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hep3b p53null  (DSMZ)


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    DSMZ hep3b p53null
    Figure 1. Effect of panobinostat (LBH589) on gene expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and fms-like tyrosine kinase-1 (FLT-1) in vitro in HepG2 and <t>Hep3B</t> cells. (A) Quantitative real-time RT-PCR analysis after 24, 48 and 72 h treatment with 0.01 µM panobinostat (A) and 0.1 µM panobinostat (B) in HepG2 cells, with 0.01 µM panobinostat (C) and 0.1 µM panobinostat (D) in Hep3B cells. Gene expression was normalized to β-actin and expressed relative to untreated controls (set at 1.0). Asterisks indicate statistically significant differences in gene expression vs. the untreated controls (p<0.01). The symbol (x) indicates that very few viable cells remained after 72 h of treatment in these cells.
    Hep3b P53null, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 73 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hep3b+p53null/HEP-3B/pm26202945-36-8-21
    Average 94 stars, based on 73 article reviews
    hep3b p53null - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression."

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.

    Journal: International journal of oncology

    doi: 10.3892/ijo.2015.3087

    Figure 1. Effect of panobinostat (LBH589) on gene expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and fms-like tyrosine kinase-1 (FLT-1) in vitro in HepG2 and Hep3B cells. (A) Quantitative real-time RT-PCR analysis after 24, 48 and 72 h treatment with 0.01 µM panobinostat (A) and 0.1 µM panobinostat (B) in HepG2 cells, with 0.01 µM panobinostat (C) and 0.1 µM panobinostat (D) in Hep3B cells. Gene expression was normalized to β-actin and expressed relative to untreated controls (set at 1.0). Asterisks indicate statistically significant differences in gene expression vs. the untreated controls (p<0.01). The symbol (x) indicates that very few viable cells remained after 72 h of treatment in these cells.
    Figure Legend Snippet: Figure 1. Effect of panobinostat (LBH589) on gene expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and fms-like tyrosine kinase-1 (FLT-1) in vitro in HepG2 and Hep3B cells. (A) Quantitative real-time RT-PCR analysis after 24, 48 and 72 h treatment with 0.01 µM panobinostat (A) and 0.1 µM panobinostat (B) in HepG2 cells, with 0.01 µM panobinostat (C) and 0.1 µM panobinostat (D) in Hep3B cells. Gene expression was normalized to β-actin and expressed relative to untreated controls (set at 1.0). Asterisks indicate statistically significant differences in gene expression vs. the untreated controls (p<0.01). The symbol (x) indicates that very few viable cells remained after 72 h of treatment in these cells.

    Techniques Used: Gene Expression, In Vitro, Quantitative RT-PCR

    Figure 2. Western blot analysis of expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (FLT-1), kinase insert domain containing receptor (KDR), MAPK, p-MAPK in vitro and densitometric quantification. HepG2 and Hep3B cells were incubated with 0.1 and 0.01 µM panobinostat for 12, 24 and 48 h. Western blot results show representative examples for expression of CTGF, VEGF, FLT-1, KDR, MAPK and p-MAPK as well as β-actin, which served as loading control (A). Protein expression analyzed using western blot analysis was quantified by densitometry (B). Shown are expression values for CTGF, MAPK, p-MAPK, KDR and VEGF after treatment of HepG2 and Hep3B cell lines with 0.01 and 0.1 µM of panobinostat for 12-48 h.
    Figure Legend Snippet: Figure 2. Western blot analysis of expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (FLT-1), kinase insert domain containing receptor (KDR), MAPK, p-MAPK in vitro and densitometric quantification. HepG2 and Hep3B cells were incubated with 0.1 and 0.01 µM panobinostat for 12, 24 and 48 h. Western blot results show representative examples for expression of CTGF, VEGF, FLT-1, KDR, MAPK and p-MAPK as well as β-actin, which served as loading control (A). Protein expression analyzed using western blot analysis was quantified by densitometry (B). Shown are expression values for CTGF, MAPK, p-MAPK, KDR and VEGF after treatment of HepG2 and Hep3B cell lines with 0.01 and 0.1 µM of panobinostat for 12-48 h.

    Techniques Used: Western Blot, Expressing, In Vitro, Incubation, Control

    Related Articles

    Gene Expression:

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.
    Article Snippet: Cell culture.Cell culture.. The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).. Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).

    In Vitro:

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.
    Article Snippet: Cell culture.Cell culture.. The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).. Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).

    Quantitative RT-PCR:

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.
    Article Snippet: Cell culture.Cell culture.. The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).. Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).

    Western Blot:

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.
    Article Snippet: Cell culture.Cell culture.. The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).. Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).

    Expressing:

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.
    Article Snippet: Cell culture.Cell culture.. The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).. Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).

    Incubation:

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.
    Article Snippet: Cell culture.Cell culture.. The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).. Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).

