Target intelligence / Profile preview

NF-kappa-B inhibitor zeta (IκBζ)

Target
IκBζ
Molecular classification
Transcription factor, NF-kappa B family regulatory protein, Nuclear IkappaB protein, Ankyrin-repeat protein
01

Overview

NF-kappa-B inhibitor zeta (IκBζ) is a nuclear regulatory protein encoded by the NFKBIZ gene. It is an atypical member of the IkappaB protein family, characterized by its ankyrin-repeat domains and distinct nuclear localization. IκBζ is induced by inflammatory stimuli such as interleukin-1 and lipopolysaccharide, and regulates the activity of NF-κB transcription factor complexes by directly interacting with p50 and p65 subunits. It can act both as an inhibitor and activator of NF-κB-dependent gene expression. IκBζ is essential for the transcriptional regulation of several cytokines, participates in chromatin remodeling, and its dysregulation is implicated in a range of diseases including autoimmune conditions, cancer (especially certain lymphomas), and psoriasis. The protein exists in several isoforms generated by alternative splicing, with IκBζ(L) being the major physiologically active form[1][3][4][5].

Other names
NFKBIZIKBZINAPMAILmolecule possessing ankyrin repeats induced by lipopolysaccharideIL-1 inducible nuclear ankyrin-repeat proteinnuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor zetaNF-kappa-B inhibitor zeta
02

Mechanism of action

Modulation of NF-kappa B signaling via transcriptional regulation, Inhibition or activation of NF-κB-dependent gene expression through interaction with p50 homodimers and heterodimers, Chromatin remodeling at target gene promoters

03

Biological functions

Regulation of NF-kappa-B transcriptional activityControl of cytokine expressionChromatin remodelingImmune response regulationInflammatory responseRegulation of cell proliferation and apoptosis
04

Disease associations

Cancer (notably diffuse large B-cell lymphoma)PsoriasisAutoimmune diseasesKidney injuryInflammation
05

Safety considerations

Given its central role in regulating inflammation and immune responses, non-specific inhibition or overactivation could broadly disrupt immune homeostasis, potentially leading to immunosuppression or autoimmune phenomena
06

Interacting drugs

Apigenin (reduces expression of IκBζ)

1 more in the full profile.

07

Biomarkers

Overexpression or mutation in DLBCL (diagnostic/prognostic marker)expression changes in inflammatory disorders

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