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  • 95
    Sino Biological cd36
    Results from multiple bond flow assay obtained at 37 and 41°C. Shown is the cellular lifetime against shear stress for IRBC-ICAM-1 and <t>IRBC-CD36</t> bonds at 37°C ( a and b ) and 41°C ( c and d ). Shown is an overlay of cellular lifetime against force graphs of IRBC-ICAM-1 and IRBC-CD36 interactions at all three temperatures ( e and f ), 37°C, and 41°C, respectively. Cellular lifetimes are plotted as mean ± SEM. To see this figure in color, go online.
    Cd36, supplied by Sino Biological, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cd36/product/Sino Biological
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd36 - by Bioz Stars, 2021-04
    95/100 stars
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    89
    Sino Biological ifnar1
    Knockout of the gene encoding CK1α induces β-catenin stabilization and Wnt hyperactivation in murine intestines from <t>Ifnar1</t> −/− mice. (A) Immunohistochemistry analysis of β-catenin expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (B) Immunohistochemistry analysis of cyclin D1 expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (C) Relative mRNA levels of the indicated Wnt target genes in intestinal epithelial cells from mice of the indicated genotypes as assessed by quantitative PCR (levels in untreated Csnk1a1 lox/lox ; Ifnar1 +/+ mice are taken as 1.0). Data are shown as averages ± SEM; an asterisk above Csnk1a1 Δ gut (SKO) indicates a significant difference between wild-type (WT) and SKO mice. *, P
    Ifnar1, supplied by Sino Biological, used in various techniques. Bioz Stars score: 89/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ifnar1/product/Sino Biological
    Average 89 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ifnar1 - by Bioz Stars, 2021-04
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    93
    Sino Biological ox 40
    Knockout of the gene encoding CK1α induces β-catenin stabilization and Wnt hyperactivation in murine intestines from <t>Ifnar1</t> −/− mice. (A) Immunohistochemistry analysis of β-catenin expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (B) Immunohistochemistry analysis of cyclin D1 expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (C) Relative mRNA levels of the indicated Wnt target genes in intestinal epithelial cells from mice of the indicated genotypes as assessed by quantitative PCR (levels in untreated Csnk1a1 lox/lox ; Ifnar1 +/+ mice are taken as 1.0). Data are shown as averages ± SEM; an asterisk above Csnk1a1 Δ gut (SKO) indicates a significant difference between wild-type (WT) and SKO mice. *, P
    Ox 40, supplied by Sino Biological, 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/result/ox 40/product/Sino Biological
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ox 40 - by Bioz Stars, 2021-04
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    86
    Bellen Chemistry attb p acman apr vector
    Knockout of the gene encoding CK1α induces β-catenin stabilization and Wnt hyperactivation in murine intestines from <t>Ifnar1</t> −/− mice. (A) Immunohistochemistry analysis of β-catenin expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (B) Immunohistochemistry analysis of cyclin D1 expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (C) Relative mRNA levels of the indicated Wnt target genes in intestinal epithelial cells from mice of the indicated genotypes as assessed by quantitative PCR (levels in untreated Csnk1a1 lox/lox ; Ifnar1 +/+ mice are taken as 1.0). Data are shown as averages ± SEM; an asterisk above Csnk1a1 Δ gut (SKO) indicates a significant difference between wild-type (WT) and SKO mice. *, P
    Attb P Acman Apr Vector, supplied by Bellen Chemistry, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/attb p acman apr vector/product/Bellen Chemistry
    Average 86 stars, based on 1 article reviews
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    attb p acman apr vector - by Bioz Stars, 2021-04
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    Image Search Results


    Results from multiple bond flow assay obtained at 37 and 41°C. Shown is the cellular lifetime against shear stress for IRBC-ICAM-1 and IRBC-CD36 bonds at 37°C ( a and b ) and 41°C ( c and d ). Shown is an overlay of cellular lifetime against force graphs of IRBC-ICAM-1 and IRBC-CD36 interactions at all three temperatures ( e and f ), 37°C, and 41°C, respectively. Cellular lifetimes are plotted as mean ± SEM. To see this figure in color, go online.

