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pka inhibitor fragment  (Tocris)


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    Structured Review

    Tocris pka inhibitor fragment
    Pka Inhibitor Fragment, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pka+inhibitor+fragment/PKA+Inhibitor+Fragment+(6-22)+amide/10__1096_slash_fj__202504690r-54-69-89
    Average 93 stars, based on 55 article reviews
    pka inhibitor fragment - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    Recombinant:

    Article Title: Morphine Protects against Intracellular Amyloid Toxicity by Inducing Estradiol Release and Upregulation of Hsp70
    Article Snippet: .. Chemicals, peptides, recombinant proteins, cDNA constructs, siRNAs, and antibodies Morphine hydrochloride (China Drug Regulation Bureau, Beijing, China), EM-1 (Tocris Bioscience), EM-2 (Tocris Bioscience), naloxone (Tocris Bioscience), naltrindole (Tocris Bioscience), -funaltrexamine ( -FNA; Tocris Bioscience), nor-binaltorphimine (nor-BNI; Tocris Bioscience), tamoxifen (Tax; Sigma), phenol red (Sigma), lipofectamine 2000 (Invitrogen), staurosporine (STS; Sigma), etoposide (Etop; Sigma), glutamate (Glu; Sigma), kainic acid (KA; Sigma), H2O2 (Beijing Chemicals), TNF- (Sigma), tunicamycin (Tocris Bioscience), thapsigargin (Tocris Bioscience), phorbol esters (Sigma), PKA inhibitor fragment (6 – 22; Tocris Bioscience), bovine serum albumin (BSA)-conjugated morphine (BAS-M; a kind gift from Dr. Z. Gong, Institute for Military Medical Sciences, Beijing, China), 17- -estradiol ( E2; Sigma), MG-132, a potent and cell permeable proteasome inhibitor (Sigma), lactacystein (Promega), and Z-VEID-fmk (CalBiochem) were used in the experiments. .. A 1– 42 and the reversed control A 42–1 peptides (Bachem) were dissolved in sterile distilled water at 25 M and immediately frozen at 20°C.

    Article Title: Morphine Protects against Intracellular Amyloid Toxicity by Inducing Estradiol Release and Upregulation of Hsp70
    Article Snippet: For medium absorption, precleaned protein-A Sepharose beads (Sigma) were coated with antibodies for overnight at 4°C and used for absorption of conditioned medium. β Secretase Activity Assay Kit (Abcam; Ab65357) and γ-Secretase Activity Kit (R & D Systems; FP003) were used to measure β- and γ-secretase activities as described by the manufacturer. .. Chemicals, peptides, recombinant proteins, cDNA constructs, siRNAs, and antibodies Morphine hydrochloride (China Drug Regulation Bureau, Beijing, China), EM-1 (Tocris Bioscience), EM-2 (Tocris Bioscience), naloxone (Tocris Bioscience), naltrindole (Tocris Bioscience), β-funaltrexamine (β-FNA; Tocris Bioscience), nor-binaltorphimine (nor-BNI; Tocris Bioscience), tamoxifen (Tax; Sigma), phenol red (Sigma), lipofectamine 2000 (Invitrogen), staurosporine (STS; Sigma), etoposide (Etop; Sigma), glutamate (Glu; Sigma), kainic acid (KA; Sigma), H 2 O 2 (Beijing Chemicals), TNF-α (Sigma), tunicamycin (Tocris Bioscience), thapsigargin (Tocris Bioscience), phorbol esters (Sigma), PKA inhibitor fragment (6–22; Tocris Bioscience), bovine serum albumin (BSA)-conjugated morphine (BAS-M; a kind gift from Dr. Z. Gong, Institute for Military Medical Sciences, Beijing, China), 17-β-estradiol (βE 2 ; Sigma), MG-132, a potent and cell permeable proteasome inhibitor (Sigma), lactacystein (Promega), and Z-VEID-fmk (CalBiochem) were used in the experiments. .. Aβ 1–42 and the reversed control Aβ 42–1 peptides (Bachem) were dissolved in sterile distilled water at 25 μ m and immediately frozen at −20°C.

