forskolin  (Alomone Labs)


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    Structured Review

    Alomone Labs forskolin
    Neurite outgrowth is regulated by cAMP signaling. A. Plated neurospheres were treated with 10 μM <t>forskolin</t> for 24 h. The number of neurites crossing a circular mask around the neurosphere was used for quantification. B. Micrographs of control and 10 μM forskolin-treated neurospheres immunostained for beta III tubulin (green). Nuclei counterstained with DAPI (blue). C. Number of neurites crossing the circle (**p
    Forskolin, supplied by Alomone Labs, 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/result/forskolin/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    forskolin - by Bioz Stars, 2022-01
    94/100 stars

    Images

    1) Product Images from "Quantitative profiling of axonal guidance proteins during the differentiation of human neurospheres"

    Article Title: Quantitative profiling of axonal guidance proteins during the differentiation of human neurospheres

    Journal: bioRxiv

    doi: 10.1101/2021.02.21.432144

    Neurite outgrowth is regulated by cAMP signaling. A. Plated neurospheres were treated with 10 μM forskolin for 24 h. The number of neurites crossing a circular mask around the neurosphere was used for quantification. B. Micrographs of control and 10 μM forskolin-treated neurospheres immunostained for beta III tubulin (green). Nuclei counterstained with DAPI (blue). C. Number of neurites crossing the circle (**p
    Figure Legend Snippet: Neurite outgrowth is regulated by cAMP signaling. A. Plated neurospheres were treated with 10 μM forskolin for 24 h. The number of neurites crossing a circular mask around the neurosphere was used for quantification. B. Micrographs of control and 10 μM forskolin-treated neurospheres immunostained for beta III tubulin (green). Nuclei counterstained with DAPI (blue). C. Number of neurites crossing the circle (**p

    Techniques Used:

    2) Product Images from "Functional and Molecular Evidence for Kv7 Channel Subtypes in Human Detrusor from Patients with and without Bladder Outflow Obstruction"

    Article Title: Functional and Molecular Evidence for Kv7 Channel Subtypes in Human Detrusor from Patients with and without Bladder Outflow Obstruction

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0117350

    At low depolarisation K v 7 channel inhibition reduces the response to forskolin. Strips pre-constricted with 20 mM KPSS were treated with either 0.1 μM isoprenaline (A) or 1 μM forskolin (B). Pre-treatment with K v 7 channel modulators revealed a reduction in response to isoprenaline and forskolin when blocking K v 7 channels by XE991 (10 μM) whereas retigabine (10μM) did not affect the response to isoprenaline. Pre-treatment with vehicle control (0.1% DMSO). ** P
    Figure Legend Snippet: At low depolarisation K v 7 channel inhibition reduces the response to forskolin. Strips pre-constricted with 20 mM KPSS were treated with either 0.1 μM isoprenaline (A) or 1 μM forskolin (B). Pre-treatment with K v 7 channel modulators revealed a reduction in response to isoprenaline and forskolin when blocking K v 7 channels by XE991 (10 μM) whereas retigabine (10μM) did not affect the response to isoprenaline. Pre-treatment with vehicle control (0.1% DMSO). ** P

    Techniques Used: Inhibition, Blocking Assay

    Modulation of K v 7 channels does not affect Gs mediated relaxation at 1 μM carbachol-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 1 μM carbachol. * P
    Figure Legend Snippet: Modulation of K v 7 channels does not affect Gs mediated relaxation at 1 μM carbachol-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 1 μM carbachol. * P

    Techniques Used: Produced, Incubation

    Modulation of K v 7 channels does not affect Gs mediated relaxation at 40 mM KPSS-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 40 mM KPSS. Neither of the K v 7 channel modulators affected the response to isoprenaline or forskolin.
    Figure Legend Snippet: Modulation of K v 7 channels does not affect Gs mediated relaxation at 40 mM KPSS-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 40 mM KPSS. Neither of the K v 7 channel modulators affected the response to isoprenaline or forskolin.