    Journal: Biophysical Journal

    Article Title: Temperature-Induced Catch-Slip to Slip Bond Transit in Plasmodium falciparum-Infected Erythrocytes

    doi: 10.1016/j.bpj.2019.11.016

    Figure Lengend Snippet: Results from multiple bond flow assay obtained at 37 and 41°C. Shown is the cellular lifetime against shear stress for IRBC-ICAM-1 and IRBC-CD36 bonds at 37°C ( a and b ) and 41°C ( c and d ). Shown is an overlay of cellular lifetime against force graphs of IRBC-ICAM-1 and IRBC-CD36 interactions at all three temperatures ( e and f ), 37°C, and 41°C, respectively. Cellular lifetimes are plotted as mean ± SEM. To see this figure in color, go online.

    Article Snippet: In our multiple bond flow assay, the concentration of ICAM-1 used to functionalize the glass substrate was 25 times that of CD36.

    Techniques:

    Knockout of the gene encoding CK1α induces β-catenin stabilization and Wnt hyperactivation in murine intestines from Ifnar1 −/− mice. (A) Immunohistochemistry analysis of β-catenin expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (B) Immunohistochemistry analysis of cyclin D1 expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (C) Relative mRNA levels of the indicated Wnt target genes in intestinal epithelial cells from mice of the indicated genotypes as assessed by quantitative PCR (levels in untreated Csnk1a1 lox/lox ; Ifnar1 +/+ mice are taken as 1.0). Data are shown as averages ± SEM; an asterisk above Csnk1a1 Δ gut (SKO) indicates a significant difference between wild-type (WT) and SKO mice. *, P

    Journal: Molecular and Cellular Biology

    Article Title: Type I Interferons Control Proliferation and Function of the Intestinal Epithelium

    doi: 10.1128/MCB.00988-15

    Figure Lengend Snippet: Knockout of the gene encoding CK1α induces β-catenin stabilization and Wnt hyperactivation in murine intestines from Ifnar1 −/− mice. (A) Immunohistochemistry analysis of β-catenin expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (B) Immunohistochemistry analysis of cyclin D1 expression in intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (C) Relative mRNA levels of the indicated Wnt target genes in intestinal epithelial cells from mice of the indicated genotypes as assessed by quantitative PCR (levels in untreated Csnk1a1 lox/lox ; Ifnar1 +/+ mice are taken as 1.0). Data are shown as averages ± SEM; an asterisk above Csnk1a1 Δ gut (SKO) indicates a significant difference between wild-type (WT) and SKO mice. *, P

    Article Snippet: Collectively, these data suggest that the ablation of CK1α leads to the accumulation of IFNAR1, induction of IFN expression, and activation of expression of IFN-stimulated genes in the intestinal epithelium.

    Techniques: Knock-Out, Mouse Assay, Immunohistochemistry, Expressing, Real-time Polymerase Chain Reaction

    Inhibition of IFN signaling suppresses DNA damage responses in CK1α-deficient mouse intestines. (A) Immunofluorescence analysis of γH2AX expression in intestinal tissues from mice of the indicated genotypes. Bar, 100 μm. (B) Quantitation of the number of γH2AX-positive foci per basal crypt in small intestines of three mice (30 to 50 crypts/villi were analyzed for each mouse). Data are shown as averages ± SEM; asterisks above Csnk1a1 Δ gut (SKO) indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) indicate a significant difference between SKO and DKO mice. *, P

    Journal: Molecular and Cellular Biology

    Article Title: Type I Interferons Control Proliferation and Function of the Intestinal Epithelium

    doi: 10.1128/MCB.00988-15

    Figure Lengend Snippet: Inhibition of IFN signaling suppresses DNA damage responses in CK1α-deficient mouse intestines. (A) Immunofluorescence analysis of γH2AX expression in intestinal tissues from mice of the indicated genotypes. Bar, 100 μm. (B) Quantitation of the number of γH2AX-positive foci per basal crypt in small intestines of three mice (30 to 50 crypts/villi were analyzed for each mouse). Data are shown as averages ± SEM; asterisks above Csnk1a1 Δ gut (SKO) indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) indicate a significant difference between SKO and DKO mice. *, P

    Article Snippet: Collectively, these data suggest that the ablation of CK1α leads to the accumulation of IFNAR1, induction of IFN expression, and activation of expression of IFN-stimulated genes in the intestinal epithelium.

