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Interleukin-1 receptor-associated kinase 1-binding protein 1 (IRAK1BP1)
- Target
- IRAK1BP1
- Molecular classification
- Signal transduction adaptor protein, Other (not a receptor, enzyme, transporter, channel, or transcription factor; acts as a scaffold/adaptor in immune signaling)
01
Overview
Interleukin-1 receptor-associated kinase 1-binding protein 1 (IRAK1BP1) is a cytoplasmic and nuclear protein that functions as a signaling adaptor in the IRAK1-dependent TNFRSF1A pathway, leading to activation of NF-κB and regulation of cell survival[1][4][7]. IRAK1BP1 modulates the balance between pro- and anti-inflammatory responses by promoting the nuclear translocation of inhibitory p50/p50 NF-κB homodimers over p65/p50 heterodimers, facilitating increased IL-10 (anti-inflammatory cytokine) production and suppressing proinflammatory cytokines such as IL-6[2]. This protein thus serves as an innate immune modulator, supporting the resolution phase of inflammation and contributing to endotoxin (LPS) tolerance in macrophages[2]. While not a classic drug target (enzyme, receptor, channel), it is an emerging candidate for modulation in diseases of excessive or insufficient inflammation, though no specific therapeutics are approved for direct IRAK1BP1 targeting.
- Other names
- AIP70SIMPLActA binding protein 3IRAK1-binding protein 1Interleukin-1 receptor-associated kinase 1 binding protein 1
02
Biological functions
Signal transduction (main effector is the NF-κB pathway)Immune response (modulates innate immune signaling through inflammation resolution)Cell survival (required for cell survival under cytokine stimulation)
03
Disease associations
Inflammation (modulator of pro- and anti-inflammatory responses)Infection (shapes response to immune stimuli such as Toll-like receptor agonists)Other (linked to syndromic disease such as Chung-Jansen Syndrome and Schizophrenia, but these associations are not well defined mechanistically)
04
Safety considerations
No direct therapeutic interventions; but as a central modulator of inflammatory signaling, non-specific inhibition or activation could present risks of immune dysfunction or excessive inflammation[2]
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