    Techniques Used: Produced, Incubation

    Effect of isoprenaline and forskolin in human DSM at 1 μM carbachol- and 40 mM KPSS-induced contractions. Cumulative concentration-responses were induced with isoprenaline and forskolin. Initial tone was achieved by pre-constriction with 1 μM carbachol (A and B) and 40 mM KPSS (C and D) bladder strips. * P
    Figure Legend Snippet: Effect of isoprenaline and forskolin in human DSM at 1 μM carbachol- and 40 mM KPSS-induced contractions. Cumulative concentration-responses were induced with isoprenaline and forskolin. Initial tone was achieved by pre-constriction with 1 μM carbachol (A and B) and 40 mM KPSS (C and D) bladder strips. * P

    Techniques Used: Concentration Assay

    3) Product Images from "Regulation of basal expression of hepatic PEPCK and G6Pase by AKT2"

    Article Title: Regulation of basal expression of hepatic PEPCK and G6Pase by AKT2

    Journal: The Biochemical journal

    doi: 10.1042/BCJ20190570

    CREB phosphorylation mediates AKT2-regulated induction of PEPCK. ( A ) CREB phosphorylation induced by PTEN loss is regulated by AKT2. Liver lysates from mice with different genotypes were analysis for p-CREB. PM, Pten deleted; DM, Pten and Akt2 deleted; AM, Akt2 deleted. Two biological replicas are included for each genotype group. Protein levels of p-AKT, PTEN and p-GSK3 are analyzed and showed up-regulation of AKT and GSK-3 with PTEN loss and inhibition when AKT2 is lost. Phosphorylation of CREB is only observed when PTEN is lost. AKT2 loss together with PTEN blocked this phosphorylation in the DM livers. ( B ) Akt2 +/+ and Akt2 − / − cell were treated with forskolin (100 μM) for 24 h to induce cAMP and CREB phosphorylation or vehicle as controls. Phosphorylation of CREB is detected and showed to be lower when AKT2 is lost. When forskolin is added to induce cAMP, protein expression of p-CREB is evaluated in both Akt2 +/+ and Akt2 − / − cells even though its levels remains lower in the Akt2 − / − cells. Vinculin is probed as loading control. ( C ) Introduction of CREB-133A and wtCREB to Akt2 +/+ and Akt2 −/− hepatocytes. Expression of PEPCK is analyzed using quantitative PCR analysis. Left panel, CREB-S133A is introduced to Akt2 +/+ cells. Middle panel, wtCREB is introduced to Akt2 −/− cells; Right panel, wtCREB is introduced to Akt2 +/+ cells. n = 3. Data presented as mean ± SEM. * P ≤ 0.05. Different from vector transfected cells of the same genotype. Experiments repeated at least three times.
    Figure Legend Snippet: CREB phosphorylation mediates AKT2-regulated induction of PEPCK. ( A ) CREB phosphorylation induced by PTEN loss is regulated by AKT2. Liver lysates from mice with different genotypes were analysis for p-CREB. PM, Pten deleted; DM, Pten and Akt2 deleted; AM, Akt2 deleted. Two biological replicas are included for each genotype group. Protein levels of p-AKT, PTEN and p-GSK3 are analyzed and showed up-regulation of AKT and GSK-3 with PTEN loss and inhibition when AKT2 is lost. Phosphorylation of CREB is only observed when PTEN is lost. AKT2 loss together with PTEN blocked this phosphorylation in the DM livers. ( B ) Akt2 +/+ and Akt2 − / − cell were treated with forskolin (100 μM) for 24 h to induce cAMP and CREB phosphorylation or vehicle as controls. Phosphorylation of CREB is detected and showed to be lower when AKT2 is lost. When forskolin is added to induce cAMP, protein expression of p-CREB is evaluated in both Akt2 +/+ and Akt2 − / − cells even though its levels remains lower in the Akt2 − / − cells. Vinculin is probed as loading control. ( C ) Introduction of CREB-133A and wtCREB to Akt2 +/+ and Akt2 −/− hepatocytes. Expression of PEPCK is analyzed using quantitative PCR analysis. Left panel, CREB-S133A is introduced to Akt2 +/+ cells. Middle panel, wtCREB is introduced to Akt2 −/− cells; Right panel, wtCREB is introduced to Akt2 +/+ cells. n = 3. Data presented as mean ± SEM. * P ≤ 0.05. Different from vector transfected cells of the same genotype. Experiments repeated at least three times.

