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psb12379  (Tocris)


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    Structured Review

    Tocris psb12379
    Psb12379, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/psb12379/PSB+12379/pm41887305-94-33-36
    Average 94 stars, based on 16 article reviews
    psb12379 - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Over Expression:

    Article Title: Characterization of ecto-5'-nucleotidase (CD73) involved in inflammatory regulation in Japanese flounder (Paralichthys olivaceus).
    Article Snippet: 31 Ecto-5’-nucleotidase (CD73) is a plasma membrane glycoprotein that regulates 32 inflammation by generating the anti-inflammatory signaling molecule adenosine in the 33 extracellular milieu in mammals.. However, the expression and immunological 34 functions of CD73 in lower vertebrates remain unclear.. In this study, we identified and 35 characterized a CD73 homolog, designated PoCD73, in Japanese flounder 36 (Paralichthys olivaceus) by RACE-PCR and genome walking.

    Inhibition:

    Article Title: Characterization of ecto-5'-nucleotidase (CD73) involved in inflammatory regulation in Japanese flounder (Paralichthys olivaceus).
    Article Snippet: 31 Ecto-5’-nucleotidase (CD73) is a plasma membrane glycoprotein that regulates 32 inflammation by generating the anti-inflammatory signaling molecule adenosine in the 33 extracellular milieu in mammals.. However, the expression and immunological 34 functions of CD73 in lower vertebrates remain unclear.. In this study, we identified and 35 characterized a CD73 homolog, designated PoCD73, in Japanese flounder 36 (Paralichthys olivaceus) by RACE-PCR and genome walking.

    Article Title: Assessment of adenosinergic activity of small extracellular vesicles in plasma of cancer patients and healthy donors
    Article Snippet: The isolated and counted sEV (1×109) were incubated (37°C) in phosphate-buffered saline (PBS; 100 μL) with either N6-etheno-ATP (eATP), N6-etheno-ADP (eADP) or N6etheno-AMP (eAMP) and with or without ecto-nucleotidase inhibitors. ePurines, including eATP, eADP, eAMP and N6-etheno-adenosine (eADO), were obtained from BioLog Life Science Institute (Hayward, CA). .. We recently evaluated the selectivity of several commercially available ecto-nucleotidase inhibitors and found that L-p-bromotetramisole (L-p-BT; Santa Cruz Biotechnology, Dallas, TX) and PSB12379 (Tocris Biosciences, Minneapolis, MN) were highly selective and effective for inhibiting tissue nonspecific alkaline phosphatase (TNAP) and ecto-5’nucleotidase (CD73), respectively; whereas, ARL67156 (Millipore Sigma, Burlington, MA) was highly effective and relatively selective for CD39 (with low (partial) off-target inhibition of CD203a). .. POM-1 (Tocris Biosciences) was a highly effective “broad-spectrum” ecto-nucleotidase inhibitor that substantially blocked the enzymatic activity of CD39 (ENTPD1), ENTPD2, ENTPD3, CD203a and TNAP [11]. sEV, with and without these inhibitors, were incubated with eATP or eADP for 3 h or with eAMP for 20 min. “Background” samples with substrate, but without sEV, were incubated and analyzed, and background levels of product ePurines were subtracted from product ePurine levels in sEV samples to correct for any non-enzymatic production of product or trace contamination of substrates with product.

    Expressing:

    Article Title: Characterization of ecto-5'-nucleotidase (CD73) involved in inflammatory regulation in Japanese flounder (Paralichthys olivaceus).
    Article Snippet: 31 Ecto-5’-nucleotidase (CD73) is a plasma membrane glycoprotein that regulates 32 inflammation by generating the anti-inflammatory signaling molecule adenosine in the 33 extracellular milieu in mammals.. However, the expression and immunological 34 functions of CD73 in lower vertebrates remain unclear.. In this study, we identified and 35 characterized a CD73 homolog, designated PoCD73, in Japanese flounder 36 (Paralichthys olivaceus) by RACE-PCR and genome walking.



