Abstract
IκBζ, an atypical member of the nuclear IκB family of proteins, is expressed at low levels in most resting cells, but is induced upon stimulation of Toll-like/IL-1 receptors through an IRAK1/IRAK4/NFκB-dependent pathway. Like its homolog Bcl3, IκBζ can regulate the transcription of a set of inflamatory genes through its association with the p50 or p52 subunits of NF-κB. Long studied as a key component of the immune response, IκBζ emerges as an important regulator of inflammation, cell proliferation and survival. As a result, growing evidence support the role of this transcription factor in the pathogenesis number of human hematological and solid malignancies.
| Original language | English |
|---|---|
| Pages (from-to) | 66310-66322 |
| Number of pages | 13 |
| Journal | Oncotarget |
| Volume | 7 |
| Issue number | 40 |
| DOIs | |
| Publication status | Published - 4 Oct 2016 |
Keywords
- Animals
- Gene Expression Regulation, Neoplastic
- Humans
- I-kappa B Proteins/genetics
- Neoplasms/genetics
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