    Techniques Used: Mouse Assay, Inhibition, Expressing, Real-time Polymerase Chain Reaction, Plasmid Preparation, Transfection

    4) Product Images from "Caveolin-1 and Lipid Microdomains Regulate Gs Trafficking and Attenuate Gs/Adenylyl Cyclase Signaling"

    Article Title: Caveolin-1 and Lipid Microdomains Regulate Gs Trafficking and Attenuate Gs/Adenylyl Cyclase Signaling

    Journal: Molecular Pharmacology

    doi: 10.1124/mol.109.060160

    Caveolin knockdown increases forskolin- and fluoride-stimulated Gα s /adenylyl cyclase signaling. A, wild-type C6 cells (WT C6) or caveolin-1 stable knockdown cells (CAV-1 RNAi) were incubated with [2,8- 3 H]adenine for 18 h to label cellular ATP.
    Figure Legend Snippet: Caveolin knockdown increases forskolin- and fluoride-stimulated Gα s /adenylyl cyclase signaling. A, wild-type C6 cells (WT C6) or caveolin-1 stable knockdown cells (CAV-1 RNAi) were incubated with [2,8- 3 H]adenine for 18 h to label cellular ATP.

    Techniques Used: Incubation

    Caveolin-1 knockout increases fluoride and forskolin-stimulated adenylyl cyclase activity in mouse striatum. Ten- to 12-week-old wild-type or caveolin-1 knockout littermate mice were colony bred, brains were obtained, and striatum was microdissected.
    Figure Legend Snippet: Caveolin-1 knockout increases fluoride and forskolin-stimulated adenylyl cyclase activity in mouse striatum. Ten- to 12-week-old wild-type or caveolin-1 knockout littermate mice were colony bred, brains were obtained, and striatum was microdissected.

    Techniques Used: Knock-Out, Activity Assay, Mouse Assay

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    Alomone Labs forskolin
    Neurite outgrowth is regulated by cAMP signaling. A. Plated neurospheres were treated with 10 μM <t>forskolin</t> for 24 h. The number of neurites crossing a circular mask around the neurosphere was used for quantification. B. Micrographs of control and 10 μM forskolin-treated neurospheres immunostained for beta III tubulin (green). Nuclei counterstained with DAPI (blue). C. Number of neurites crossing the circle (**p
    Forskolin, supplied by Alomone Labs, 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/result/forskolin/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    forskolin - by Bioz Stars, 2022-01
    94/100 stars
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    Neurite outgrowth is regulated by cAMP signaling. A. Plated neurospheres were treated with 10 μM forskolin for 24 h. The number of neurites crossing a circular mask around the neurosphere was used for quantification. B. Micrographs of control and 10 μM forskolin-treated neurospheres immunostained for beta III tubulin (green). Nuclei counterstained with DAPI (blue). C. Number of neurites crossing the circle (**p

    Journal: bioRxiv

    Article Title: Quantitative profiling of axonal guidance proteins during the differentiation of human neurospheres

    doi: 10.1101/2021.02.21.432144

    Figure Lengend Snippet: Neurite outgrowth is regulated by cAMP signaling. A. Plated neurospheres were treated with 10 μM forskolin for 24 h. The number of neurites crossing a circular mask around the neurosphere was used for quantification. B. Micrographs of control and 10 μM forskolin-treated neurospheres immunostained for beta III tubulin (green). Nuclei counterstained with DAPI (blue). C. Number of neurites crossing the circle (**p

    Article Snippet: 10-day old neurospheres were treated with 10 μM forskolin (Alomone Labs) 24 hours after plating and analyzed 24 h after treatment.