    Construct:

    Article Title: Morphine Protects against Intracellular Amyloid Toxicity by Inducing Estradiol Release and Upregulation of Hsp70
    Article Snippet: .. Chemicals, peptides, recombinant proteins, cDNA constructs, siRNAs, and antibodies Morphine hydrochloride (China Drug Regulation Bureau, Beijing, China), EM-1 (Tocris Bioscience), EM-2 (Tocris Bioscience), naloxone (Tocris Bioscience), naltrindole (Tocris Bioscience), -funaltrexamine ( -FNA; Tocris Bioscience), nor-binaltorphimine (nor-BNI; Tocris Bioscience), tamoxifen (Tax; Sigma), phenol red (Sigma), lipofectamine 2000 (Invitrogen), staurosporine (STS; Sigma), etoposide (Etop; Sigma), glutamate (Glu; Sigma), kainic acid (KA; Sigma), H2O2 (Beijing Chemicals), TNF- (Sigma), tunicamycin (Tocris Bioscience), thapsigargin (Tocris Bioscience), phorbol esters (Sigma), PKA inhibitor fragment (6 – 22; Tocris Bioscience), bovine serum albumin (BSA)-conjugated morphine (BAS-M; a kind gift from Dr. Z. Gong, Institute for Military Medical Sciences, Beijing, China), 17- -estradiol ( E2; Sigma), MG-132, a potent and cell permeable proteasome inhibitor (Sigma), lactacystein (Promega), and Z-VEID-fmk (CalBiochem) were used in the experiments. .. A 1– 42 and the reversed control A 42–1 peptides (Bachem) were dissolved in sterile distilled water at 25 M and immediately frozen at 20°C.

    Article Title: Morphine Protects against Intracellular Amyloid Toxicity by Inducing Estradiol Release and Upregulation of Hsp70
    Article Snippet: For medium absorption, precleaned protein-A Sepharose beads (Sigma) were coated with antibodies for overnight at 4°C and used for absorption of conditioned medium. β Secretase Activity Assay Kit (Abcam; Ab65357) and γ-Secretase Activity Kit (R & D Systems; FP003) were used to measure β- and γ-secretase activities as described by the manufacturer. .. Chemicals, peptides, recombinant proteins, cDNA constructs, siRNAs, and antibodies Morphine hydrochloride (China Drug Regulation Bureau, Beijing, China), EM-1 (Tocris Bioscience), EM-2 (Tocris Bioscience), naloxone (Tocris Bioscience), naltrindole (Tocris Bioscience), β-funaltrexamine (β-FNA; Tocris Bioscience), nor-binaltorphimine (nor-BNI; Tocris Bioscience), tamoxifen (Tax; Sigma), phenol red (Sigma), lipofectamine 2000 (Invitrogen), staurosporine (STS; Sigma), etoposide (Etop; Sigma), glutamate (Glu; Sigma), kainic acid (KA; Sigma), H 2 O 2 (Beijing Chemicals), TNF-α (Sigma), tunicamycin (Tocris Bioscience), thapsigargin (Tocris Bioscience), phorbol esters (Sigma), PKA inhibitor fragment (6–22; Tocris Bioscience), bovine serum albumin (BSA)-conjugated morphine (BAS-M; a kind gift from Dr. Z. Gong, Institute for Military Medical Sciences, Beijing, China), 17-β-estradiol (βE 2 ; Sigma), MG-132, a potent and cell permeable proteasome inhibitor (Sigma), lactacystein (Promega), and Z-VEID-fmk (CalBiochem) were used in the experiments. .. Aβ 1–42 and the reversed control Aβ 42–1 peptides (Bachem) were dissolved in sterile distilled water at 25 μ m and immediately frozen at −20°C.

    Positron Emission Tomography:

    Article Title: Mechanism of 5‐Hydroxytryptamine Receptor 4 Mediated Vasorelaxation in the Isolated Bovine Lateral Saphenous Vein
    Article Snippet: To better understand the mechanisms of 5hydroxytryptamine receptor 4 (HTR4)mediated vasorelaxation, lateral saphenous veins from cattle (n = 4 to 7) were collected and assessed for vasoactivity in response to increasing concentrations of a selective HTR4 agonist (BIMU 8) in the absence and presence of inhibitors selective for downstream proteins involved with cyclic nucleotidemediated signaling.. Vessels were precontracted with 1 × 10−4 M phenylephrine and exposed to increasing HTR4 agonist concentrations.. Vasoactive response data were normalized as a percentage of the maximum contractile response induced by the phenylephrine precontraction.

