NFKB2 Antibodies

Nuclear factor NF-kappa-B p100 subunit (NFKB2)

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 a lot of biological processes such as inflammation, immunity, differentiation, cell development, tumorigenesis and apoptosis. 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 websites 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 different cofactors or corepressors.

Gene Information

Human
Gene Name:	NFKB2
Uniprot:	Q00653
Entrez:	4791

Family

Belongs to:
No superfamily

Alternative Names

LYT10; NFkB2; NF-kB2

Molecular Weight

Mass (kDA):
96.749 kDA

Genomic Context

Human
Location:	10q24.32
Sequence:	10; NC_000010.11 (102394110..102402529)

Subcellular Localizations

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

Diseases

• Malignant Neoplasms
• Neoplasms
• Inflammation
• Leukemia
• Lymphoma
• Chromosomal Translocation
• Leukemogenesis
• Multiple Myeloma
• B-cell Lymphomas
• Immunologic Deficiency Syndromes
• Tissue Adhesions
• Cell Transformation, Neoplastic
• Hiv Infections

• Leukemia, T-cell
• Lymphoid Leukemia
• Malignant Neoplasm Of Breast
• Mammary Neoplasms
• Chronic Lymphocytic Leukemia
• Adult T-cell Lymphoma/leukemia
• Acute Lymphocytic Leukemia

Interacting Proteins

• MAP3K8
• NFKB1
• NFKBIA
• REL
• RELB

• SUMO1

Pathways

• Pathogenesis
• Immune Response
• Localization
• Cell Proliferation
• Cell Death
• Rna Interference
• Cell Adhesion
• Cell Differentiation
• Angiogenesis
• Response To Lipopolysaccharide
• Inflammatory Response
• Chemotaxis
• Lymphocyte Proliferation

• Dna Repair
• Organ Development
• Cell Growth
• Secretion
• Transport
• Osteoclast Differentiation
• Dna Integration

PTMs

• Phosphorylation
• Cleavage

• Glycosylation
• Acetylation

• Ubiquitination

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/NFKB2

Best Uses Of The NFKB2 Marker

This antibody can detect NFKB2/IL-33. Boster produces high-affinity, primary antibodies that have been well-cited by the research community for more than 25 years. They are validated in Western Blotting, Immunohistochemistry, and ELISA. Read on to discover the best use of Boster's NFKB2 antibody.

IL-33 is a proinflammatory cell cytokine

IL-33 is a member the family of cytokines. It is released during a variety events including tissue damage and cell death. Its primary function it to activate the immune systems to respond to disruptions. IL-33, which is also upregulated in mouse brains, has been implicated with inflammatory bowel disease, allergic reaction, and parasitic infection.

IL-33 is a potent activator and is produced by innate immune cell. It promotes survival of eosinophils, and increases the production IL-8 and IL-17/22. It also prevents CXCR2 deregulation and inhibits TLR4-induced Chemotaxis.

IL-33 has been implicated for several respiratory disorders including allergic airway inflammation. Blocking the IL-33/ST2 axis causes severe impairment of lung function and reduced tissue remodeling in mice. Intranasal IL-33 could play a role after viral infections in the physiological remodeling and repair of the lungs. Numerous studies have also shown that IL-33 is a factor in pulmonary fibrosis.

Although it is not known what role IL-33 has in allergies and innate immune system, it was found in a variety tissue types, including adipocytes. IL-33 acts as a transcriptional regulator, in addition to its proinflammatory effects. Although it was initially thought that this protein was restricted to certain cell types, recent studies have shown its widespread presence in the body.

IL-33 is a proinflammatory antiinflammatorin that exhibits enigmatic nuclear localization, chromatin binding activity, and enigmatic nuclear localization. IL-33's overexpression does not cause any changes in gene expression, despite its low mobility in the nucleus. IL-333 has a shorter intranuclear time-live than IL-1a and is therefore more mobile. IL-33 has a linear release following membrane dissolution and the release of histones.

Studies have shown that IL33 induces a change in ST2's conformation and dimerizes a pair of proteins that activate MyD88's downstream signaling pathway. IL-33 can also be used to stimulate the synthesis and release of multiple cytokines from TH2 cell-related tissues. It is also a 17.9-kDa-protein found in murine D10S cell. It has a specific activity level of 2 x107 units/mg.

Among all the alarmins, IL-33 is notable for its ability to inhibit proinflammatory macrophage differentiation. Transplants without this cell cytokine showed increased infiltration of proinflammatory microphages and graft losses. IL33-expressing heart grafts demonstrated a high degree phenotype, increased metabolic reprograming, decreased infiltration of proinflammatory macules, and a high level of reparative phenotype.

While the effects of IL33 have been examined on innate immunity cell cells, further studies are required to determine the role of IL33 in innate immune reactions. The findings of this study highlight the need for future research. Future research should take into account differences in protein production or degradation. WT IL33 has a higher potency than its mature, enzymatically produced form.