    Techniques:

    At low depolarisation K v 7 channel inhibition reduces the response to forskolin. Strips pre-constricted with 20 mM KPSS were treated with either 0.1 μM isoprenaline (A) or 1 μM forskolin (B). Pre-treatment with K v 7 channel modulators revealed a reduction in response to isoprenaline and forskolin when blocking K v 7 channels by XE991 (10 μM) whereas retigabine (10μM) did not affect the response to isoprenaline. Pre-treatment with vehicle control (0.1% DMSO). ** P

    Journal: PLoS ONE

    Article Title: Functional and Molecular Evidence for Kv7 Channel Subtypes in Human Detrusor from Patients with and without Bladder Outflow Obstruction

    doi: 10.1371/journal.pone.0117350

    Figure Lengend Snippet: At low depolarisation K v 7 channel inhibition reduces the response to forskolin. Strips pre-constricted with 20 mM KPSS were treated with either 0.1 μM isoprenaline (A) or 1 μM forskolin (B). Pre-treatment with K v 7 channel modulators revealed a reduction in response to isoprenaline and forskolin when blocking K v 7 channels by XE991 (10 μM) whereas retigabine (10μM) did not affect the response to isoprenaline. Pre-treatment with vehicle control (0.1% DMSO). ** P

    Article Snippet: Organ bath studies Retigabine and forskolin were purchased from Alamone Labs (Jerusalem, Israel) whereas XE991 was kindly provided by NeuroSearch (Ballerup, Denmark), and ML213 and ML277 were kindly provided by Vanderbilt University (Nashville, TN, USA (MLCPN probes)).

    Techniques: Inhibition, Blocking Assay

    Modulation of K v 7 channels does not affect Gs mediated relaxation at 1 μM carbachol-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 1 μM carbachol. * P

    Journal: PLoS ONE

    Article Title: Functional and Molecular Evidence for Kv7 Channel Subtypes in Human Detrusor from Patients with and without Bladder Outflow Obstruction

    doi: 10.1371/journal.pone.0117350

    Figure Lengend Snippet: Modulation of K v 7 channels does not affect Gs mediated relaxation at 1 μM carbachol-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 1 μM carbachol. * P

    Article Snippet: Organ bath studies Retigabine and forskolin were purchased from Alamone Labs (Jerusalem, Israel) whereas XE991 was kindly provided by NeuroSearch (Ballerup, Denmark), and ML213 and ML277 were kindly provided by Vanderbilt University (Nashville, TN, USA (MLCPN probes)).

    Techniques: Produced, Incubation

    Modulation of K v 7 channels does not affect Gs mediated relaxation at 40 mM KPSS-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 40 mM KPSS. Neither of the K v 7 channel modulators affected the response to isoprenaline or forskolin.

    Journal: PLoS ONE

    Article Title: Functional and Molecular Evidence for Kv7 Channel Subtypes in Human Detrusor from Patients with and without Bladder Outflow Obstruction

    doi: 10.1371/journal.pone.0117350

    Figure Lengend Snippet: Modulation of K v 7 channels does not affect Gs mediated relaxation at 40 mM KPSS-induced contractility. Cumulative concentrations-responses for isoprenaline (A and B) and forskolin (C) were produced with pre-incubation of 10 μM XE991 (A and C), 10 μM retigabine (B) or vehicle control (0.1% DMSO). Initial tone was achieved by pre-constriction with 40 mM KPSS. Neither of the K v 7 channel modulators affected the response to isoprenaline or forskolin.

