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pka inhibitor pki 14-22 #2546  (Tocris)


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    Tocris pka inhibitor pki 14-22 #2546
    Pka Inhibitor Pki 14 22 #2546, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pka+inhibitor+pki/pki+14+22+amide/pmc11543937-240-8-14
    Average 90 stars, based on 1 article reviews
    pka inhibitor pki 14-22 #2546 - by Bioz Stars, 2026-09
    90/100 stars

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    Related Articles

    other:

    Article Title: Endothelial CD99 signals through soluble adenylyl cyclase and PKA to regulate leukocyte transendothelial migration.
    Article Snippet: In TEM assays where ECs were treated with various inhibitors, before the addition of PBMCs, HUVECs were preincubated with the following inhibitors in preconditioned media for 1 h at 37°C: PKI (5 μM PKA inhibitor; Tocris), KH7 (50 μM sAC inhibitor; Cayman Chemical Co.), 2’,5-dideoxyadenosine (ddAdo; 25 μM tmAC inhibitor; Sigma-Aldrich), diphenhydramine (10 μM H1-R antagonist; Sigma-Aldrich), ranitidine (10 μM H2-R antagonist; Sigma-Aldrich), or JNJ-10191584 (10 μM H4-R antagonist; Sigma-Aldrich) or DMSO (carrier control).

    Article Title: Age-Dependent D1-D2 Receptor Coactivation in the Lateral Orbitofrontal Cortex Potentiates NMDA Receptors and Facilitates Cognitive Flexibility.
    Article Snippet: Protein kinase A (PKA) inhibitor (PKI; 20 μM; Tocris), phospholipase C (PLC) inhibitor U73122 (1 μM; Tocris), or 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA) (10 mM; Tocris) was dissolved in internal solution.

    Molecular Weight:

    Article Title: Activation of InsP 3 receptors is sufficient for inducing graded intrinsic plasticity in rat hippocampal pyramidal neurons
    Article Snippet: .. Drugs used in the experiments were d -myo-InsP 3 (InsP 3 ; Sigma Aldrich or Tocris Bioscience), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 10 μM (+)bicuculline, 10 μM picrotoxin, 50 μM d,l -2-amino-5-phosphonovaleric acid ( d,l -APV), and 2 μM {"type":"entrez-protein","attrs":{"text":"CGP55845","term_id":"875097176","term_text":"CGP55845"}} CGP55845 (all synaptic blockers from Allied Scientific), 50 μM NiCl 2 (Sigma-Aldrich), 10 μM nimodipine (Tocris Bioscience), 1 mg/ml heparin (20,000–25,000 molecular weight; Calbiochem), 20 μM ZD7288 (Tocris Bioscience), 20 mM BAPTA (Life Technologies), 20 μM PKA inhibitor (PKI) (14-22) amide, myristoylated (PKAi peptide; Tocris Bioscience), and 500 nM KT5720 (Tocris Bioscience). ..

    Incubation:

    Article Title: Calcium/calmodulin‐dependent kinase II and nitric oxide synthase 1‐dependent modulation of ryanodine receptors during β‐adrenergic stimulation is restricted to the dyadic cleft
    Article Snippet: .. The PKA inhibitor PKI (PKI myristoylated‐(14‐22)‐amide; Tocris Bioscience, Bristol, UK) was used at 20 μ m with incubation for 30 min and included in the pipette solution. .. The PKA inhibitor H‐89 (Sigma‐Aldrich, St Louis, MO, USA) was used at 10 μ m with pre‐incubation for 15 min and then included in the pipette solution.

    Transferring:

    Article Title: Calcium/calmodulin‐dependent kinase II and nitric oxide synthase 1‐dependent modulation of ryanodine receptors during β‐adrenergic stimulation is restricted to the dyadic cleft
    Article Snippet: .. The PKA inhibitor PKI (PKI myristoylated‐(14‐22)‐amide; Tocris Bioscience, Bristol, UK) was used at 20 μ m with incubation for 30 min and included in the pipette solution. .. The PKA inhibitor H‐89 (Sigma‐Aldrich, St Louis, MO, USA) was used at 10 μ m with pre‐incubation for 15 min and then included in the pipette solution.

