IKBKB: A Nuclear Factor NF-kappa-B Inhibitor Kinase Beta as a Drug Target and Biomarker

Target Name: IKBKB

NCBI ID: G3551

IKBKB: A Nuclear Factor NF-kappa-B Inhibitor Kinase Beta as a Drug Target and Biomarker

The nuclear factor kappa B (NF-kappa-B) is a protein that plays a crucial role in regulating various cellular processes. It is a cytoplasmic protein that can be activated by various factors, including stress, infection, and inflammation. The NF-kappa-B signaling pathway is involved in the regulation of inflammation, cell growth, and apoptosis. It is a complex protein that consists of several subunits, including IKBKB (Nuclear factor NF-kappa-B inhibitor kinase beta).

IKBKB is a 14-kDa protein that is located in the nucleotide-binding oligomerization domain (NBD) of the NF-kappa-B signaling pathway. It is a key regulator of the NF-kappa-B signaling pathway and is involved in the inhibition of NF-kappa-B signaling. IKBKB functions by phosphorylation and negative feedback inhibition of NF-kappa-B signaling. It can inhibit the activity of NF-kappa-B-activating enzymes and modulate the activity of NF-kappa-B-inhibitors.

IKBKB has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative diseases, and autoimmune diseases. Its functions in these diseases have been attributed to its role in the regulation of NF-kappa-B signaling.

In cancer, IKBKB has been shown to play a negative role in the regulation of cell growth and apoptosis. It has been shown to inhibit the activity of NF-kappa-B signaling, which can lead to the inhibition of cell proliferation and the initiation of cell apoptosis . Therefore, IKBKB may be a useful target for cancer treatment.

In neurodegenerative diseases, IKBKB has been shown to be involved in the regulation of neuroinflammation and neurodegeneration. It has been shown to modulate the activity of microglial cells, which are a type of immune cell in the central nervous system. Therefore, IKBKB may be a useful target for neurodegenerative diseases.

In autoimmune diseases, IKBKB has been shown to play a negative role in the regulation of immune cell function. It has been shown to inhibit the activity of NF-kappa-B signaling, which can lead to the inhibition of immune cell function and the development of autoimmune diseases. Therefore, IKBKB may be a useful target for autoimmune diseases.

IKBKB has also been shown to have potential therapeutic applications in other diseases, including cardiovascular diseases and chronic obstructive pulmonary diseases (COPD). In cardiovascular diseases, IKBKB has been shown to play a negative role in the regulation of blood pressure and myocardial function. It has been shown to inhibit the activity of NF-kappa-B signaling, which can lead to the inhibition of blood pressure regulation and myocardial function. Therefore, IKBKB may be a useful target for cardiovascular diseases. In COPD, IKBKB has been shown to play a negative role in the regulation of airway inflammation and fibrosis. It has been shown to inhibit the activity of NF-kappa-B signaling, which can lead to the inhibition of airway inflammation and fibrosis. Therefore, IKBKB may be a useful target for COPD.

In conclusion, IKBKB is a 14-kDa protein that is involved in the regulation of various cellular processes, including the NF-kappa-B signaling pathway. It has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative diseases, autoimmune diseases, and cardiovascular diseases. Its functions in these diseases have been attributed to its role in the regulation of NF-kappa-B signaling. Further research is needed to fully understand the role of IKBKB in

Protein Name: Inhibitor Of Nuclear Factor Kappa B Kinase Subunit Beta

Functions: Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses (PubMed:30337470). Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation. Phosphorylates inhibitors of NF-kappa-B on 2 critical serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome. In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis. In addition to the NF-kappa-B inhibitors, phosphorylates several other components of the signaling pathway including NEMO/IKBKG, NF-kappa-B subunits RELA and NFKB1, as well as IKK-related kinases TBK1 and IKBKE (PubMed:11297557, PubMed:20410276). IKK-related kinase phosphorylations may prevent the overproduction of inflammatory mediators since they exert a negative regulation on canonical IKKs. Phosphorylates FOXO3, mediating the TNF-dependent inactivation of this pro-apoptotic transcription factor (PubMed:15084260). Also phosphorylates other substrates including NCOA3, BCL10 and IRS1 (PubMed:17213322). Within the nucleus, acts as an adapter protein for NFKBIA degradation in UV-induced NF-kappa-B activation (PubMed:11297557). Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity). Phosphorylates the C-terminus of IRF5, stimulating IRF5 homodimerization and translocation into the nucleus (PubMed:25326418)

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