    Phospho-proteomics:

    Article Title: Mechanism of 5‐Hydroxytryptamine Receptor 4 Mediated Vasorelaxation in the Isolated Bovine Lateral Saphenous Vein
    Article Snippet: To better understand the mechanisms of 5hydroxytryptamine receptor 4 (HTR4)mediated vasorelaxation, lateral saphenous veins from cattle (n = 4 to 7) were collected and assessed for vasoactivity in response to increasing concentrations of a selective HTR4 agonist (BIMU 8) in the absence and presence of inhibitors selective for downstream proteins involved with cyclic nucleotidemediated signaling.. Vessels were precontracted with 1 × 10−4 M phenylephrine and exposed to increasing HTR4 agonist concentrations.. Vasoactive response data were normalized as a percentage of the maximum contractile response induced by the phenylephrine precontraction.

    other:

    Article Title: Dopamine increases protein synthesis in hippocampal neurons enabling dopamine-dependent LTP
    Article Snippet: The following drugs were used in this study: 100 μM dopamine hydrochloride (Sigma- Aldrich, Dorset, United Kingdom), 10 μM CHX (Tocris Bioscience), 0.5 mM AM (stock solution in EtOH; Tocris Bioscience), 1 μM PKA inhibitor fragment (6- 22) amide (Tocris Bioscience), 100 μM 1- naphthyl acetyl spermine trihydrochloride (NASPM trihydrochloride; Tocris Bioscience), 10 μM N,N,H,-trimethyl- 5-[(tricyclo[3.3.1.13,7]dec- 1- ylmethyl) amino]–1- pentanaminiumbromide hydrobromide (IEM1460; Tocris Bioscience).

    Article Title: Atypical Protein Kinase C Is a Novel Mediator of Dopamine-Enhanced Firing in Nucleus Accumbens Neurons
    Article Snippet: PKA inhibitor fragment (6 –22) amide (PKI) was from Tocris Cookson (Ballwin, MO).



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    GPR35 attenuates inflammatory response in macrophages through the <t>Gαs-cAMP-PKA</t> pathway. ( A ) Co-IP detection of GPR35 and Gαs in peritoneal macrophages stimulated with or without KA. ( B ) Levels of cAMP in peritoneal macrophages pretreated with FSK, KA, or DSCG. GPR35 agonist KA (4 mM), or DSCG (200 µg/ml) was administered 1 h before treatment with LPS. Adenylate cyclase activator FSK (10 µM) was used to stimulate cAMP in peritoneal macrophages 1 h before treatment with LPS. ( C ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages after stimulation with LPS in the presence of FSK, KA, or DSCG. ( D ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. ( E ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. <t>Gαs</t> <t>inhibitor</t> NF449, AC inhibitor SQ22536, or PKA inhibitor H89 was added to the culture 30 min before treatment with GPR35 agonist KA or DSCG. The data are representative of three independent experiments and shown as the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001
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    GPR35 attenuates inflammatory response in macrophages through the <t>Gαs-cAMP-PKA</t> pathway. ( A ) Co-IP detection of GPR35 and Gαs in peritoneal macrophages stimulated with or without KA. ( B ) Levels of cAMP in peritoneal macrophages pretreated with FSK, KA, or DSCG. GPR35 agonist KA (4 mM), or DSCG (200 µg/ml) was administered 1 h before treatment with LPS. Adenylate cyclase activator FSK (10 µM) was used to stimulate cAMP in peritoneal macrophages 1 h before treatment with LPS. ( C ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages after stimulation with LPS in the presence of FSK, KA, or DSCG. ( D ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. ( E ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. <t>Gαs</t> <t>inhibitor</t> NF449, AC inhibitor SQ22536, or PKA inhibitor H89 was added to the culture 30 min before treatment with GPR35 agonist KA or DSCG. The data are representative of three independent experiments and shown as the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001
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    GPR35 attenuates inflammatory response in macrophages through the <t>Gαs-cAMP-PKA</t> pathway. ( A ) Co-IP detection of GPR35 and Gαs in peritoneal macrophages stimulated with or without KA. ( B ) Levels of cAMP in peritoneal macrophages pretreated with FSK, KA, or DSCG. GPR35 agonist KA (4 mM), or DSCG (200 µg/ml) was administered 1 h before treatment with LPS. Adenylate cyclase activator FSK (10 µM) was used to stimulate cAMP in peritoneal macrophages 1 h before treatment with LPS. ( C ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages after stimulation with LPS in the presence of FSK, KA, or DSCG. ( D ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. ( E ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. <t>Gαs</t> <t>inhibitor</t> NF449, AC inhibitor SQ22536, or PKA inhibitor H89 was added to the culture 30 min before treatment with GPR35 agonist KA or DSCG. The data are representative of three independent experiments and shown as the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001
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    GPR35 attenuates inflammatory response in macrophages through the <t>Gαs-cAMP-PKA</t> pathway. ( A ) Co-IP detection of GPR35 and Gαs in peritoneal macrophages stimulated with or without KA. ( B ) Levels of cAMP in peritoneal macrophages pretreated with FSK, KA, or DSCG. GPR35 agonist KA (4 mM), or DSCG (200 µg/ml) was administered 1 h before treatment with LPS. Adenylate cyclase activator FSK (10 µM) was used to stimulate cAMP in peritoneal macrophages 1 h before treatment with LPS. ( C ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages after stimulation with LPS in the presence of FSK, KA, or DSCG. ( D ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. ( E ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. <t>Gαs</t> <t>inhibitor</t> NF449, AC inhibitor SQ22536, or PKA inhibitor H89 was added to the culture 30 min before treatment with GPR35 agonist KA or DSCG. The data are representative of three independent experiments and shown as the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001
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    https://www.bioz.com/product/pka+inhibitor+fragment/PKA+Inhibitor+Fragment+(6-22)+amide/pmc11893101-172-32-37
    Average 93 stars, based on 1 article reviews
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    Image Search Results


