Antibodies against p p65 and p65

Manufactured by Cell Signaling Technology

Antibodies against p-P65 and P65 are lab equipment products offered by Cell Signaling Technology. These antibodies are designed to detect the phosphorylated and non-phosphorylated forms of the NF-κB subunit p65 (also known as RelA). They can be used in various applications such as Western blotting, immunohistochemistry, and immunocytochemistry to study the activation and regulation of the NF-κB signaling pathway.

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Lab products found in correlation

Horseradish peroxidase hrp conjugated secondary antibody, by Santa Cruz Biotechnology (2 mentions) Sulforaphane sf, by Santa Cruz Biotechnology (2 mentions) 8 oxo dg antibody, by Bio-Techne (2 mentions) Hmvec l, by Lonza (1 mentions) H1299, by American Type Culture Collection (1 mentions) Gentamycin, by Thermo Fisher Scientific (1 mentions) Bronchial epithelial growth medium (begm), by Lonza (1 mentions) Alexa fluor 488 conjugated secondary antibody, by Thermo Fisher Scientific (1 mentions) Bixin, by Merck Group (1 mentions) Sodium arsenite as 3, by Merck Group (1 mentions) Primary antibodies against nrf2, by Santa Cruz Biotechnology (1 mentions) Normal human bronchial epithelial cells nhbe, by Lonza (1 mentions) Cycloheximide (chx), by Merck Group (1 mentions) Mg132, by Merck Group (1 mentions)

Spelling variants of this product

Antibodies against p65 (7 citations) P65 and P-p65 (2 citations) P65 antibodies (2 citations)

2 protocols using antibodies against p p65 and p65

Nrf2 Activation Pathway Analysis

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Bixin, tBHQ, and sodium arsenite (As(III)) were purchased from Sigma, and sulforaphane (SF) was from Santa Cruz. Primary antibodies against NRF2, KEAP1, GCLM, HO-1, GAPDH, and the hemagglutinin (HA) epitope, as well as horseradish peroxidase (HRP)-conjugated secondary antibodies were from Santa Cruz. Antibodies against p-P65 and P65 were from Cell Signaling, and the 8-oxo-dG antibody was from Trevigen. The Alexa Fluor 488-conjugated secondary antibody was from Invitrogen. The human non-small cell carcinoma H1299 cells were purchased from ATCC and were grown in RPMI 1640 medium supplemented with 10% FBS (Atlanta Biological) and 0.1% gentamycin (Invitrogen). Normal human bronchial epithelial cells (NHBE) and normal lung microvascular endothelial cells (HMVEC-L) were purchased from Lonza and were grown in Bronchial Epithelial Growth Medium (BEGM, Lonza) and Endothelial Cell Growth Medium (EGM, Lonza), respectively, according to the supplier’s instructions. All cells were maintained at 37 °C in a humidified incubator containing 5% CO₂.

Tao S., Rojo de la Vega M., Quijada H., Wondrak G.T., Wang T., Garcia J.G, & Zhang D.D. (2016). Bixin protects mice against ventilation-induced lung injury in an NRF2-dependent manner. Scientific Reports, 6, 18760.

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Oxidative Stress Regulation in Keratinocytes

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Bixin was purchased from Spectrum (New Brunswick, NJ); sodium arsenite (As), cycloheximide, and MG132 were from Sigma (St. Louis, MO); sulforaphane (SF) was purchased from Santa Cruz (Santa Cruz, CA); primary antibodies against NRF2, KEAP1, GCLM, AKR1C1, NQO1, AKR1C2, HO-1, TrxR, FTH (heavy), MMP9, Ki67, and GAPDH, as well as horseradish peroxidase (HRP)-conjugated secondary antibodies were purchased from Santa Cruz. Antibodies against p-P65 and P65 were purchased from Cell Signaling. The anti-Thymine Dimer (H3) CPD antibody was purchased from Novus (Littleton, CO). The hemagglutinin (HA) epitope antibody was purchased from Covance (Branford, CT). The 8-oxo-dG antibody was purchased from Trevigen (Gaithersburg, MD). Human immortalized HaCaT keratinocytes were grown in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum and 0.1% gentamycin, and primary human epidermal keratinocytes [adult HEKa (C-005-5C)] were cultured on collagen matrix protein-coated dishes using Epilife medium (EDGS growth supplement; Life Technologies, Carlsbad, CA).

Tao S., Park S.L., de la Vega M.R., Zhang D.D, & Wondrak G.T. (2015). Systemic administration of the apocarotenoid bixin protects skin against solar UV-induced damage through activation of NRF2. Free radical biology & medicine, 89, 690-700.

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