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    EAC cells are sensitive to HIF1α and NT5E inhibition, with enhanced effects under hypoxic conditions. ( A , B ) HIF1α and NT5E expression measured by qPCR ( A ) and cell viability measurements expressed as % growth (cell titer relative to day 0) ( B ) upon NT5E knockdown; qPCR data represent mean ± SEM of n = 4; statistical significance determined by unpaired two-tailed t -test. ( C ) Cell viability in HIF1α knockdown alone and in combination with NT5E knockdown under normoxic or hypoxic conditions at 72 h; data are mean ± SEM ( n = 3); comparisons analyzed by two-way ANOVA with Dunnet’s correction. ( D ) % cell growth (cell titer relative to day 0) comparing acriflavine treatment in normoxic and hypoxic conditions. ( E ) % cell growth for combined treatment with acriflavine and <t>PSB12379</t> under normoxic and hypoxic conditions, showing synergistic viability reduction. ( F ) NT5E CRISPR dependency scores from DepMap across cancer lineages, indicating NT5E is broadly non-essential. ns = not significant; * p -value < 0.05; ** p < 0.01; **** p < 0.0001.
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    EAC cells are sensitive to HIF1α and NT5E inhibition, with enhanced effects under hypoxic conditions. ( A , B ) HIF1α and NT5E expression measured by qPCR ( A ) and cell viability measurements expressed as % growth (cell titer relative to day 0) ( B ) upon NT5E knockdown; qPCR data represent mean ± SEM of n = 4; statistical significance determined by unpaired two-tailed t -test. ( C ) Cell viability in HIF1α knockdown alone and in combination with NT5E knockdown under normoxic or hypoxic conditions at 72 h; data are mean ± SEM ( n = 3); comparisons analyzed by two-way ANOVA with Dunnet’s correction. ( D ) % cell growth (cell titer relative to day 0) comparing acriflavine treatment in normoxic and hypoxic conditions. ( E ) % cell growth for combined treatment with acriflavine and <t>PSB12379</t> under normoxic and hypoxic conditions, showing synergistic viability reduction. ( F ) NT5E CRISPR dependency scores from DepMap across cancer lineages, indicating NT5E is broadly non-essential. ns = not significant; * p -value < 0.05; ** p < 0.01; **** p < 0.0001.
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    Image Search Results


    EAC cells are sensitive to HIF1α and NT5E inhibition, with enhanced effects under hypoxic conditions. ( A , B ) HIF1α and NT5E expression measured by qPCR ( A ) and cell viability measurements expressed as % growth (cell titer relative to day 0) ( B ) upon NT5E knockdown; qPCR data represent mean ± SEM of n = 4; statistical significance determined by unpaired two-tailed t -test. ( C ) Cell viability in HIF1α knockdown alone and in combination with NT5E knockdown under normoxic or hypoxic conditions at 72 h; data are mean ± SEM ( n = 3); comparisons analyzed by two-way ANOVA with Dunnet’s correction. ( D ) % cell growth (cell titer relative to day 0) comparing acriflavine treatment in normoxic and hypoxic conditions. ( E ) % cell growth for combined treatment with acriflavine and PSB12379 under normoxic and hypoxic conditions, showing synergistic viability reduction. ( F ) NT5E CRISPR dependency scores from DepMap across cancer lineages, indicating NT5E is broadly non-essential. ns = not significant; * p -value < 0.05; ** p < 0.01; **** p < 0.0001.

    Journal: Cancers

    Article Title: Synergistic Disruption of Survival and Metastatic Potential in Esophageal Adenocarcinoma Cells Through Combined Inhibition of HIF1α and CD73

    doi: 10.3390/cancers17244016

    Figure Lengend Snippet: EAC cells are sensitive to HIF1α and NT5E inhibition, with enhanced effects under hypoxic conditions. ( A , B ) HIF1α and NT5E expression measured by qPCR ( A ) and cell viability measurements expressed as % growth (cell titer relative to day 0) ( B ) upon NT5E knockdown; qPCR data represent mean ± SEM of n = 4; statistical significance determined by unpaired two-tailed t -test. ( C ) Cell viability in HIF1α knockdown alone and in combination with NT5E knockdown under normoxic or hypoxic conditions at 72 h; data are mean ± SEM ( n = 3); comparisons analyzed by two-way ANOVA with Dunnet’s correction. ( D ) % cell growth (cell titer relative to day 0) comparing acriflavine treatment in normoxic and hypoxic conditions. ( E ) % cell growth for combined treatment with acriflavine and PSB12379 under normoxic and hypoxic conditions, showing synergistic viability reduction. ( F ) NT5E CRISPR dependency scores from DepMap across cancer lineages, indicating NT5E is broadly non-essential. ns = not significant; * p -value < 0.05; ** p < 0.01; **** p < 0.0001.

