For IHC: Use at an assay dependent dilution. For IP: Use at an assay dependent dilution. For WB: Use at an assay dependent dilution. Optimal dilutions/concentrations should be determined by the researcher.
NFkB p52 (C20) DB036 reacts with NFkB p52 and p100 of mouse, rat, and human origin.
Phosphate-buffered saline containing 0.1% sodium azide and 0.2% gelatin
Store as concentrated solution. Centrifuge briefly prior to opening vial. Store at 4ºC. DO NOT FREEZE.
0.2 mg/ml (Please refer to the vial label for the specific concentration.)
Synthetic peptide (Mouse) (C terminal).
For laboratory use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
In resting cells, NFkB is retained in the cytoplasm bound to inhibitory proteins of the IkB family. Degradation of IkB proteins occurs with cell activation, via of variety of signals, including inflammatory cytokines and bacterial lipopolysaccharides (LPS) as well as oxidative and fluid mechanical stress. This results in nuclear translocation of NFkB and the transcriptional gene activation of pro-inflammatory genes (1,9). NFkB plays a role in the development of numerous pathological states. Activation of NFkB induces gene programs leading to transcription of factors that promote inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines. It is also thought that there are some substances with possible anti-inflammatory effects that are also NFkappaB regulated. There is some evidence indicating NFkB as a key factor in the pathophysiology of cardiac ischemia-reperfusion injury as well as the development of insulin dependent Diabetes Mellitus (3-4).