    Article Snippet: Organ bath studies Retigabine and forskolin were purchased from Alamone Labs (Jerusalem, Israel) whereas XE991 was kindly provided by NeuroSearch (Ballerup, Denmark), and ML213 and ML277 were kindly provided by Vanderbilt University (Nashville, TN, USA (MLCPN probes)).

    Techniques: Produced, Incubation

    Effect of isoprenaline and forskolin in human DSM at 1 μM carbachol- and 40 mM KPSS-induced contractions. Cumulative concentration-responses were induced with isoprenaline and forskolin. Initial tone was achieved by pre-constriction with 1 μM carbachol (A and B) and 40 mM KPSS (C and D) bladder strips. * P

    Journal: PLoS ONE

    Article Title: Functional and Molecular Evidence for Kv7 Channel Subtypes in Human Detrusor from Patients with and without Bladder Outflow Obstruction

    doi: 10.1371/journal.pone.0117350

    Figure Lengend Snippet: Effect of isoprenaline and forskolin in human DSM at 1 μM carbachol- and 40 mM KPSS-induced contractions. Cumulative concentration-responses were induced with isoprenaline and forskolin. Initial tone was achieved by pre-constriction with 1 μM carbachol (A and B) and 40 mM KPSS (C and D) bladder strips. * P

    Article Snippet: Organ bath studies Retigabine and forskolin were purchased from Alamone Labs (Jerusalem, Israel) whereas XE991 was kindly provided by NeuroSearch (Ballerup, Denmark), and ML213 and ML277 were kindly provided by Vanderbilt University (Nashville, TN, USA (MLCPN probes)).

    Techniques: Concentration Assay

    CREB phosphorylation mediates AKT2-regulated induction of PEPCK. ( A ) CREB phosphorylation induced by PTEN loss is regulated by AKT2. Liver lysates from mice with different genotypes were analysis for p-CREB. PM, Pten deleted; DM, Pten and Akt2 deleted; AM, Akt2 deleted. Two biological replicas are included for each genotype group. Protein levels of p-AKT, PTEN and p-GSK3 are analyzed and showed up-regulation of AKT and GSK-3 with PTEN loss and inhibition when AKT2 is lost. Phosphorylation of CREB is only observed when PTEN is lost. AKT2 loss together with PTEN blocked this phosphorylation in the DM livers. ( B ) Akt2 +/+ and Akt2 − / − cell were treated with forskolin (100 μM) for 24 h to induce cAMP and CREB phosphorylation or vehicle as controls. Phosphorylation of CREB is detected and showed to be lower when AKT2 is lost. When forskolin is added to induce cAMP, protein expression of p-CREB is evaluated in both Akt2 +/+ and Akt2 − / − cells even though its levels remains lower in the Akt2 − / − cells. Vinculin is probed as loading control. ( C ) Introduction of CREB-133A and wtCREB to Akt2 +/+ and Akt2 −/− hepatocytes. Expression of PEPCK is analyzed using quantitative PCR analysis. Left panel, CREB-S133A is introduced to Akt2 +/+ cells. Middle panel, wtCREB is introduced to Akt2 −/− cells; Right panel, wtCREB is introduced to Akt2 +/+ cells. n = 3. Data presented as mean ± SEM. * P ≤ 0.05. Different from vector transfected cells of the same genotype. Experiments repeated at least three times.

    Journal: The Biochemical journal

    Article Title: Regulation of basal expression of hepatic PEPCK and G6Pase by AKT2

