Overexpression of NFkB (p65) stabilizes cell lines

NFkB is composed of five homodimers, NFkB1 (p50), NFkB2 (p52), RelA (p65), RelB, and c-Rel (Rel), from the Rel family. The main RelA (p65)/p50 dimer is free in the cytoplasmic matrix that is not stimulated by IKBs. Signal induction leads to dissociation and degradation of IkB, and activates NFkB complexes. The activated NFkB complex transfers to the nucleus, binds to the DNA kB binding motif, and then initiates transcription of the target gene. NFKB plays an important role in many biological processes, such as differentiation, proliferation, and apoptosis. The dysfunction of NFkB can cause many diseases, such as inflammation and cancer. The overexpression of NFkB (P65) in Signosis stabilizes the COS-7 cell line and can be effectively used for studying the NFkB pathway.
A. Advantages:
Continuous stability - wild-type p65 protein is stably expressed in cells to avoid experimental differences;
Save time - cell lines can be immediately used to study the p65 signaling pathway;
B. Principle:
The cell line was established by transfection with NFkB (p65) CMV myc tag expression vector. The expression vector is labeled with a hygromycin screening marker, and the resistant clones to hygromycin are screened using NFkB (p65) and myc tag expression. Clones with high expression are selected and propagated into cell lines.