    Article Snippet: Cells were treated with acriflavine (Sigma-Aldrich, St. Louis, MO, USA) as a HIF1α inhibitor and PSB12379 (MedChemExpress, Monmouth Junction, NJ, USA) as a CD73/NT5E inhibitor at the indicated concentrations under normoxic or hypoxic conditions for 24–72 h prior to viability, migration, or metabolite assays.

    Techniques: Inhibition, Expressing, Knockdown, Two Tailed Test, CRISPR

    HIF1α and NT5E inhibition alter purinergic metabolite levels in esophageal adenocarcinoma cells. ( A ) Schematic illustrating hypoxia-induced NT5E expression and the enzymatic conversion of AMP to adenosine. ( B ) Intracellular and extracellular adenosine levels in FLO-1 cells measured by LC-MS, cultured under normoxia or hypoxia. Data represent mean ± SD ( n = 3 biological replicates); significance determined by unpaired two-tailed t -test. ( C ) Intracellular and extracellular AMP levels under the same conditions. Data represent mean ± SD ( n = 3); significance determined by unpaired two-tailed t -test. ( D ) Dose-dependent changes in intracellular adenosine following treatment with PSB12379 , acriflavine, or their combination under hypoxia. Data represent mean ± SD ( n = 3); analyzed by two-way ANOVA with Tukey’s multiple comparison test. ( E ) Adenosine levels in conditioned media from the same experiment, showing dose-dependent accumulation at low and intermediate PSB12379 concentrations, followed by reduction at the highest dose. Data represent mean ± SD ( n = 3); analyzed by two-way ANOVA with Tukey’s post hoc test. ( F ) Intracellular AMP levels under the same treatment conditions; PSB12379 -induced AMP accumulation further enhanced by acriflavine co-treatment. Data represent mean ± SD ( n = 3); analyzed by two-way ANOVA with Tukey’s multiple comparison test. ns = not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Journal: Cancers

    Article Title: Synergistic Disruption of Survival and Metastatic Potential in Esophageal Adenocarcinoma Cells Through Combined Inhibition of HIF1α and CD73

    doi: 10.3390/cancers17244016

    Figure Lengend Snippet: HIF1α and NT5E inhibition alter purinergic metabolite levels in esophageal adenocarcinoma cells. ( A ) Schematic illustrating hypoxia-induced NT5E expression and the enzymatic conversion of AMP to adenosine. ( B ) Intracellular and extracellular adenosine levels in FLO-1 cells measured by LC-MS, cultured under normoxia or hypoxia. Data represent mean ± SD ( n = 3 biological replicates); significance determined by unpaired two-tailed t -test. ( C ) Intracellular and extracellular AMP levels under the same conditions. Data represent mean ± SD ( n = 3); significance determined by unpaired two-tailed t -test. ( D ) Dose-dependent changes in intracellular adenosine following treatment with PSB12379 , acriflavine, or their combination under hypoxia. Data represent mean ± SD ( n = 3); analyzed by two-way ANOVA with Tukey’s multiple comparison test. ( E ) Adenosine levels in conditioned media from the same experiment, showing dose-dependent accumulation at low and intermediate PSB12379 concentrations, followed by reduction at the highest dose. Data represent mean ± SD ( n = 3); analyzed by two-way ANOVA with Tukey’s post hoc test. ( F ) Intracellular AMP levels under the same treatment conditions; PSB12379 -induced AMP accumulation further enhanced by acriflavine co-treatment. Data represent mean ± SD ( n = 3); analyzed by two-way ANOVA with Tukey’s multiple comparison test. ns = not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Article Snippet: Cells were treated with acriflavine (Sigma-Aldrich, St. Louis, MO, USA) as a HIF1α inhibitor and PSB12379 (MedChemExpress, Monmouth Junction, NJ, USA) as a CD73/NT5E inhibitor at the indicated concentrations under normoxic or hypoxic conditions for 24–72 h prior to viability, migration, or metabolite assays.

    Techniques: Inhibition, Expressing, Liquid Chromatography with Mass Spectroscopy, Cell Culture, Two Tailed Test, Comparison