cyclin d1 cell signaling technology 2978s wb Search Results


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Cell Signaling Technology Inc rabbit cyclin d1
A. β-catenin mRNA expression was not significantly altered in HCT116 and HT29 cells with HDGF knockdown by real-time PCR analysis, respectively; B. HDGF knockdown dramatically inhibited β-catenin and c-Myc, <t>cyclin</t> <t>D1</t> and MMP9 and phos-GSK3β (Ser9) expression in HCT116 cells; C. - D. Nuclear and cytoplasmic β-catenin, c-Myc, cyclin D1, MMP9, and phos-GSK-3β (Ser9) expression were suppressed in HCT116 C. and HT29 D. cells with HDGF knock-down; E. rHDGF enhanced nuclear and cytoplasmic β-catenin, c-Myc, cyclin D1, MMP9, and phos-GSK-3β(Ser9) protein expression in LOVO cells; F. rHDGF reversed the nuclear and cytoplasmic protein expression suppression of β-catenin c-Myc, cyclin D1, MMP9, and phos-GSK-3β (Ser9) in HCT116 upon HDGF knock-down by Western blot analysis. GAPDH was considered as loading control. Lamin B1 was considered as nuclear loading control.
Rabbit Cyclin D1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A. β-catenin mRNA expression was not significantly altered in HCT116 and HT29 cells with HDGF knockdown by real-time PCR analysis, respectively; B. HDGF knockdown dramatically inhibited β-catenin and c-Myc, cyclin D1 and MMP9 and phos-GSK3β (Ser9) expression in HCT116 cells; C. - D. Nuclear and cytoplasmic β-catenin, c-Myc, cyclin D1, MMP9, and phos-GSK-3β (Ser9) expression were suppressed in HCT116 C. and HT29 D. cells with HDGF knock-down; E. rHDGF enhanced nuclear and cytoplasmic β-catenin, c-Myc, cyclin D1, MMP9, and phos-GSK-3β(Ser9) protein expression in LOVO cells; F. rHDGF reversed the nuclear and cytoplasmic protein expression suppression of β-catenin c-Myc, cyclin D1, MMP9, and phos-GSK-3β (Ser9) in HCT116 upon HDGF knock-down by Western blot analysis. GAPDH was considered as loading control. Lamin B1 was considered as nuclear loading control.

Journal: Oncotarget

Article Title: Positive feedback loop of hepatoma-derived growth factor and β-catenin promotes carcinogenesis of colorectal cancer

doi:

Figure Lengend Snippet: A. β-catenin mRNA expression was not significantly altered in HCT116 and HT29 cells with HDGF knockdown by real-time PCR analysis, respectively; B. HDGF knockdown dramatically inhibited β-catenin and c-Myc, cyclin D1 and MMP9 and phos-GSK3β (Ser9) expression in HCT116 cells; C. - D. Nuclear and cytoplasmic β-catenin, c-Myc, cyclin D1, MMP9, and phos-GSK-3β (Ser9) expression were suppressed in HCT116 C. and HT29 D. cells with HDGF knock-down; E. rHDGF enhanced nuclear and cytoplasmic β-catenin, c-Myc, cyclin D1, MMP9, and phos-GSK-3β(Ser9) protein expression in LOVO cells; F. rHDGF reversed the nuclear and cytoplasmic protein expression suppression of β-catenin c-Myc, cyclin D1, MMP9, and phos-GSK-3β (Ser9) in HCT116 upon HDGF knock-down by Western blot analysis. GAPDH was considered as loading control. Lamin B1 was considered as nuclear loading control.

Article Snippet: The membranes were incubated with primary antibodies including rabbit HDGF (Abcam, dilution 1:1000), rabbit β-catenin, rabbit cyclin D1, rabbit c-Myc, rabbit phosphorylated- glycogen synthase kinase 3β (phos-GSK-3β) (Ser9), and rabbit MMP9 (Cell Signaling Technology, Danvers, MA, dilution 1:1000) at 4°C overnight.

Techniques: Expressing, Knockdown, Real-time Polymerase Chain Reaction, Western Blot, Control

A. - B. β-catenin knockdown significantly suppressed HDGF mRNA expression in HCT116 A. and HT29 B. cells by real-time PCR analysis, respectively; C. - E. β-catenin knockdown inhibited HDGF protein expression in HCT116 cells C. and mainly inhibited nuclear HDGF, β-catenin, c-Myc, cyclin D1, MMP9 and phos-GSK-3β (Ser9) protein expression in HCT116 D. and HT29 E. cells; F. Recombinant Wnt3a and DKK1 increased and decreased HDGF and β-catenin expression in HCT116 cells, respectively; G. - I. Recombinant Wnt3a and DKK1 increased and decreased nuclear and cytoplasmic HDGF, β-catenin, c-Myc, cyclin D1, MMP9 and phos-GSK-3β (Ser9) protein expression in HCT116 G. , I. and LOVO H. cells by Western blot analysis, respectively.

Journal: Oncotarget

Article Title: Positive feedback loop of hepatoma-derived growth factor and β-catenin promotes carcinogenesis of colorectal cancer

doi:

Figure Lengend Snippet: A. - B. β-catenin knockdown significantly suppressed HDGF mRNA expression in HCT116 A. and HT29 B. cells by real-time PCR analysis, respectively; C. - E. β-catenin knockdown inhibited HDGF protein expression in HCT116 cells C. and mainly inhibited nuclear HDGF, β-catenin, c-Myc, cyclin D1, MMP9 and phos-GSK-3β (Ser9) protein expression in HCT116 D. and HT29 E. cells; F. Recombinant Wnt3a and DKK1 increased and decreased HDGF and β-catenin expression in HCT116 cells, respectively; G. - I. Recombinant Wnt3a and DKK1 increased and decreased nuclear and cytoplasmic HDGF, β-catenin, c-Myc, cyclin D1, MMP9 and phos-GSK-3β (Ser9) protein expression in HCT116 G. , I. and LOVO H. cells by Western blot analysis, respectively.

Article Snippet: The membranes were incubated with primary antibodies including rabbit HDGF (Abcam, dilution 1:1000), rabbit β-catenin, rabbit cyclin D1, rabbit c-Myc, rabbit phosphorylated- glycogen synthase kinase 3β (phos-GSK-3β) (Ser9), and rabbit MMP9 (Cell Signaling Technology, Danvers, MA, dilution 1:1000) at 4°C overnight.

Techniques: Knockdown, Expressing, Real-time Polymerase Chain Reaction, Recombinant, Western Blot