    GPR35 attenuates inflammatory response in macrophages through the Gαs-cAMP-PKA pathway. ( A ) Co-IP detection of GPR35 and Gαs in peritoneal macrophages stimulated with or without KA. ( B ) Levels of cAMP in peritoneal macrophages pretreated with FSK, KA, or DSCG. GPR35 agonist KA (4 mM), or DSCG (200 µg/ml) was administered 1 h before treatment with LPS. Adenylate cyclase activator FSK (10 µM) was used to stimulate cAMP in peritoneal macrophages 1 h before treatment with LPS. ( C ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages after stimulation with LPS in the presence of FSK, KA, or DSCG. ( D ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. ( E ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. Gαs inhibitor NF449, AC inhibitor SQ22536, or PKA inhibitor H89 was added to the culture 30 min before treatment with GPR35 agonist KA or DSCG. The data are representative of three independent experiments and shown as the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: GPR35 prevents drug-induced liver injury via the Gαs-cAMP-PKA axis in macrophages

    doi: 10.1007/s00018-025-05751-4

    Figure Lengend Snippet: GPR35 attenuates inflammatory response in macrophages through the Gαs-cAMP-PKA pathway. ( A ) Co-IP detection of GPR35 and Gαs in peritoneal macrophages stimulated with or without KA. ( B ) Levels of cAMP in peritoneal macrophages pretreated with FSK, KA, or DSCG. GPR35 agonist KA (4 mM), or DSCG (200 µg/ml) was administered 1 h before treatment with LPS. Adenylate cyclase activator FSK (10 µM) was used to stimulate cAMP in peritoneal macrophages 1 h before treatment with LPS. ( C ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages after stimulation with LPS in the presence of FSK, KA, or DSCG. ( D ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. ( E ) Levels of TNF-α and IL-1β in supernatants from peritoneal macrophages with indicated pretreatment after LPS stimulation. Gαs inhibitor NF449, AC inhibitor SQ22536, or PKA inhibitor H89 was added to the culture 30 min before treatment with GPR35 agonist KA or DSCG. The data are representative of three independent experiments and shown as the mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001

    Article Snippet: To investigate the role of Gαs-cyclic AMP-protein kinase A (Gαs-cAMP-PKA) in the GPR35-mediated effect on macrophages, the Gαs inhibitor NF449 (25 µM, Santa Cruz Biotechnology, TEX, USA), AC inhibitor SQ22536 (50 µM, MedChemExpress, NJ, USA), or PKA inhibitor H89 (10 µM, MedChemExpress, NJ, USA), PKA inhibitor fragment [ – ] amide (10 μm, TargetMol, BOS, USA) was added to the culture 30 min prior to treatment with the GPR35 agonist.

    Techniques: Co-Immunoprecipitation Assay