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  • N/A
    Adenylate cyclase activator
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    99
    Millipore forskolin
    Pulmonary ionocytes are a major source of CFTR activity. a , Immunofluorescence for Krt5 (green) and Foxi1 (red) in mouse tracheae at homeostasis (left, n=3) or 3 days post injury (right, n=3). Arrowhead: Foxi1 + Krt5 + cells. Arrow: Foxi1 + Krt5 - cell. Scale bars, 20μm. b , Immunofluorescence and quantification for ionocytes (FOXI1 + , red, arrowheads) and ciliated cells (FOXJ1 + , green) in HBEC cultures treated with DMSO or DAPT, scale bar, 100 μm, (n=4 experiments in one donor). *p-value=0.01, ***p-value=1.1×10 −6 by two-tailed t-test c , HBECs were treated with DMSO or DAPT upon culture at ALI. After differentiation (2–3 weeks), cultures were loaded into Ussing chambers and short circuit current (I sc ) was recorded during addition of Amiloride, <t>Forskolin,</t> and a CFTR-inhibitor, CFTR(inh)-172. Shown is a representative tracing from Donor 1 (n=11). d , Change in short circuit current (ΔI sc ) in response to Forskolin measured in DMSO (n=7 cultures per donor) and DAPT-treated cultures, (n=8 cultures per donor). ***p-value
    Forskolin, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/forskolin/product/Millipore
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    forskolin - by Bioz Stars, 2021-04
    99/100 stars
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    99
    Tocris nkh 477
    G protein activation and βarr2 recruitment in absence and presence of active G proteins. a Inhibition of <t>forskolin-mediated</t> cAMP accumulation by C3-activated FFA2 in FFA2-HEK293 cells, in the presence or absence of PTX. b IP1 accumulation of C3-stimulated FFA2, in the presence or absence of FR. c , d FRET measurements of Gi ( c ) and Gq ( d ) activation-induced conformational changes in wild-type (WT) HEK293 cells expressing FFA2 after stimulation with C3 in absence and presence of G protein inhibitors. e , f C3-induced β-arrestin2 recruitment to FFA2 in wild-type (WT) ( e ) or ΔG12/13 HEK293 cells ( f ), in the absence and presence of PTX and FR. Shown are representative FRET traces with the indicated number of total cells per condition ( c , d ) and bar diagrams are averages from three independent experiments. Data are mean ± s.e.m. ( a , b , e , f ) or + s.d. ( c , d ) of three experiments each performed in triplicate. For statistical analysis, two-tailed unpaired t -test ( c , d ) and two-sample paired Wilcoxon test ( e , f ) was applied to paired points at different concentrations. * P
    Nkh 477, supplied by Tocris, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nkh 477/product/Tocris
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nkh 477 - by Bioz Stars, 2021-04
    99/100 stars
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    N/A
    Cyclic AMP cAMP is an important signal carrier necessary for the proper biological response of cells to hormones neurotransmitters and other extracellular signals Forskolin is a naturally occurring diterpene that
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    Labdane diterpene found in Coleus PP2A and adenylyl cyclase activator
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    N/A
    StemMACS Forskolin is a small molecule activator of adenylate cyclase
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    Image Search Results


    Pulmonary ionocytes are a major source of CFTR activity. a , Immunofluorescence for Krt5 (green) and Foxi1 (red) in mouse tracheae at homeostasis (left, n=3) or 3 days post injury (right, n=3). Arrowhead: Foxi1 + Krt5 + cells. Arrow: Foxi1 + Krt5 - cell. Scale bars, 20μm. b , Immunofluorescence and quantification for ionocytes (FOXI1 + , red, arrowheads) and ciliated cells (FOXJ1 + , green) in HBEC cultures treated with DMSO or DAPT, scale bar, 100 μm, (n=4 experiments in one donor). *p-value=0.01, ***p-value=1.1×10 −6 by two-tailed t-test c , HBECs were treated with DMSO or DAPT upon culture at ALI. After differentiation (2–3 weeks), cultures were loaded into Ussing chambers and short circuit current (I sc ) was recorded during addition of Amiloride, Forskolin, and a CFTR-inhibitor, CFTR(inh)-172. Shown is a representative tracing from Donor 1 (n=11). d , Change in short circuit current (ΔI sc ) in response to Forskolin measured in DMSO (n=7 cultures per donor) and DAPT-treated cultures, (n=8 cultures per donor). ***p-value