    Transfection:

    Article Title: Characterization of a Threonine-Rich Cluster in Hepatitis C Virus Nonstructural Protein 5A and Its Contribution to Hyperphosphorylation
    Article Snippet: 20 21 Pharmacological inhibition of NS5A phosphorylation 22 Huh7-Lunet T7 cells were seeded with a density of 2x106 cells per 6-Well dish and 23 transfected 24 h later with LT1 transfection agent (Mirus Bio LLC, Madison, WI, USA) 24 according to manufacturer’s instruction. .. For drug treatment the supernatant was replaced 4 h 25 on S eptem ber 28, 2018 by guest http://jvi.asm .org/ D ow nloaded from 10 after transfection with complete DMEM containing either 5 μM of the PI4KA inhibitor G1 1 (GlaxoSmithKline, Munich, Germany) (60), 10 μM of the CKIα inhibitor H479 (61), 500nM 2 of the CKII inhibitor TBBz (Sigma-Aldrich, Darmstadt, Germany) (62), 30 μM of the Polo-3 like Kinase 1 inhibitor Poloxin (Sigma-Aldrich, Darmstadt, Germany) (63),100 nM of the 4 Polo-like Kinase 2/3 inhibitor TC-S 7005 (Tocris, Wiesbaden-Nordenstadt, Germany), 1 μM 5 GSK3 inhibitor BIO (Sigma-Aldrich, Darmstadt, Germany) (64),10 μM PKA inhibitor PKI 6 5-24 (Tocris, Wiesbaden-Nordenstadt, Germany) (65) or 5 μM CamK2D inhibitor KN93 7 (50). ..

    Concentration Assay:

    Article Title: SYK kinase mediates brown fat differentiation and activation
    Article Snippet: .. SYK-i1/ER27319 (Tocris Bioscience), SYK-i2/BAY61-3606 (Sigma-Aldrich), SYK-i3/R406 (free base, Selleck Chemicals #S1533), SYK-i4/PRT062607 (Selleck Chemicals #S8032) and SHP1 inhibitor 3AC (EMD Millipore #5658351) were reconstituted in DMSO and stored at −80 °C. mTOR inhibitors (Torin 1, torin 2, KU0063794), Akt inhibitor API-2, PKA inhibitor PKI 14-22 were all obtained from Tocris Bioscience, PKA inhibitor H89 was purchased from Santa Cruz Biotechnology were all reconstituted in DMSO, stored at −80 °C and used at a final concentration of 10 μM. ..



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    Image Search Results


    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: Retrograde adenosine/A 2A receptor signaling facilitates excitatory synaptic transmission and seizures

    doi: 10.1016/j.celrep.2024.114382

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: PKI 6-22 amide , Tocris Bioscience , Cat#1904.

    Techniques: Virus, Plasmid Preparation, Recombinant, Software

    ( A–C ) lhx1a mRNA levels were assessed by RT-PCR at 7 dpi. β-actin was used as a sample control. ( D–K ) lhx1a whole-mount in situ hybridization (WISH) showing the trunk kidney region at 7 dpi. XAV939 ( F ) could reduce the number of lhx1a + cell aggregates and dmPGE2 could rescue the influence of XAV939 treatment ( G ); ICRT 14 ( H ) or ICG-001 ( J ) could reduce the number of lhx1a + cell aggregates and dmPGE2 could not rescue the influence of ICRT 14 ( I ) or ICG-001 ( K ) treatment. n = 5–7 in each condition. ( L ) lhx1a + cell aggregates of whole kidney were calculated using ImageJ. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. ( M–V ) Immunofluorescence staining of β-catenin in Tg(lhx1a:DsRed ) zebrafish kidneys at 5 dpi. ( M, N ) Zebrafish injected DMSO as a control group, and the amount of β-catenin could be detected in lhx1a + cell aggregates during renal progenitor cell (RPC) aggregation ( M ) or proliferation ( N ). ( O ) β-catenin level in lhx1a + cell aggregates of cox2a -/- was significantly less than the control group, and injection of dmPGE2 ( P, Q ) could rescue the influence of Cox2a deficiency. ( R ) β-catenin level in lhx1a + cell aggregates of wnt4a -/- was significantly less than the control group, and injection of dmPGE2 ( S, T ) could rescue the influence of Wnt4a deficiency. Injection of PKI ( U ) could reduce β-catenin level in lhx1a + cell aggregates, while injection of dmPGE2 ( V ) could not rescue the influence of PKI treatment. n = 3–6 in ( M–V ). Scale bar in ( M–V ), 50 μm. ( W ) Bar chart depicting β-catenin levels following acute kidney injury (AKI) ( M–V ). Fluorescent intensities per unit area were measured at the lhx1a + RPC aggregates using ImageJ. β-catenin levels of lhx1a + RPCs during RPC aggregation normalized as 1. Ag, aggregation; Pr, proliferation. n = 3–6 in each condition. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. Figure 6—source data 1. Original gel files of . Figure 6—source data 2. Numerical data for , , , and .

