PI3K/Akt/mTOR · target hub
NF-kappa-B inhibitor alpha (NFKBIA)
NFKBIA is a PDK1–Akt axis or canonical effector on the PI3K/Akt/mTOR axis. Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL (RELA/p65 and NFKB1/p50) dimers in the cytoplasm by masking their nuclear localization signals. On cellular stimulation by immune and pro-inflammatory responses, becomes phosphorylated promoting ubiquitinat… It is indexed under "Canonical Akt substrates & effectors (selected)" on our pathway page for antibodies, inhibitors, and assay guidance.
| Type / example | Domain / context (brief) |
|---|---|
| Expression context | Tissue/cell-type–dependent expression |
| Rare variants | Sporadic variants—require functional validation |
| Pathway coupling | Co-occurs with neighboring nodes on the hub |
Naming and prevalence vary by cohort and assay—annotate clinically with COSMIC, ClinVar, OncoKB, and datasheets; research context only.
Examples below reflect common literature and public resources (e.g., CCLE, DepMap)—validate genotypes, expression, and passage in your own stocks before committing assays.
Human tissues and primary cells require ethics/IRB approval; tumors are heterogeneous—record histotype, site, and preservation conditions.
Overexpression vs endogenous NFKBIA can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.
Adds NFKBIA keyword bias atop the PI3K/Akt/mTOR antibody pool—if sparse, use presets above or global search.
This content supports research reagents and pathway education—not medical advice. Annotate mutations, drug indications, and protocols with authoritative databases, datasheets, and institutional oversight.
Last reviewed: 2026-05-18
See the PI3K/Akt/mTOR hub for neighboring nodes and assay guidance—cross-check MAPK, RTK, metabolism, and autophagy pages as needed.