    Journal: Nature

    Article Title: A single cell atlas of the tracheal epithelium reveals the CFTR-rich pulmonary ionocyte

    doi: 10.1038/s41586-018-0394-6

    Figure Lengend Snippet: Pulmonary ionocytes are a major source of CFTR activity. a , Immunofluorescence for Krt5 (green) and Foxi1 (red) in mouse tracheae at homeostasis (left, n=3) or 3 days post injury (right, n=3). Arrowhead: Foxi1 + Krt5 + cells. Arrow: Foxi1 + Krt5 - cell. Scale bars, 20μm. b , Immunofluorescence and quantification for ionocytes (FOXI1 + , red, arrowheads) and ciliated cells (FOXJ1 + , green) in HBEC cultures treated with DMSO or DAPT, scale bar, 100 μm, (n=4 experiments in one donor). *p-value=0.01, ***p-value=1.1×10 −6 by two-tailed t-test c , HBECs were treated with DMSO or DAPT upon culture at ALI. After differentiation (2–3 weeks), cultures were loaded into Ussing chambers and short circuit current (I sc ) was recorded during addition of Amiloride, Forskolin, and a CFTR-inhibitor, CFTR(inh)-172. Shown is a representative tracing from Donor 1 (n=11). d , Change in short circuit current (ΔI sc ) in response to Forskolin measured in DMSO (n=7 cultures per donor) and DAPT-treated cultures, (n=8 cultures per donor). ***p-value

    Article Snippet: Amiloride (Sigma, A9561) was added apically at 10μM to inhibit Na+ absorption, then Forskolin (Sigma, F6886) was added apically at 20μM to stimulate cAMP and finally, CFTR-172 (Sigma-Aldrich, C2992) inhibitor was added apically and basally at 30μM.

    Techniques: Activity Assay, Immunofluorescence, Two Tailed Test

    G protein activation and βarr2 recruitment in absence and presence of active G proteins. a Inhibition of forskolin-mediated cAMP accumulation by C3-activated FFA2 in FFA2-HEK293 cells, in the presence or absence of PTX. b IP1 accumulation of C3-stimulated FFA2, in the presence or absence of FR. c , d FRET measurements of Gi ( c ) and Gq ( d ) activation-induced conformational changes in wild-type (WT) HEK293 cells expressing FFA2 after stimulation with C3 in absence and presence of G protein inhibitors. e , f C3-induced β-arrestin2 recruitment to FFA2 in wild-type (WT) ( e ) or ΔG12/13 HEK293 cells ( f ), in the absence and presence of PTX and FR. Shown are representative FRET traces with the indicated number of total cells per condition ( c , d ) and bar diagrams are averages from three independent experiments. Data are mean ± s.e.m. ( a , b , e , f ) or + s.d. ( c , d ) of three experiments each performed in triplicate. For statistical analysis, two-tailed unpaired t -test ( c , d ) and two-sample paired Wilcoxon test ( e , f ) was applied to paired points at different concentrations. * P

    Journal: Nature Communications

    Article Title: Lack of beta-arrestin signaling in the absence of active G proteins

    doi: 10.1038/s41467-017-02661-3

    Figure Lengend Snippet: G protein activation and βarr2 recruitment in absence and presence of active G proteins. a Inhibition of forskolin-mediated cAMP accumulation by C3-activated FFA2 in FFA2-HEK293 cells, in the presence or absence of PTX. b IP1 accumulation of C3-stimulated FFA2, in the presence or absence of FR. c , d FRET measurements of Gi ( c ) and Gq ( d ) activation-induced conformational changes in wild-type (WT) HEK293 cells expressing FFA2 after stimulation with C3 in absence and presence of G protein inhibitors. e , f C3-induced β-arrestin2 recruitment to FFA2 in wild-type (WT) ( e ) or ΔG12/13 HEK293 cells ( f ), in the absence and presence of PTX and FR. Shown are representative FRET traces with the indicated number of total cells per condition ( c , d ) and bar diagrams are averages from three independent experiments. Data are mean ± s.e.m. ( a , b , e , f ) or + s.d. ( c , d ) of three experiments each performed in triplicate. For statistical analysis, two-tailed unpaired t -test ( c , d ) and two-sample paired Wilcoxon test ( e , f ) was applied to paired points at different concentrations. * P