    Journal: eLife

    Article Title: Renal interstitial cells promote nephron regeneration by secreting prostaglandin E2

    doi: 10.7554/eLife.81438

    Figure Lengend Snippet: ( A–C ) lhx1a mRNA levels were assessed by RT-PCR at 7 dpi. β-actin was used as a sample control. ( D–K ) lhx1a whole-mount in situ hybridization (WISH) showing the trunk kidney region at 7 dpi. XAV939 ( F ) could reduce the number of lhx1a + cell aggregates and dmPGE2 could rescue the influence of XAV939 treatment ( G ); ICRT 14 ( H ) or ICG-001 ( J ) could reduce the number of lhx1a + cell aggregates and dmPGE2 could not rescue the influence of ICRT 14 ( I ) or ICG-001 ( K ) treatment. n = 5–7 in each condition. ( L ) lhx1a + cell aggregates of whole kidney were calculated using ImageJ. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. ( M–V ) Immunofluorescence staining of β-catenin in Tg(lhx1a:DsRed ) zebrafish kidneys at 5 dpi. ( M, N ) Zebrafish injected DMSO as a control group, and the amount of β-catenin could be detected in lhx1a + cell aggregates during renal progenitor cell (RPC) aggregation ( M ) or proliferation ( N ). ( O ) β-catenin level in lhx1a + cell aggregates of cox2a -/- was significantly less than the control group, and injection of dmPGE2 ( P, Q ) could rescue the influence of Cox2a deficiency. ( R ) β-catenin level in lhx1a + cell aggregates of wnt4a -/- was significantly less than the control group, and injection of dmPGE2 ( S, T ) could rescue the influence of Wnt4a deficiency. Injection of PKI ( U ) could reduce β-catenin level in lhx1a + cell aggregates, while injection of dmPGE2 ( V ) could not rescue the influence of PKI treatment. n = 3–6 in ( M–V ). Scale bar in ( M–V ), 50 μm. ( W ) Bar chart depicting β-catenin levels following acute kidney injury (AKI) ( M–V ). Fluorescent intensities per unit area were measured at the lhx1a + RPC aggregates using ImageJ. β-catenin levels of lhx1a + RPCs during RPC aggregation normalized as 1. Ag, aggregation; Pr, proliferation. n = 3–6 in each condition. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. Figure 6—source data 1. Original gel files of . Figure 6—source data 2. Numerical data for , , , and .

    Article Snippet: During the nephron regeneration stage, the Indo (I7378-5G, Sigma; 400 μM, 10 μL per fish), NS-398 (N194-5MG, Sigma; 140 μM, 10 μL per fish), TG4-155 (S6793, Selleck; 400 μM, 10 μL per fish), dmPGE2 (D0160, Sigma; 600 μM, 10 μL per fish), GW627368X (T1978, TOPSCIENCE; 200 μM, 10 μL per fish), XAV939 (S1180, Selleck; 200 μM, 10 μL per fish), ICRT 14 (HY-16665, MCE; 10 μM, 10 μL per fish), ICG-001 (HY-14428, MCE; 100 μM, 10 μL per fish), PKI (HY-P1290A, MCE; 20 μM, 10 μL per fish), and H89 (HY-15979, MCE; 200 μM, 10 μL per fish) were intraperitoneally injected into zebrafish at 2, 4, and 6 dpi.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Control, In Situ Hybridization, Immunofluorescence, Staining, Injection

