Rabbit anti-Human Phospho-NFKB1-S932 Polyclonal Antibody

Uniprot Id

P19838

Target Species

Human

Target Name

NFKB1

Target Full Name

Nuclear factor NF-kappa-B p105 subunit

Target Function

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52 and the heterodimeric p65-p50 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.

Target Involvement

Immunodeficiency, common variable, 12 (CVID12)

Target Subcellular Location

Nucleus. Cytoplasm. Note=Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B).

Target Research Area

Apoptosis, Cancer

Target Synonyms

DKFZp686C01211; DNA binding factor KBF1; DNA binding factor KBF1 EBP1; DNA-binding factor KBF1; EBP 1; EBP-1; EBP1; KBF1; MGC54151; nf b; NF kappa B; NF kappaB; NF kappabeta; NF kB1; NF-kappaB; NFkappaB; NFKB 1; NFKB p105; NFKB p50; NFKB-p105; Nfkb1; NFKB1_HUMAN; Nuclear factor kappa B DNA binding subunit; Nuclear factor kappa-B; Nuclear factor kappa-B, subunit 1; Nuclear factor NF kappa B p105 subunit; Nuclear factor NF kappa B p50 subunit; Nuclear factor NF-kappa-B p50 subunit; Nuclear factor of kappa light chain gene enhancer in B cells 1; Nuclear factor of kappa light polypeptide gene enhancer in B cells 1; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1; p105; p50; p84/NF-kappa-B1 p98; Transcription factor NFKB1

Target Background

This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. NFKB is a critical regulator of the immediate-early response to viral infection. Alternative splicing results in multiple transcript variants encoding different isoforms, at least one of which is proteolytically processed.