    doi: 10.1042/BCJ20190570

    Figure Lengend Snippet: CREB phosphorylation mediates AKT2-regulated induction of PEPCK. ( A ) CREB phosphorylation induced by PTEN loss is regulated by AKT2. Liver lysates from mice with different genotypes were analysis for p-CREB. PM, Pten deleted; DM, Pten and Akt2 deleted; AM, Akt2 deleted. Two biological replicas are included for each genotype group. Protein levels of p-AKT, PTEN and p-GSK3 are analyzed and showed up-regulation of AKT and GSK-3 with PTEN loss and inhibition when AKT2 is lost. Phosphorylation of CREB is only observed when PTEN is lost. AKT2 loss together with PTEN blocked this phosphorylation in the DM livers. ( B ) Akt2 +/+ and Akt2 − / − cell were treated with forskolin (100 μM) for 24 h to induce cAMP and CREB phosphorylation or vehicle as controls. Phosphorylation of CREB is detected and showed to be lower when AKT2 is lost. When forskolin is added to induce cAMP, protein expression of p-CREB is evaluated in both Akt2 +/+ and Akt2 − / − cells even though its levels remains lower in the Akt2 − / − cells. Vinculin is probed as loading control. ( C ) Introduction of CREB-133A and wtCREB to Akt2 +/+ and Akt2 −/− hepatocytes. Expression of PEPCK is analyzed using quantitative PCR analysis. Left panel, CREB-S133A is introduced to Akt2 +/+ cells. Middle panel, wtCREB is introduced to Akt2 −/− cells; Right panel, wtCREB is introduced to Akt2 +/+ cells. n = 3. Data presented as mean ± SEM. * P ≤ 0.05. Different from vector transfected cells of the same genotype. Experiments repeated at least three times.

    Article Snippet: The medium was replaced with fresh medium with 100 μM Forskolin (Alomone Labs Cat# F-500) or vehicle and incubated for 24 h before harvesting.

    Techniques: Mouse Assay, Inhibition, Expressing, Real-time Polymerase Chain Reaction, Plasmid Preparation, Transfection

    Caveolin knockdown increases forskolin- and fluoride-stimulated Gα s /adenylyl cyclase signaling. A, wild-type C6 cells (WT C6) or caveolin-1 stable knockdown cells (CAV-1 RNAi) were incubated with [2,8- 3 H]adenine for 18 h to label cellular ATP.

    Journal: Molecular Pharmacology

    Article Title: Caveolin-1 and Lipid Microdomains Regulate Gs Trafficking and Attenuate Gs/Adenylyl Cyclase Signaling

    doi: 10.1124/mol.109.060160

    Figure Lengend Snippet: Caveolin knockdown increases forskolin- and fluoride-stimulated Gα s /adenylyl cyclase signaling. A, wild-type C6 cells (WT C6) or caveolin-1 stable knockdown cells (CAV-1 RNAi) were incubated with [2,8- 3 H]adenine for 18 h to label cellular ATP.

    Article Snippet: Cells were subsequently exposed to agonist or drug at 37°C for 30 min at the following concentrations: 10 pM to 10 μM isoproterenol (Sigma), 0.01 to 100 mIU/ml bovine TSH (Sigma), and 100 μM forskolin (Alomone Labs, Jerusalem, Israel).

    Techniques: Incubation

    Caveolin-1 knockout increases fluoride and forskolin-stimulated adenylyl cyclase activity in mouse striatum. Ten- to 12-week-old wild-type or caveolin-1 knockout littermate mice were colony bred, brains were obtained, and striatum was microdissected.

    Journal: Molecular Pharmacology

    Article Title: Caveolin-1 and Lipid Microdomains Regulate Gs Trafficking and Attenuate Gs/Adenylyl Cyclase Signaling

    doi: 10.1124/mol.109.060160

    Figure Lengend Snippet: Caveolin-1 knockout increases fluoride and forskolin-stimulated adenylyl cyclase activity in mouse striatum. Ten- to 12-week-old wild-type or caveolin-1 knockout littermate mice were colony bred, brains were obtained, and striatum was microdissected.

    Article Snippet: Cells were subsequently exposed to agonist or drug at 37°C for 30 min at the following concentrations: 10 pM to 10 μM isoproterenol (Sigma), 0.01 to 100 mIU/ml bovine TSH (Sigma), and 100 μM forskolin (Alomone Labs, Jerusalem, Israel).

    Techniques: Knock-Out, Activity Assay, Mouse Assay