    ( A, B ) lhx1a mRNA levels were evaluated by RT-PCR at 7 dpi. β-actin was used as a sample control. ( C–H ) lhx1a whole-mount in situ hybridization (WISH) showing the trunk kidney region at 7 dpi. PKI ( E ) or H89 ( G ) treatment reduced the number of lhx1a + cell aggregates, while injection of dmPGE2 could not rescue the influence of PKI ( F ) or H89 ( H ) treatment. ( I ) lhx1a + cell aggregates of whole kidney were calculated using ImageJ. n = 5–7 in each condition. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. ( J–N ) Immunofluorescence staining of p-S9-GSK3β (arrowheads) in Tg(lhx1a:DsRed ) zebrafish kidneys at 5 dpi. ( J, K ) Zebrafish injected with DMSO as a control group, and the amount of p-S9-GSK3β could be detected in lhx1a + cell aggregates cytoplasm during RPC aggregation ( J ) or proliferation ( K ). ( L ) p-S9-GSK3β in lhx1a + cell aggregates of cox2a -/- was hardly detectable, and injection of dmPGE2 ( M, N ) could rescue the influence of Cox2a deficiency. Injection of PKI ( O ) could reduce p-S9-GSK3β level in lhx1a + cell aggregates, while injection of dmPGE2 ( P ) could not rescue the influence of PKI treatment. ( Q–W ) Immunofluorescence staining of p-S675-β-catenin in Tg(lhx1a:DsRed ) zebrafish kidneys at 5 dpi. ( Q, R ) Injection of DMSO as a control group and amounts of p-S675-β-catenin could be detected in lhx1a + cell aggregates during RPC aggregation ( Q ) or proliferation ( R ). ( S ) p-S675-β-catenin level in lhx1a + cell aggregates of cox2a -/- was hardly detectable, and injection of dmPGE2 ( T, U ) could rescue the influence of Cox2a deficiency. Injection of PKI ( V ) could reduce p-S675-β-catenin level in lhx1a + cell aggregates, while injection of dmPGE2 ( W ) could not rescue the influence of PKI treatment. Scale bar, 50 μm. ( X, Y ) Bar chart depicting p-S9-GSK3β ( X ) and p-S675-β-catenin ( Y ) levels following acute kidney injury (AKI) ( J–W ). Fluorescent intensities per unit area were measured at the lhx1a + RPC aggregates using ImageJ. p-S9-GSK3β or p-S675-β-catenin levels of lhx1a + RPCs during RPC aggregation normalized as 1. Ag, aggregation; Pr, proliferation. n = 3–6 in each condition. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. Figure 7—source data 1. Original gel files of . Figure 7—source data 2. Numerical data for .

    Journal: eLife

    Article Title: Renal interstitial cells promote nephron regeneration by secreting prostaglandin E2

    doi: 10.7554/eLife.81438

    Figure Lengend Snippet: ( A, B ) lhx1a mRNA levels were evaluated by RT-PCR at 7 dpi. β-actin was used as a sample control. ( C–H ) lhx1a whole-mount in situ hybridization (WISH) showing the trunk kidney region at 7 dpi. PKI ( E ) or H89 ( G ) treatment reduced the number of lhx1a + cell aggregates, while injection of dmPGE2 could not rescue the influence of PKI ( F ) or H89 ( H ) treatment. ( I ) lhx1a + cell aggregates of whole kidney were calculated using ImageJ. n = 5–7 in each condition. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. ( J–N ) Immunofluorescence staining of p-S9-GSK3β (arrowheads) in Tg(lhx1a:DsRed ) zebrafish kidneys at 5 dpi. ( J, K ) Zebrafish injected with DMSO as a control group, and the amount of p-S9-GSK3β could be detected in lhx1a + cell aggregates cytoplasm during RPC aggregation ( J ) or proliferation ( K ). ( L ) p-S9-GSK3β in lhx1a + cell aggregates of cox2a -/- was hardly detectable, and injection of dmPGE2 ( M, N ) could rescue the influence of Cox2a deficiency. Injection of PKI ( O ) could reduce p-S9-GSK3β level in lhx1a + cell aggregates, while injection of dmPGE2 ( P ) could not rescue the influence of PKI treatment. ( Q–W ) Immunofluorescence staining of p-S675-β-catenin in Tg(lhx1a:DsRed ) zebrafish kidneys at 5 dpi. ( Q, R ) Injection of DMSO as a control group and amounts of p-S675-β-catenin could be detected in lhx1a + cell aggregates during RPC aggregation ( Q ) or proliferation ( R ). ( S ) p-S675-β-catenin level in lhx1a + cell aggregates of cox2a -/- was hardly detectable, and injection of dmPGE2 ( T, U ) could rescue the influence of Cox2a deficiency. Injection of PKI ( V ) could reduce p-S675-β-catenin level in lhx1a + cell aggregates, while injection of dmPGE2 ( W ) could not rescue the influence of PKI treatment. Scale bar, 50 μm. ( X, Y ) Bar chart depicting p-S9-GSK3β ( X ) and p-S675-β-catenin ( Y ) levels following acute kidney injury (AKI) ( J–W ). Fluorescent intensities per unit area were measured at the lhx1a + RPC aggregates using ImageJ. p-S9-GSK3β or p-S675-β-catenin levels of lhx1a + RPCs during RPC aggregation normalized as 1. Ag, aggregation; Pr, proliferation. n = 3–6 in each condition. Data were analyzed by ANOVA, ***p<0.001; ns, no significant difference. Figure 7—source data 1. Original gel files of . Figure 7—source data 2. Numerical data for .

