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h89 2hcl  (TargetMol)


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    TargetMol h89 2hcl
    Effects of E 2 -BSA (2 nM, 3 h) on PGR mRNA level in female chick pituitary cells in the presence of distinct pharmacological drugs, including U73 (PLC inhibitor, 3 μM), 2-APB (IP3R antagonist, 10 μM), AEB (pan-PKC inhibitor, 10 μM), GSK (MEK1/2 inhibitor, 10 μM), LY (ERK1/2 inhibitor, 10 μM), NIL (calcium channel blocker, 3 μM), JNK8 (JNK1/2/3 inhibitor, 2 μM), GW (p38 MAPK inhibitor, 10 μM), ZSTK (PI3K inhibitor, 10 μM), MK (AKT1/2/3 inhibitor, 2 μM), MDL (AC inhibitor, 10 μM) and <t>H89</t> (PKA inhibitor, 1 μM). The expression level of PGR was normalized by β-actin and expressed as the fold change compared with control group (without drug treatment). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s test, each value represents the mean ± SEM of four replicates (n = 4). Exact p-values are shown for significant comparisons, ‘ns’ indicates no statistical significance (p>0.05).
    H89 2hcl, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/h89 2hcl/product/TargetMol
    Average 94 stars, based on 15 article reviews
    h89 2hcl - by Bioz Stars, 2026-02
    94/100 stars

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    1) Product Images from "17β-estradiol mediates sex-biased progesterone receptor expression via estrogen receptor α in chicken pituitary"

    Article Title: 17β-estradiol mediates sex-biased progesterone receptor expression via estrogen receptor α in chicken pituitary

    Journal: Poultry Science

    doi: 10.1016/j.psj.2025.106210

    Effects of E 2 -BSA (2 nM, 3 h) on PGR mRNA level in female chick pituitary cells in the presence of distinct pharmacological drugs, including U73 (PLC inhibitor, 3 μM), 2-APB (IP3R antagonist, 10 μM), AEB (pan-PKC inhibitor, 10 μM), GSK (MEK1/2 inhibitor, 10 μM), LY (ERK1/2 inhibitor, 10 μM), NIL (calcium channel blocker, 3 μM), JNK8 (JNK1/2/3 inhibitor, 2 μM), GW (p38 MAPK inhibitor, 10 μM), ZSTK (PI3K inhibitor, 10 μM), MK (AKT1/2/3 inhibitor, 2 μM), MDL (AC inhibitor, 10 μM) and H89 (PKA inhibitor, 1 μM). The expression level of PGR was normalized by β-actin and expressed as the fold change compared with control group (without drug treatment). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s test, each value represents the mean ± SEM of four replicates (n = 4). Exact p-values are shown for significant comparisons, ‘ns’ indicates no statistical significance (p>0.05).
    Figure Legend Snippet: Effects of E 2 -BSA (2 nM, 3 h) on PGR mRNA level in female chick pituitary cells in the presence of distinct pharmacological drugs, including U73 (PLC inhibitor, 3 μM), 2-APB (IP3R antagonist, 10 μM), AEB (pan-PKC inhibitor, 10 μM), GSK (MEK1/2 inhibitor, 10 μM), LY (ERK1/2 inhibitor, 10 μM), NIL (calcium channel blocker, 3 μM), JNK8 (JNK1/2/3 inhibitor, 2 μM), GW (p38 MAPK inhibitor, 10 μM), ZSTK (PI3K inhibitor, 10 μM), MK (AKT1/2/3 inhibitor, 2 μM), MDL (AC inhibitor, 10 μM) and H89 (PKA inhibitor, 1 μM). The expression level of PGR was normalized by β-actin and expressed as the fold change compared with control group (without drug treatment). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s test, each value represents the mean ± SEM of four replicates (n = 4). Exact p-values are shown for significant comparisons, ‘ns’ indicates no statistical significance (p>0.05).

    Techniques Used: Expressing, Control



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    Effects of E 2 -BSA (2 nM, 3 h) on PGR mRNA level in female chick pituitary cells in the presence of distinct pharmacological drugs, including U73 (PLC inhibitor, 3 μM), 2-APB (IP3R antagonist, 10 μM), AEB (pan-PKC inhibitor, 10 μM), GSK (MEK1/2 inhibitor, 10 μM), LY (ERK1/2 inhibitor, 10 μM), NIL (calcium channel blocker, 3 μM), JNK8 (JNK1/2/3 inhibitor, 2 μM), GW (p38 MAPK inhibitor, 10 μM), ZSTK (PI3K inhibitor, 10 μM), MK (AKT1/2/3 inhibitor, 2 μM), MDL (AC inhibitor, 10 μM) and <t>H89</t> (PKA inhibitor, 1 μM). The expression level of PGR was normalized by β-actin and expressed as the fold change compared with control group (without drug treatment). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s test, each value represents the mean ± SEM of four replicates (n = 4). Exact p-values are shown for significant comparisons, ‘ns’ indicates no statistical significance (p>0.05).
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    Effects of E 2 -BSA (2 nM, 3 h) on PGR mRNA level in female chick pituitary cells in the presence of distinct pharmacological drugs, including U73 (PLC inhibitor, 3 μM), 2-APB (IP3R antagonist, 10 μM), AEB (pan-PKC inhibitor, 10 μM), GSK (MEK1/2 inhibitor, 10 μM), LY (ERK1/2 inhibitor, 10 μM), NIL (calcium channel blocker, 3 μM), JNK8 (JNK1/2/3 inhibitor, 2 μM), GW (p38 MAPK inhibitor, 10 μM), ZSTK (PI3K inhibitor, 10 μM), MK (AKT1/2/3 inhibitor, 2 μM), MDL (AC inhibitor, 10 μM) and H89 (PKA inhibitor, 1 μM). The expression level of PGR was normalized by β-actin and expressed as the fold change compared with control group (without drug treatment). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s test, each value represents the mean ± SEM of four replicates (n = 4). Exact p-values are shown for significant comparisons, ‘ns’ indicates no statistical significance (p>0.05).

