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Total p38α mapk

Manufactured by Cell Signaling Technology
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Total p38α MAPK is a lab equipment product that measures the total amount of p38α mitogen-activated protein kinase (MAPK) in a sample. p38α MAPK is a protein that plays a crucial role in cellular signaling pathways.

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Lab products found in correlation

Total irak4, by Cell Signaling Technology (2 mentions) Gapdh, by Cell Signaling Technology (2 mentions) Phloretin, by Merck Group (1 mentions) Phospho sapk jnk, by Cell Signaling Technology (1 mentions) Total sapk jnk, by Cell Signaling Technology (1 mentions) Sb203580, by Merck Group (1 mentions) Total erk1 2, by Cell Signaling Technology (1 mentions) Anti β actin antibody, by Merck Group (1 mentions) Cell culture medium and supplements, by Thermo Fisher Scientific (1 mentions) Ara a, by Merck Group (1 mentions) Phospho p38α mapk, by Cell Signaling Technology (1 mentions) Phospho erk1 2, by Cell Signaling Technology (1 mentions) Pd98059, by Merck Group (1 mentions) Sp600125, by Merck Group (1 mentions) Phospho creb, by Cell Signaling Technology (1 mentions) Phospho atf2, by Cell Signaling Technology (1 mentions) Phospho msk1, by Cell Signaling Technology (1 mentions) Total creb, by Cell Signaling Technology (1 mentions) Total msk1, by Cell Signaling Technology (1 mentions) Calf serum, by Thermo Fisher Scientific (1 mentions)

4 protocols using total p38α mapk

1

AMPK Signaling Pathway Regulation

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Cell culture medium and supplements were purchased from GIBCO-BRL (Rockville, MD, USA). Phloretin, the AMPK inhibitor ara-A, the MEK inhibitor PD98059, the JNK inhibitor SP600125, the p38 inhibitor SB203580, and the anti-β actin antibody were purchased from Sigma–Aldrich (St. Louis, MO, USA). Antibodies against phospho-AMPKα (Thr172), total AMPKα, phospho-ERK1/2, total-ERK1/2, phospho-SAPK/JNK, total-SAPK/JNK, phospho-p38α MAPK, and total-p38α MAPK were purchased from Cell Signaling Technology (Beverly, MA, USA).
Takeno A., Kanazawa I., Notsu M., Tanaka K.I, & Sugimoto T. (2018). Phloretin Promotes Adipogenesis via Mitogen-Activated Protein Kinase Pathways in Mouse Marrow Stromal ST2 Cells. International Journal of Molecular Sciences, 19(6), 1772.
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2

Antibodies for Signaling Pathway Analysis

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Antibodies recognizing p105/NFκB1 phosphorylated at Ser933, p38α MAPK phosphorylated at its Thr-Gly-Tyr motif, total p38α MAPK, total IRAK4 and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were from Cell Signalling Technology. An antibody recognizing IRAK4 phosphorylated at both Thr345 and Ser346 was provided by Vikram Rao, Pfizer Inc. (31 (link)). An antibody recognizing JNKs phosphorylated at their Thr-Pro-Tyr motif was from Invitrogen, and a rabbit secondary antibody conjugated to horseradish peroxidase (HRP) was from Pierce.
Nanda S.K., Lopez-Pelaez M., Arthur J.S., Marchesi F, & Cohen P. (2016). Suppression of IRAK1 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding–Defective Mutant of ABIN1. The Journal of Immunology Author Choice, 197(11), 4266-4273.
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3

Signaling Pathway Activation Analysis

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Chemical reagents, including arsenic trioxide (As2O3) and basal medium eagle (BME) were purchased from Sigma-Aldrich (St. Louis, MO). Calf serum (CS) was from GIBCO (Grand Island, NY). The prestained protein marker and protease inhibitor cocktail were from GenDEPOT (Barker, TX). Antibodies against phospho-p38 MAPK, total p38α MAPK, phospho-MSK1, total MSK1, phospho-CREB, total CREB, phospho-ATF2 and total ATF2 were from Cell Signaling Technology, Inc. (Beverly, MA).
Kim H.G., Shi C., Bode A.M, & Dong Z. (2015). p38α MAPK is required for arsenic-induced cell transformation. Molecular carcinogenesis, 55(5), 910-917.
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4

Antibody Validation for Signaling Proteins

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Abs recognizing p105/NFκB1 phosphorylated at Ser933, p38α MAPK phosphorylated at its Thr-Gly-Tyr motif, total p38α MAPK, total IRAK4, and GAPDH were from Cell Signaling Technology. An Ab recognizing IRAK4 phosphorylated at Thr345 and Ser346 was provided by V. Rao (Pfizer) (31 (link)). An Ab recognizing JNKs phosphorylated at their Thr-Pro-Tyr motif was from Invitrogen, and a rabbit secondary Ab conjugated to HRP was from Pierce.
Nanda S.K., Lopez-Pelaez M., Arthur J.S., Marchesi F, & Cohen P. (2016). Suppression of IRAK1 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding–Defective Mutant of ABIN1. The Journal of Immunology Author Choice, 197(11), 4266-4273.
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