    Control:

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.
    Article Snippet: Cell culture.Cell culture.. The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).. Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).Panobinostat (LBH589) was provided by novartis Pharma AG (basel, Switzerland) and was prepared as previously described (41,45).



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    hep3b p53null  (DSMZ)
    94
    DSMZ hep3b p53null
    Figure 1. Effect of panobinostat (LBH589) on gene expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and fms-like tyrosine kinase-1 (FLT-1) in vitro in HepG2 and <t>Hep3B</t> cells. (A) Quantitative real-time RT-PCR analysis after 24, 48 and 72 h treatment with 0.01 µM panobinostat (A) and 0.1 µM panobinostat (B) in HepG2 cells, with 0.01 µM panobinostat (C) and 0.1 µM panobinostat (D) in Hep3B cells. Gene expression was normalized to β-actin and expressed relative to untreated controls (set at 1.0). Asterisks indicate statistically significant differences in gene expression vs. the untreated controls (p<0.01). The symbol (x) indicates that very few viable cells remained after 72 h of treatment in these cells.
    Hep3b P53null, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hep3b+p53null/HEP-3B/pm26202945-36-8-21
    Average 94 stars, based on 1 article reviews
    hep3b p53null - by Bioz Stars, 2026-09
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    Figure 1. Effect of panobinostat (LBH589) on gene expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and fms-like tyrosine kinase-1 (FLT-1) in vitro in HepG2 and Hep3B cells. (A) Quantitative real-time RT-PCR analysis after 24, 48 and 72 h treatment with 0.01 µM panobinostat (A) and 0.1 µM panobinostat (B) in HepG2 cells, with 0.01 µM panobinostat (C) and 0.1 µM panobinostat (D) in Hep3B cells. Gene expression was normalized to β-actin and expressed relative to untreated controls (set at 1.0). Asterisks indicate statistically significant differences in gene expression vs. the untreated controls (p<0.01). The symbol (x) indicates that very few viable cells remained after 72 h of treatment in these cells.

    Journal: International journal of oncology

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.

    doi: 10.3892/ijo.2015.3087

    Figure Lengend Snippet: Figure 1. Effect of panobinostat (LBH589) on gene expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) and fms-like tyrosine kinase-1 (FLT-1) in vitro in HepG2 and Hep3B cells. (A) Quantitative real-time RT-PCR analysis after 24, 48 and 72 h treatment with 0.01 µM panobinostat (A) and 0.1 µM panobinostat (B) in HepG2 cells, with 0.01 µM panobinostat (C) and 0.1 µM panobinostat (D) in Hep3B cells. Gene expression was normalized to β-actin and expressed relative to untreated controls (set at 1.0). Asterisks indicate statistically significant differences in gene expression vs. the untreated controls (p<0.01). The symbol (x) indicates that very few viable cells remained after 72 h of treatment in these cells.

    Article Snippet: The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).

    Techniques: Gene Expression, In Vitro, Quantitative RT-PCR

    Figure 2. Western blot analysis of expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (FLT-1), kinase insert domain containing receptor (KDR), MAPK, p-MAPK in vitro and densitometric quantification. HepG2 and Hep3B cells were incubated with 0.1 and 0.01 µM panobinostat for 12, 24 and 48 h. Western blot results show representative examples for expression of CTGF, VEGF, FLT-1, KDR, MAPK and p-MAPK as well as β-actin, which served as loading control (A). Protein expression analyzed using western blot analysis was quantified by densitometry (B). Shown are expression values for CTGF, MAPK, p-MAPK, KDR and VEGF after treatment of HepG2 and Hep3B cell lines with 0.01 and 0.1 µM of panobinostat for 12-48 h.

    Journal: International journal of oncology

    Article Title: The pan-deacetylase inhibitor panobinostat affects angiogenesis in hepatocellular carcinoma models via modulation of CTGF expression.

    doi: 10.3892/ijo.2015.3087

    Figure Lengend Snippet: Figure 2. Western blot analysis of expression of connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (FLT-1), kinase insert domain containing receptor (KDR), MAPK, p-MAPK in vitro and densitometric quantification. HepG2 and Hep3B cells were incubated with 0.1 and 0.01 µM panobinostat for 12, 24 and 48 h. Western blot results show representative examples for expression of CTGF, VEGF, FLT-1, KDR, MAPK and p-MAPK as well as β-actin, which served as loading control (A). Protein expression analyzed using western blot analysis was quantified by densitometry (B). Shown are expression values for CTGF, MAPK, p-MAPK, KDR and VEGF after treatment of HepG2 and Hep3B cell lines with 0.01 and 0.1 µM of panobinostat for 12-48 h.

    Article Snippet: The human hepatoma cell lines HepG2 (p53wt) and Hep3B (p53null) were obtained from the German collection of microorganisms and cell cultures (DSMZ, braunschweig, Germany) and maintained under standard conditions as described previously (41).

    Techniques: Western Blot, Expressing, In Vitro, Incubation, Control