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 |
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Keywords
- IκB
- Mustard
- NF-κB
- NPR1
- p50
- p65
- U373
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Cell Biology
- Molecular Biology
Cite this
Mustard NPR1, a mammalian IκB homologue inhibits NF-κB activation in human GBM cell lines. / Kesanakurti, Divya; Sareddy, Gangadhara R; Babu, Phanithi Prakash; Kirti, Pulugurtha Bharadwaja.
In: Biochemical and Biophysical Research Communications, Vol. 390, No. 3, 18.12.2009, p. 427-433.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mustard NPR1, a mammalian IκB homologue inhibits NF-κB activation in human GBM cell lines
AU - Kesanakurti, Divya
AU - Sareddy, Gangadhara R
AU - Babu, Phanithi Prakash
AU - Kirti, Pulugurtha Bharadwaja
PY - 2009/12/18
Y1 - 2009/12/18
N2 - 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.
AB - 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.
KW - IκB
KW - Mustard
KW - NF-κB
KW - NPR1
KW - p50
KW - p65
KW - U373
UR - http://www.scopus.com/inward/record.url?scp=70449715125&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70449715125&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2009.09.046
DO - 10.1016/j.bbrc.2009.09.046
M3 - Article
C2 - 19766095
AN - SCOPUS:70449715125
VL - 390
SP - 427
EP - 433
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -