Abstract
NF-κB activity is tightly regulated by IκB class of proteins. IκB proteins possess ankyrin repeats for binding to and inhibiting NF-κB. The regulatory protein, NPR1 from Brassica juncea possesses ankyrin repeats with sequence similarity to IκBα subgroup. Therefore, we examined whether stably expressed BjNPR1 could function as IκB in inhibiting NF-κB in human glioblastoma cell lines. We observed that BjNPR1 bound to NF-κB and inhibited its nuclear translocation. Further, BjNPR1 expression down-regulated the NF-κB target genes iNOS, Cox-2, c-Myc and cyclin D1 and reduced the proliferation rate of U373 cells. Finally, BjNPR1 decreased the levels of pERK, pJNK and PKCα and increased the Caspase-3 and Caspase-8 activities. These results suggested that inhibition of NF-κB activation by BjNPR1 can be a promising therapy in NF-κB dependent pathologies.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 427-433 |
| Number of pages | 7 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 390 |
| Issue number | 3 |
| DOIs | |
| State | Published - Dec 18 2009 |
| Externally published | Yes |
Keywords
- IκB
- Mustard
- NF-κB
- NPR1
- U373
- p50
- p65
ASJC Scopus subject areas
- Molecular Biology
- Biophysics
- Biochemistry
- Cell Biology