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Inhibitor of nuclear factor kappa-B kinase-interacting protein (IKBIP)

Target
IKBIP
Molecular classification
Other (adaptor/regulatory protein; not a classical enzyme, receptor, or ion channel)
01

Overview

Inhibitor of nuclear factor kappa-B kinase-interacting protein (IKBIP, also known as IKIP) is an adaptor protein involved in the regulation of cell stress and inflammatory signaling. It acts as a direct target of p53, promoting apoptosis after cellular stress or DNA damage, and is also a negative regulator of the NF-κB pathway, acting by interfering with IKKα/β complex activation[1][3][7]. This dual role positions IKBIP at the crossroads of apoptosis and immune modulation. IKBIP has been implicated as a biomarker of poor prognosis in glioma and is being explored as a potential regulator of epithelial-mesenchymal transition (EMT) in tumors[1]. There are currently no approved drugs that directly target IKBIP; however, research into peptide-based inhibitors suggests it may have future therapeutic relevance in controlling inflammation and tumor progression[1].

Other names
IKBKB interacting proteinIKIPI kappa-B kinase-interacting proteinIKBKB-interacting proteinIKK-interacting proteinFLJ31051I kappa B kinase interacting proteinIKIP_HUMAN
02

Mechanism of action

no known drugs directly targeting IKBIP; research on peptide-based NF-κB pathway inhibition ongoing[1]

03

Biological functions

Immune responseApoptosis (pro-apoptotic role downstream of p53)Negative regulation of NF-κB signalingCellular stress response
04

Disease associations

Cancer (glioma prognosis, pro-apoptotic in certain tumor settings)Inflammation (regulator of inflammatory signaling)Other (linked to Cole-Carpenter Syndrome[3])
05

Biomarkers

Poor glioma prognosis (elevated IKBIP expression predicts poor survival in glioma patients[1])Potential EMT-related marker in glioma[1]

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