    Article Snippet: The cells were treated with vehicle, 100 nM arginine vasopressin (Peptide Institutes, Japan) or 100 µM NKH-477 (Tocris) (10 µL of 5X solution per well).

    Techniques: Activation Assay, Inhibition, Expressing, Two Tailed Test

    DMR biosensing of G protein- and arrestin-mediated cellular responses. DMR recordings in absence ( a – c ) and presence of G protein inhibitors ( d – f ) of agonist-mediated DP2 ( a , d ), GPR17 ( b , e ) and FFA2 ( c , f ) in wild-type (WT) HEK293 cells. Concentration-response-curves of DMR peak values in absence and presence of G protein inhibitors of DP2 ( g ), GPR17 ( h ), and FFA2 ( i ) response in wild-type HEK293 cells. j C3-mediated and forskolin-mediated DMR response of FFA2 in ΔG12/13 cells in the absence and presence of PTX/FR. k C3-induced DMR response of FFA2 in vector- or Gα 12/13 -transfected ΔG12/13 cells. l C3- or forskolin-mediated DMR response of FFA2 in vector- or β-arrestin2-transfected ΔG12/13 cells in the presence of PTX/FR. Inset shows βarr2-GFP transfected ΔG12/13 cells, scale bar 50 µm. m – o Agonist-induced DMR response of DP2 ( m ), GPR17 ( n ), or FFA2 ( o ) in vector- or β-arrestin2-transfected Δβarr1/2 cells in absence and presence of G protein inhibitors. a – f , j – o Shown are representative traces (mean + s.e.m.) of three independent experiments, each performed in triplicate. g – i Data are mean ± s.e.m. of three independent experiments (three technical replicates)

    Journal: Nature Communications

    Article Title: Lack of beta-arrestin signaling in the absence of active G proteins

    doi: 10.1038/s41467-017-02661-3

    Figure Lengend Snippet: DMR biosensing of G protein- and arrestin-mediated cellular responses. DMR recordings in absence ( a – c ) and presence of G protein inhibitors ( d – f ) of agonist-mediated DP2 ( a , d ), GPR17 ( b , e ) and FFA2 ( c , f ) in wild-type (WT) HEK293 cells. Concentration-response-curves of DMR peak values in absence and presence of G protein inhibitors of DP2 ( g ), GPR17 ( h ), and FFA2 ( i ) response in wild-type HEK293 cells. j C3-mediated and forskolin-mediated DMR response of FFA2 in ΔG12/13 cells in the absence and presence of PTX/FR. k C3-induced DMR response of FFA2 in vector- or Gα 12/13 -transfected ΔG12/13 cells. l C3- or forskolin-mediated DMR response of FFA2 in vector- or β-arrestin2-transfected ΔG12/13 cells in the presence of PTX/FR. Inset shows βarr2-GFP transfected ΔG12/13 cells, scale bar 50 µm. m – o Agonist-induced DMR response of DP2 ( m ), GPR17 ( n ), or FFA2 ( o ) in vector- or β-arrestin2-transfected Δβarr1/2 cells in absence and presence of G protein inhibitors. a – f , j – o Shown are representative traces (mean + s.e.m.) of three independent experiments, each performed in triplicate. g – i Data are mean ± s.e.m. of three independent experiments (three technical replicates)

    Article Snippet: The cells were treated with vehicle, 100 nM arginine vasopressin (Peptide Institutes, Japan) or 100 µM NKH-477 (Tocris) (10 µL of 5X solution per well).

    Techniques: Concentration Assay, Plasmid Preparation, Transfection