    Article Snippet: During the nephron regeneration stage, the Indo (I7378-5G, Sigma; 400 μM, 10 μL per fish), NS-398 (N194-5MG, Sigma; 140 μM, 10 μL per fish), TG4-155 (S6793, Selleck; 400 μM, 10 μL per fish), dmPGE2 (D0160, Sigma; 600 μM, 10 μL per fish), GW627368X (T1978, TOPSCIENCE; 200 μM, 10 μL per fish), XAV939 (S1180, Selleck; 200 μM, 10 μL per fish), ICRT 14 (HY-16665, MCE; 10 μM, 10 μL per fish), ICG-001 (HY-14428, MCE; 100 μM, 10 μL per fish), PKI (HY-P1290A, MCE; 20 μM, 10 μL per fish), and H89 (HY-15979, MCE; 200 μM, 10 μL per fish) were intraperitoneally injected into zebrafish at 2, 4, and 6 dpi.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Control, In Situ Hybridization, Injection, Immunofluorescence, Staining

    S. cerevisiae Sup35p is phosphorylated by PKA in vitro . Proteins were incubated with the PKA catalytic subunit and [γ- 32 P]ATP, submitted to SDS-PAGE, and visualized by autoradiography. (a) Phosphorylation of wild-type Sup35p in the presence of PKA or PKI. (b) Phosphorylation of A and D mutant proteins by PKA. (c) Recognition of the different proteins by a specific PKA-phosphorylated substrate antibody. Wild-type, A or D mutant proteins were phosphorylated or not by PKA before western blotting and detection using a secondary antibody linked to the alkaline phosphatase. (d) Phosphorylation of C-terminal proteins by PKA.

    Journal: BMC Molecular Biology

    Article Title: A novel mutant of the Sup35 protein of Saccharomyces cerevisiae defective in translation termination and in GTPase activity still supports cell viability

    doi: 10.1186/1471-2199-9-22

    Figure Lengend Snippet: S. cerevisiae Sup35p is phosphorylated by PKA in vitro . Proteins were incubated with the PKA catalytic subunit and [γ- 32 P]ATP, submitted to SDS-PAGE, and visualized by autoradiography. (a) Phosphorylation of wild-type Sup35p in the presence of PKA or PKI. (b) Phosphorylation of A and D mutant proteins by PKA. (c) Recognition of the different proteins by a specific PKA-phosphorylated substrate antibody. Wild-type, A or D mutant proteins were phosphorylated or not by PKA before western blotting and detection using a secondary antibody linked to the alkaline phosphatase. (d) Phosphorylation of C-terminal proteins by PKA.

    Article Snippet: To test for the specificity of the reaction for PKA, 30 μg of PKA inhibitor (PKI) (Sigma) were added to the reaction buffer to specifically inhibit the activity of PKA.

    Techniques: In Vitro, Incubation, SDS Page, Autoradiography, Mutagenesis, Western Blot