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pka rii  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology pka rii
    Pka Rii, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    pka rii - by Bioz Stars, 2026-01
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA <t>RIIα,</t> or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA <t>RIIα,</t> or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA <t>RIIα,</t> or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA <t>RIIα,</t> or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA <t>RIIα,</t> or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.
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    2011 pka rii α santa cruz biotech sc  (Santa Cruz Biotechnology)
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA <t>RIIα,</t> or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA <t>RIIα,</t> or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.
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    SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA RIIα, or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.

    Journal: Journal of Virology

    Article Title: Small Hepatitis B Virus Surface Antigen Promotes Hepatic Gluconeogenesis via Enhancing Glucagon/cAMP/Protein Kinase A/CREB Signaling

    doi: 10.1128/jvi.01020-22

    Figure Lengend Snippet: SHBs elevates cAMP levels by regulating AC. (A) cAMP levels in the liver of LSL-SHBs and LSL-SHBs/Alb-Cre mice fasted for 16 h ( n = 6 to 7 mice/group). (B to E) Effect of AC inhibitor SQ22536 or PDE inhibitor IBMX on cAMP levels (B), glucose production (C), gluconeogenic gene expression (D), CREB phosphorylation, and PKA activity (E) in Ad-SHBs-infected mouse primary hepatocytes and in Huh7-SHBs cells. Cells were treated with SQ22536 (500 μM) or IBMX (500 μM) for 1 h and then with glucagon (100 nM) stimulation or FSK (10 μM) for 15 min (B), 6 h (C), 2 h (D) and 30 min (E). (F) Huh7 cells were transfected with pcDNA 3.1-SHBs-Flag for 48 h, and then co-IP assays were performed to determine the interaction between SHBs and PKA subunits. The immunoprecipitated complexes with anti-Flag antibody were subjected to immunoblotting with PKA Cα, PKA RIα/β, PKA RIIα, or PKA RIIβ antibody. The glycosylated (gp) and nonglycosylated (p) forms of SHBs were indicated. Arrowhead points to phospho-CREB. Data are presented as means ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significant difference.

    Article Snippet: The primary antibodies used in this studies included anti-Flag (F1804; Sigma-Aldrich), anti-SHBs (DMABT-51328MH; Creative-Diagnostics, Shirley, NY), anti-CREB (9197S; Cell Signaling Technology [CST], Beverly, MA), anti-phospho-CREB (9198S; CST), anti-phospho-PKA substrate (9624S; CST), anti-PKA Cα (4782S; CST), anti-PKA RIα/β (3927; CST), anti-β-Actin (3700; CST), anti-PKA RIIα (MAB8000; R&D Systems, Minneapolis, MN), anti-PKA RIIβ (PAB18374; Abnova Inc., Walnut, CA), and anti-AC1 (LS-C314759; LifeSpan Biosciences, Seattle, WA).

    Techniques: Gene Expression, Phospho-proteomics, Activity Assay, Infection, Transfection, Co-Immunoprecipitation Assay, Immunoprecipitation, Western Blot