    Journal: Poultry Science

    Article Title: 17β-estradiol mediates sex-biased progesterone receptor expression via estrogen receptor α in chicken pituitary

    doi: 10.1016/j.psj.2025.106210

    Figure Lengend Snippet: Effects of E 2 -BSA (2 nM, 3 h) on PGR mRNA level in female chick pituitary cells in the presence of distinct pharmacological drugs, including U73 (PLC inhibitor, 3 μM), 2-APB (IP3R antagonist, 10 μM), AEB (pan-PKC inhibitor, 10 μM), GSK (MEK1/2 inhibitor, 10 μM), LY (ERK1/2 inhibitor, 10 μM), NIL (calcium channel blocker, 3 μM), JNK8 (JNK1/2/3 inhibitor, 2 μM), GW (p38 MAPK inhibitor, 10 μM), ZSTK (PI3K inhibitor, 10 μM), MK (AKT1/2/3 inhibitor, 2 μM), MDL (AC inhibitor, 10 μM) and H89 (PKA inhibitor, 1 μM). The expression level of PGR was normalized by β-actin and expressed as the fold change compared with control group (without drug treatment). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s test, each value represents the mean ± SEM of four replicates (n = 4). Exact p-values are shown for significant comparisons, ‘ns’ indicates no statistical significance (p>0.05).

    Article Snippet: Pharmacological drugs targeting the components of signaling pathways, including ZSTK474 (ZSTK, Cat#S1072), MK-2206 dihydrochloride (MK, Cat#S1078), GSK1120212 (GSK, Cat#S2673), LY3214996 (LY, Cat#S8534), H89 2HCl (H89, Cat#S1582), nilvadipine (NIL, Cat#2721), U-73122 (U73, Cat#S8011), AEB071 (AEB, Cat#S2791), losmapimod (GW, Cat#S7215), MDL-12330A (MDL, Cat#E6418), and 2-aminoethoxydiphenyl borate (2-APB, Cat#S6657), were obtained from Selleck Chemicals (Houston, US), while JNK-IN-8 (JNK8, Cat#HY-13319) was supplied by TargetMol.

    Techniques: Expressing, Control

    A U87 cells overexpressing SFB-tagged GLYCTK2 stimulated with or without glucose deprivation in the presence or absence of 20 μM SB202190 (p38 inhibitor), 10 μM Compound C (AMPK inhibitor), 20 μM U0126-EtOH (ERK inhibitor), 20 μM H89 (PKA inhibitor), 2.5 μM TSC7010 (Aurora A Inhibitor I), 25 μM SP600125 (JNK inhibitor), 20 μM KU-55933 (ATM inhibitor) or 1 μM PF-04691502 (PI3K/ mTOR inhibitor) for 3 h were harvested for immunoblot analysis with indicated antibodies, Tubulin as a loading control. B U87 cells stimulated with or without glucose deprivation in the presence or absence of 20 μM U0126-EtOH (ERK inhibitor), 25 μM SP600125 (JNK inhibitor), 20 μM SB202190 (p38 inhibitor) or 10 μM Compound C (AMPK inhibitor) for 3 h were harvested for immunoblot analysis with indicated antibodies. Tubulin served as a loading control. C U87 cells overexpressing SFB-tagged GLYCTK2 stimulated with or without glucose deprivation in the presence or absence of 20 μM U0126-EtOH for 3 h were harvested and immunoprecipitated with streptavidin (Strep) agarose for immunoblot analysis with indicated antibodies.

    Journal: Cell Death Discovery

    Article Title: ERK1-mediated GLYCTK2 phosphorylation promotes fructolysis to sustain glioblastoma survival under glucose deprivation

    doi: 10.1038/s41420-025-02544-3

    Figure Lengend Snippet: A U87 cells overexpressing SFB-tagged GLYCTK2 stimulated with or without glucose deprivation in the presence or absence of 20 μM SB202190 (p38 inhibitor), 10 μM Compound C (AMPK inhibitor), 20 μM U0126-EtOH (ERK inhibitor), 20 μM H89 (PKA inhibitor), 2.5 μM TSC7010 (Aurora A Inhibitor I), 25 μM SP600125 (JNK inhibitor), 20 μM KU-55933 (ATM inhibitor) or 1 μM PF-04691502 (PI3K/ mTOR inhibitor) for 3 h were harvested for immunoblot analysis with indicated antibodies, Tubulin as a loading control. B U87 cells stimulated with or without glucose deprivation in the presence or absence of 20 μM U0126-EtOH (ERK inhibitor), 25 μM SP600125 (JNK inhibitor), 20 μM SB202190 (p38 inhibitor) or 10 μM Compound C (AMPK inhibitor) for 3 h were harvested for immunoblot analysis with indicated antibodies. Tubulin served as a loading control. C U87 cells overexpressing SFB-tagged GLYCTK2 stimulated with or without glucose deprivation in the presence or absence of 20 μM U0126-EtOH for 3 h were harvested and immunoprecipitated with streptavidin (Strep) agarose for immunoblot analysis with indicated antibodies.

    Article Snippet: MG132 (S2619), Cycloheximide (S7418), SB202190 (S1077), Compound C (S7840), U0126-EtOH (S1102), H89 (S1582), TCS7010 (S1451), SP600125 (S1460), KU-55933 (S1092) and PF-04691502 (S2743) were purchased from Selleck (Shanghai, China).

    Techniques: Western Blot, Control, Immunoprecipitation