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Anti phospho pka c thr197

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Anti-Phospho-PKA C (Thr197) is a monoclonal antibody that recognizes the catalytic subunit of protein kinase A (PKA) when phosphorylated at threonine 197. This antibody can be used to detect the activated form of PKA C subunit.

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Lab products found in correlation

Polyvinylidene fluoride membrane, by Merck Group (2 mentions) Am4300, by Thermo Fisher Scientific (2 mentions) Ecl western blotting protocol, by GE Healthcare (2 mentions) Anti pde10a sab2700582, by Merck Group (2 mentions) Mabs1753, by Merck Group (2 mentions) Mab1598, by Merck Group (2 mentions) Ab34735, by Abcam (2 mentions) Anti satb2, by Abcam (2 mentions) A5060, by Merck Group (2 mentions) Ecl system, by Cytiva (1 mentions) Anti phospho γ h2ax, by Cell Signaling Technology (1 mentions)

Spelling variants of this product

Anti-PKA (9 citations) Anti-phospho-PKA (5 citations) Phospho-PKA C (4 citations) Phospho‐PKA‐C (Thr197) (2 citations)

3 protocols using anti phospho pka c thr197

1

Western Blot Analysis of Protein Samples

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Protein samples were separated on SDS-PAGE gels and then transferred to polyvinylidene fluoride membranes (Millipore). Membranes were processed according to the ECL Western Blotting Protocol (GE Healthcare). Anti-PDE10A (SAB2700582; Sigma-Aldrich), anti-SATB2 (ab34735; Abcam), anti-PTPN2 (MABS1753; Millipore), anti-DNMT3A (3598S; CST), anti-PKA C-α (4782S; CST), anti-Phospho-PKA C (Thr197) (5661S; Cell Signaling Technology), and anti-PSD-95 (MAB1598; Millipore) were used as primary anntibodies at a 1:1,000 dilution. HRP-labeled secondary antibodies were obtained from Cell Signaling Technology (7074S & 7076S) and were used at a dilution of 1:5,000. The antibodies against GAPDH (AM4300; Thermo Fisher) or Actin (A5060; Sigma-Aldrich) were used for loading controls. All Western blot quantifications were performed using ImageJ software. Full Western blotting images are summarized in Supplementary Fig. 15.
Cheng Y., Wang Z.M., Tan W., Wang X., Li Y., Bai B., Li Y., Zhang S.F., Yan H.L., Chen Z.L., Liu C.M., Mi T.W., Xia S., Zhou Z., Liu A., Tang G.B., Liu C., Dai Z.J., Wang Y.Y., Wang H., Wang X., Kang Y., Lin L., Chen Z., Xie N., Sun Q., Xie W., Peng J., Chen D., Teng Z.Q, & Jin P. (2018). Partial loss of psychiatric risk gene miR-137 in mice causes repetitive behavior and impairs sociability and learning via increased Pde10a. Nature neuroscience, 21(12), 1689-1703.
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2

Western Blot Analysis of Protein Samples

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Protein samples were separated on SDS-PAGE gels and then transferred to polyvinylidene fluoride membranes (Millipore). Membranes were processed according to the ECL Western Blotting Protocol (GE Healthcare). Anti-PDE10A (SAB2700582; Sigma-Aldrich), anti-SATB2 (ab34735; Abcam), anti-PTPN2 (MABS1753; Millipore), anti-DNMT3A (3598S; CST), anti-PKA C-α (4782S; CST), anti-Phospho-PKA C (Thr197) (5661S; Cell Signaling Technology), and anti-PSD-95 (MAB1598; Millipore) were used as primary anntibodies at a 1:1,000 dilution. HRP-labeled secondary antibodies were obtained from Cell Signaling Technology (7074S & 7076S) and were used at a dilution of 1:5,000. The antibodies against GAPDH (AM4300; Thermo Fisher) or Actin (A5060; Sigma-Aldrich) were used for loading controls. All Western blot quantifications were performed using ImageJ software. Full Western blotting images are summarized in Supplementary Fig. 15.
Cheng Y., Wang Z.M., Tan W., Wang X., Li Y., Bai B., Li Y., Zhang S.F., Yan H.L., Chen Z.L., Liu C.M., Mi T.W., Xia S., Zhou Z., Liu A., Tang G.B., Liu C., Dai Z.J., Wang Y.Y., Wang H., Wang X., Kang Y., Lin L., Chen Z., Xie N., Sun Q., Xie W., Peng J., Chen D., Teng Z.Q, & Jin P. (2018). Partial loss of psychiatric risk gene miR-137 in mice causes repetitive behavior and impairs sociability and learning via increased Pde10a. Nature neuroscience, 21(12), 1689-1703.
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3

Propranolol Modulates Radiation and Cisplatin-Induced Signaling

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PC9 and A549 cells were pre-incubated with propranolol (50 μM) for 8 h and then treated with either radiation (6 Gy) or cisplatin (0.5 μM). Protein expression analyses were performed 4 h post-treatment for phospho-gamma nucleosome core histone H2A (phospho-γH2AX) and 24 h post-treatment for phopho-protein kinase A (phospho-PKA C). Cell lysates were prepared from with 4 × LDS sample buffer and resolved on SDS-PAGE according to standard protocols. Primary antibodies used included polyclonal anti-phospho-PKA C (Thr197) and anti-phospho-γH2AX (Cell Signaling, Beverly, MA, USA). The secondary antibodies (anti-rabbit or anti-mouse) were conjugated with horseradish peroxidase. Signals were detected using the ECL system (Amersham, Pittsburgh, PA, USA). Using ImageJ software, densitometries of phospho-protein kinase A (p-PKA) and p-γH2AX protein levels were quantified by normalizing over the vinculin, which served as a loading control.
Chaudhary K.R., Yan S.X., Heilbroner S.P., Sonett J.R., Stoopler M.B., Shu C., Halmos B., Wang T.J., Hei T.K, & Cheng S.K. (2019). Effects of β-Adrenergic Antagonists on Chemoradiation Therapy for Locally Advanced Non-Small Cell Lung Cancer. Journal of Clinical Medicine, 8(5), 575.
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