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8 bromo camp  (MedChemExpress)


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    MedChemExpress 8 bromo camp
    BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or <t>1</t> <t>mM</t> <t>8-bromo-cAMP</t> for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.
    8 Bromo Camp, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/8+bromo+camp/8-Bromo-cAMP/pmc13430265-84-20-23
    Average 95 stars, based on 39 article reviews
    8 bromo camp - by Bioz Stars, 2026-10
    95/100 stars

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    1) Product Images from "BK channel deficiency promotes lipolysis via an AKT-independent activation of the cAMP/PKA/HSL pathway"

    Article Title: BK channel deficiency promotes lipolysis via an AKT-independent activation of the cAMP/PKA/HSL pathway

    Journal: Journal of Lipid Research

    doi: 10.1016/j.jlr.2026.101094

    BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or 1 mM 8-bromo-cAMP for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.
    Figure Legend Snippet: BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or 1 mM 8-bromo-cAMP for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.

    Techniques Used: Western Blot, Phospho-proteomics, Fluorescence, Two Tailed Test, MANN-WHITNEY

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    BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or <t>1</t> <t>mM</t> <t>8-bromo-cAMP</t> for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.
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    BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or <t>1</t> <t>mM</t> <t>8-bromo-cAMP</t> for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.
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    BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or <t>1</t> <t>mM</t> <t>8-bromo-cAMP</t> for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.
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    BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or 1 mM 8-bromo-cAMP for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.

    Journal: Journal of Lipid Research

    Article Title: BK channel deficiency promotes lipolysis via an AKT-independent activation of the cAMP/PKA/HSL pathway

    doi: 10.1016/j.jlr.2026.101094

    Figure Lengend Snippet: BK channel deficiency enhances lipolysis via the cAMP/PKA/HSL signaling pathway. A and B: Representative western blots (A) and quantitative analysis (B) of PKA substrate phosphorylation levels in eWAT from the indicated mouse models (n = 5). C: Glycerol release from adipocytes measured under basal conditions or following stimulation with 1 μM CL-316243 for 1 h. Cells were preincubated with or without the PKA inhibitor H89 (10 μM) for 1 h prior to stimulation (n = 6). D and E: Representative western blots (D) and quantitative analysis (E) of the phosphorylation levels of key lipolytic regulatory proteins in adipocytes following the indicated treatments (n = 5). F: Glycerol release from mature adipocytes treated with 10 μM forskolin or 1 mM 8-bromo-cAMP for 1 h, measured using a glycerol assay kit (n = 4). G and H: Representative western blots (G) and quantitative analysis (H) of lipolysis-related protein phosphorylation levels in mature adipocytes treated as described in (F) (n = 4). I and J: The average (I) and Δfold change in fluo-4 fluorescence intensity (J) in mature adipocytes treated with 1 μM CL-316243 (n = 4). Data are presented as mean ± SEM. Statistical analysis was performed using an unpaired two-tailed Student's t test for (E, H), Mann–Whitney U test for (B and C, F) and the Kruskal–Wallis test with Dunn's multiple comparisons test for (J). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. ns, not significant.

    Article Snippet: Cells were stimulated with either 1 μM CL-316243 (Cat# C5976, Sigma-Aldrich), 10 μM Forskolin (Cat# HY-15371, MCE), or 1 mM 8-Bromo-cAMP (Cat# HY-12306A, MCE) for 1 h at 37°C in an incubator with 5% CO 2 .

    Techniques: Western Blot, Phospho-proteomics, Fluorescence, Two Tailed Test, MANN-WHITNEY