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Rabbit Anti-NFKB2 Polyclonal Antibody#abs136710

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Description

Catalog-specification	Delivery time	USD price
abs136710-100ug	1-2 Weeks	301.0
abs136710-50ug	1-2 Weeks	201.0

Overview
catalog	abs136710
Description	NFkB is a crucial transcription factor complex involved in inflammation and immune function. It comprises different subunits, including the p100 subunit encoded by this gene. The p100 subunit gets processed to form the active p52 subunit. The NFkB complex can form both homo- or heterodimers with various subunits and binds specific kappa-B elements in target genes. This versatile protein serves as a transcriptional activator or repressor, depending on its dimer partner. Additionally, alternate splicing produces coding and non-coding variants of this gene.
Other names	Transcription factor NFKB2, also known as Nuclear factor of kappa light polypeptide gene enhancer in B cells 2, or NF kB2, is a DNA binding factor that plays a crucial role in cellular processes. This protein, encoded by the CVID10 gene, is also referred to as KBF2, H2TF1, Lymphocyte translocation chromosome 10 protein, LYT 10, or Oncogene Lyt 10. NFKB2 belongs to the nuclear factor kappa B (NF-κB) family of transcription factors. It acts as a subunit, specifically p52 or p100, in the NF-κB complex. This complex plays a significant role in regulating immune responses, inflammation, cell survival, and development. The activation of NF-κB signaling pathway involves the degradation of the inhibitor of kappa B (IκB) proteins, leading to the release and translocation of active NF-κB subunits into the nucleus. In the case of NFKB2, the precursor protein p100 undergoes processing to generate p52, which then translocates into the nucleus to modulate gene expression. NFKB2 is particularly important in B cells, where it regulates the expression of genes involved in B cell development, function, and differentiation. It also has implications in lymphocyte translocation, making it a key player in the immune response. Understanding the functions and mechanisms of NFKB2 and its complex interactions with other proteins and genes is crucial for deciphering the intricate regulatory networks that control various biological processes. Further research in this field will undoubtedly shed light on the therapeutic potential of targeting NFKB2 in human diseases, particularly those associated with dysregulation of the immune system.
Source	Rabbit
Specificity	The total levels of endogenous NFKB2 can be detected using the NFKB2 Antibody.
Species Reactivity	Human;Mouse;Rat
Antigen	NFKB2
Application	，。 WB1：500-1：2000，IF/ICC1：100-1：500，ELISA（）1：20000-1：40000。。
Immunogen	A synthetic peptide of humanNFKB2.
MW	97kDa
Properties
Concentration	1mg/ml
purification	The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin .
Clonality	Polyclonal Antibody
Stability & Storage	Store at -20 °C for one year. Avoid repeated freeze/thaw cycles
Storage buffer	Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt.
Target
Background	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. 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. In a non-canonical activation pathway, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. The NF-kappa-B heterodimeric RelB-p52 complex is a transcriptional activator. The NF-kappa-B p52-p52 homodimer is a transcriptional repressor. NFKB2 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p100 and generation of p52 by a cotranslational processing. The proteasome-mediated process ensures the production of both p52 and p100 and preserves their independent function. p52 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. p52 and p100 are respectively the minor and major form; the processing of p100 being relatively poor. Isoform p49 is a subunit of the NF-kappa-B protein complex, which stimulates the HIV enhancer in synergy with p65. In concert with RELB, regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer.
Posttranslational 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.
Celluar localization	Cytosol;Nucleus;
UniPort	Q00653