. pylori transcriptionally increased gastric epithelial NFIL3 expression via ERK-SP1 pathway. ( A ) AGS cells were subjected to infection with H. pylori 11,637 or 26,695 (MOI = 100, 24 h) either in the same (lower) chamber or in a separate (upper) chamber of a Transwell apparatus. The expression levels of NFIL3 were assessed using qRT-PCR ( n = 3) and WB. ( B ) The expression of NFIL3 in AGS cells infected with H. pylori TN2GF4 or its virulence mutant strains was evaluated through the GEO database ( GSE60661 ). ( C ) NFIL3 expression was further examined in AGS cells infected with H. pylori 11,637 or the Δ cagA mutant, utilizing qRT-PCR ( n = 3) and WB. ( D ) The expression of NFIL3 was also analyzed in AGS cells infected with H. pylori 26,695 or the Δ vacA mutant through qRT-PCR ( n = 3) and WB. ( E ) The expression levels of NR1D1 were investigated in AGS cells infected with H. pylori TN2GF4 or virulence mutant strains utilizing the GEO database ( GSE60661 ). ( F ) Potential transcription factor binding sites were predicted via the PROMO website, focusing on a 2000 bp segment of the NFIL3 promoter. ( G ) A conserved sequence of putative SP1 binding sites (red line) was identified in both human and mouse models. ( H ) WB and qRT-PCR ( n = 3) analyses of NFIL3 were conducted in AGS cells post-treatment with H. pylori 11,637, U0126, and Mithramycin A (MMA). ( I ) Following a 24-hour transfection with SP1 siRNA, AGS cells were subsequently infected with H. pylori 11,637 for an additional 24 h. The expression levels of NFIL3 and SP1 were analyzed using qRT-PCR ( n = 3) and WB. ( J ) NFIL3 promoter luciferase reporter assays were conducted in AGS cell lines treated with H. pylori 11,637, U0126, Mithramycin A (MMA), and the Δ cagA mutant. ( K ) Luciferase reporter assay for NFIL3-Luc and mutant-Luc. n.s. P > 0.05, ** P < 0.01, and *** P < 0.001

    Journal: Cell Communication and Signaling : CCS

    Article Title: Disruption of the biorhythm in gastric epithelial cell triggers inflammation in Helicobacter pylori -associated gastritis by aberrantly regulating NFIL3 via CagA activated ERK-SP1 pathway

    doi: 10.1186/s12964-025-02302-z

    Figure Lengend Snippet: H. pylori transcriptionally increased gastric epithelial NFIL3 expression via ERK-SP1 pathway. ( A ) AGS cells were subjected to infection with H. pylori 11,637 or 26,695 (MOI = 100, 24 h) either in the same (lower) chamber or in a separate (upper) chamber of a Transwell apparatus. The expression levels of NFIL3 were assessed using qRT-PCR ( n = 3) and WB. ( B ) The expression of NFIL3 in AGS cells infected with H. pylori TN2GF4 or its virulence mutant strains was evaluated through the GEO database ( GSE60661 ). ( C ) NFIL3 expression was further examined in AGS cells infected with H. pylori 11,637 or the Δ cagA mutant, utilizing qRT-PCR ( n = 3) and WB. ( D ) The expression of NFIL3 was also analyzed in AGS cells infected with H. pylori 26,695 or the Δ vacA mutant through qRT-PCR ( n = 3) and WB. ( E ) The expression levels of NR1D1 were investigated in AGS cells infected with H. pylori TN2GF4 or virulence mutant strains utilizing the GEO database ( GSE60661 ). ( F ) Potential transcription factor binding sites were predicted via the PROMO website, focusing on a 2000 bp segment of the NFIL3 promoter. ( G ) A conserved sequence of putative SP1 binding sites (red line) was identified in both human and mouse models. ( H ) WB and qRT-PCR ( n = 3) analyses of NFIL3 were conducted in AGS cells post-treatment with H. pylori 11,637, U0126, and Mithramycin A (MMA). ( I ) Following a 24-hour transfection with SP1 siRNA, AGS cells were subsequently infected with H. pylori 11,637 for an additional 24 h. The expression levels of NFIL3 and SP1 were analyzed using qRT-PCR ( n = 3) and WB. ( J ) NFIL3 promoter luciferase reporter assays were conducted in AGS cell lines treated with H. pylori 11,637, U0126, Mithramycin A (MMA), and the Δ cagA mutant. ( K ) Luciferase reporter assay for NFIL3-Luc and mutant-Luc. n.s. P > 0.05, ** P < 0.01, and *** P < 0.001

    Article Snippet: We utilized several strains of H. pylori , specifically the cagA and vacA -positive strain 26,695 (ATCC 700392), the vacA knockout mutant strain 26,695 (referred to as Δ vacA herein), the cagA and vacA -positive strain NCTC 11,637 (ATCC 43504, designated as H. pylori 11637 in this manuscript), the cagA knockout mutant strain NCTC 11,637 (termed Δ cagA in this article), and the cagA and vacA -positive strain PMSS1 (pre-mouse Sydney strain 1) [ , ].

    Techniques: Expressing, Infection, Quantitative RT-PCR, Mutagenesis, Binding Assay, Sequencing, Transfection, Luciferase, Reporter Assay