    Techniques: Inhibition, Immunofluorescence, Expressing, Mouse Assay, Quantitation Assay

    Inhibition of IFN signaling increases proliferation and decreases numbers of goblet cells in intestinal tissues from Csnk1a1 -deleted mice. (A) GSEA of transcriptome profiles showing a significant enrichment of genes upregulated upon APC deletion in Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) versus Csnk1a1 Δ gut (SKO) intestinal epithelial cells at day 5 after CK1α ablation. NES, normalized enrichment score; FDR, false discovery rate. (B) H E staining of small intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (C) H E staining of colonic tissues from mice of the indicated genotypes. Bars, 100 μm. (D) PAS staining of small intestinal tissues from mice of the indicated genotypes. (E) Quantitation of the number of PAS-positive goblet cells per crypt/villus axis in the small intestines of three mice (30 to 50 crypts/villi were analyzed for each mouse). Data are shown as averages ± SEM; asterisks above SKO indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above DKO indicate a significant difference between SKO and DKO mice. ***, P

    Journal: Molecular and Cellular Biology

    Article Title: Type I Interferons Control Proliferation and Function of the Intestinal Epithelium

    doi: 10.1128/MCB.00988-15

    Figure Lengend Snippet: Inhibition of IFN signaling increases proliferation and decreases numbers of goblet cells in intestinal tissues from Csnk1a1 -deleted mice. (A) GSEA of transcriptome profiles showing a significant enrichment of genes upregulated upon APC deletion in Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) versus Csnk1a1 Δ gut (SKO) intestinal epithelial cells at day 5 after CK1α ablation. NES, normalized enrichment score; FDR, false discovery rate. (B) H E staining of small intestinal tissues from mice of the indicated genotypes. Bars, 100 μm. (C) H E staining of colonic tissues from mice of the indicated genotypes. Bars, 100 μm. (D) PAS staining of small intestinal tissues from mice of the indicated genotypes. (E) Quantitation of the number of PAS-positive goblet cells per crypt/villus axis in the small intestines of three mice (30 to 50 crypts/villi were analyzed for each mouse). Data are shown as averages ± SEM; asterisks above SKO indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above DKO indicate a significant difference between SKO and DKO mice. ***, P

    Article Snippet: Collectively, these data suggest that the ablation of CK1α leads to the accumulation of IFNAR1, induction of IFN expression, and activation of expression of IFN-stimulated genes in the intestinal epithelium.

    Techniques: Inhibition, Mouse Assay, Staining, Quantitation Assay

    Endogenous IFN restrict proliferation of intestinal epithelial cells and elicit their apoptosis. (A) Double-immunofluorescence analysis of IFNAR1 and Ki67 expression in intestinal tissues from mice of the indicated genotypes. Bar, 100 μm. (B) Quantitation of the number of IFNAR1-positive, Ki67-positive, or double-positive cells per crypt/villus axis in the small intestines of three mice (30 to 50 crypts/villi were analyzed for each mouse). Data are shown as averages ± SEM; asterisks above Csnk1a1 Δ gut (SKO) indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) indicate a significant difference between SKO and DKO mice. ***, P

    Journal: Molecular and Cellular Biology

    Article Title: Type I Interferons Control Proliferation and Function of the Intestinal Epithelium

    doi: 10.1128/MCB.00988-15

    Figure Lengend Snippet: Endogenous IFN restrict proliferation of intestinal epithelial cells and elicit their apoptosis. (A) Double-immunofluorescence analysis of IFNAR1 and Ki67 expression in intestinal tissues from mice of the indicated genotypes. Bar, 100 μm. (B) Quantitation of the number of IFNAR1-positive, Ki67-positive, or double-positive cells per crypt/villus axis in the small intestines of three mice (30 to 50 crypts/villi were analyzed for each mouse). Data are shown as averages ± SEM; asterisks above Csnk1a1 Δ gut (SKO) indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) indicate a significant difference between SKO and DKO mice. ***, P

    Article Snippet: Collectively, these data suggest that the ablation of CK1α leads to the accumulation of IFNAR1, induction of IFN expression, and activation of expression of IFN-stimulated genes in the intestinal epithelium.

