NFkB p100 Recombinant Rabbit Monoclonal Antibody [JM82-03] (ET1705-45)

UNIPROT #

Q00653

PROTEIN NAME

NFkB p100

SYNONYMS

CVID10 antibody;DNA binding factor KBF2 antibody;H2TF1 antibody;Lymphocyte translocation chromosome 10 protein antibody;LYT 10 antibody;NF kB2 antibody;NFKB p52/p100 subunit antibody;Nuclear factor Kappa B subunit 2 antibody;Nuclear factor of kappa light polypeptide gene enhancer in B cells 2 (p49/p100) antibody;Nuclear factor of kappa light polypeptide gene enhancer in B cells 2 antibody;Oncogene Lyt 10 antibody;p100 antibody;Transcription factor NFKB2 antibody

POST-TRANSLATIONAL MODIFICATION

While translation occurs, the particular unfolded structure after the GRR repeat promotes the generation of p52 making it an acceptable substrate for the proteasome. This process is known as cotranslational processing. The processed form is active and the unprocessed form acts as an inhibitor (I kappa B-like), being able to form cytosolic complexes with NF-kappa B, trapping it in the cytoplasm. Complete folding of the region downstream of the GRR repeat precludes processing.; Subsequent to MAP3K14-dependent serine phosphorylation, p100 polyubiquitination occurs then triggering its proteasome-dependent processing.; Constitutive processing is tightly suppressed by its C-terminal processing inhibitory domain, named PID, which contains the death domain.

SUBCELLULAR LOCATION

Cytoplasm. Nucleus.

FUNCTION

Nuclear factor NF-kappa-B p100 subunit is a protein that in humans is encoded by the NFKB2 gene. NF-κB has been detected in numerous cell types that express cytokines, chemokines, growth factors, cell adhesion molecules, and some acute phase proteins in health and in various disease states. NF-κB is activated by a wide variety of stimuli such as cytokines, oxidant-free radicals, inhaled particles, ultraviolet irradiation, and bacterial or viral products. Inappropriate activation of NF-kappa-B has been linked to inflammatory events associated with autoimmune arthritis, asthma, septic shock, lung fibrosis, glomerulonephritis, atherosclerosis, and AIDS. In contrast, complete and persistent inhibition of NF-kappa-B has been linked directly to apoptosis, inappropriate immune cell development, and delayed cell growth.