7.3 NF-κB

NF-κB
1. NF-κB p65 Is an Important Transcription Factor
NF-κB p65 is a crucial transcription factor. It can activate the regulation of genes involved in inflammation, cell proliferation, cell apoptosis, and other processes, affecting cell apoptosis while influencing the sensitivity of tumor cells to cytotoxic drugs and ionizing radiation.
Additionally, literature reports indicate that NF-κB is activated or expressed in various human tumors, such as breast cancer, non-small cell lung cancer, thyroid cancer, T or B lymphocyte leukemia, and tumors induced by viral mutagenesis. NF-κB can protect cells from apoptosis caused by tumor necrosis factor (TNF), ionizing radiation, and other factors. Inhibiting the expression of NF-κB can increase cell apoptosis induced by TNF and other substances, as well as enhance the sensitivity of tumor cells to chemotherapy and radiotherapy.
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2. NF-κB p65 Undergoes Modifications Including Phosphorylation, Ubiquitination, Acetylation, and Methylation
NF-κB p65 undergoes modifications such as phosphorylation, ubiquitination, acetylation, and methylation, and is localized in both the cytoplasm and nucleus. In the inactive state, p65 is present in the cytoplasm in an inactive form, bound to an inhibitor (IκB). After activation, it translocates into the nucleus and induces the expression of a series of downstream genes.
During Western Blotting (WB) experiments, it is optimal to extract cytoplasmic and nuclear fractions separately, and observe the expression of p65 in different compartments to infer its activation status.