    Techniques: Immunofluorescence, Expressing, Mouse Assay, Quantitation Assay

    Activation of IFN signaling in response to CK1α ablation. (A) Relative levels of Csnk1a1 and Ifnar1 mRNAs in intestinal tissues from mice of the indicated genotypes. Levels of mRNA in intestinal tissues from untreated Csnk1a1 lox/lox ; Ifnar1 +/+ mice were taken as 1.0. Data are shown as averages ± SEM; asterisks above Csnk1a1 Δ gut (SKO) indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) indicate a significant difference between SKO and DKO mice. *, P

    Journal: Molecular and Cellular Biology

    Article Title: Type I Interferons Control Proliferation and Function of the Intestinal Epithelium

    doi: 10.1128/MCB.00988-15

    Figure Lengend Snippet: Activation of IFN signaling in response to CK1α ablation. (A) Relative levels of Csnk1a1 and Ifnar1 mRNAs in intestinal tissues from mice of the indicated genotypes. Levels of mRNA in intestinal tissues from untreated Csnk1a1 lox/lox ; Ifnar1 +/+ mice were taken as 1.0. Data are shown as averages ± SEM; asterisks above Csnk1a1 Δ gut (SKO) indicate a significant difference between wild-type (WT) and SKO mice, and asterisks above Csnk1a1 Δ gut ; Ifnar1 −/− (DKO) indicate a significant difference between SKO and DKO mice. *, P

    Article Snippet: Collectively, these data suggest that the ablation of CK1α leads to the accumulation of IFNAR1, induction of IFN expression, and activation of expression of IFN-stimulated genes in the intestinal epithelium.

    Techniques: Activation Assay, Mouse Assay

    CK1α and IFN pathways regulate intestinal barrier function. (A) Kaplan-Meier survival analysis of mice of the indicated genotypes after induction of intestinal CK1α ablation. Csnk1a1 Δ gut ; Ifnar1 −/− mice received intraperitoneal injections of 1 ml saline every day starting on day 1 after intestinal CK1α ablation (DKO+Saline) or were administered antibiotics (Ab) in drinking water. ***, P

    Journal: Molecular and Cellular Biology

    Article Title: Type I Interferons Control Proliferation and Function of the Intestinal Epithelium

    doi: 10.1128/MCB.00988-15

    Figure Lengend Snippet: CK1α and IFN pathways regulate intestinal barrier function. (A) Kaplan-Meier survival analysis of mice of the indicated genotypes after induction of intestinal CK1α ablation. Csnk1a1 Δ gut ; Ifnar1 −/− mice received intraperitoneal injections of 1 ml saline every day starting on day 1 after intestinal CK1α ablation (DKO+Saline) or were administered antibiotics (Ab) in drinking water. ***, P

    Article Snippet: Collectively, these data suggest that the ablation of CK1α leads to the accumulation of IFNAR1, induction of IFN expression, and activation of expression of IFN-stimulated genes in the intestinal epithelium.

    Techniques: Mouse Assay

    Alterations in CK1α and IFNAR1 levels affect intestinal organoid growth and survival. (A) Representative bright-field images of wild-type (WT) and Ifnar1 −/− intestinal organoids treated with 10 μM the CK1α inhibitor D4476 at day 4. (B) Quantitation of live organoids in wild-type and Ifnar1 −/− cultures compared with their vehicle-treated counterparts at day 4 (at least 10 random fields were analyzed for each culture). Data are shown as averages ± SEM. *, P

    Journal: Molecular and Cellular Biology

    Article Title: Type I Interferons Control Proliferation and Function of the Intestinal Epithelium

    doi: 10.1128/MCB.00988-15

    Figure Lengend Snippet: Alterations in CK1α and IFNAR1 levels affect intestinal organoid growth and survival. (A) Representative bright-field images of wild-type (WT) and Ifnar1 −/− intestinal organoids treated with 10 μM the CK1α inhibitor D4476 at day 4. (B) Quantitation of live organoids in wild-type and Ifnar1 −/− cultures compared with their vehicle-treated counterparts at day 4 (at least 10 random fields were analyzed for each culture). Data are shown as averages ± SEM. *, P

    Article Snippet: Collectively, these data suggest that the ablation of CK1α leads to the accumulation of IFNAR1, induction of IFN expression, and activation of expression of IFN-stimulated genes in the intestinal epithelium.

    Techniques: Quantitation Assay