IRF-2 regulates NF-{kappa}B activity by modulating the subcellular localization of NF-{kappa}B

Journal Article · Fri Jun 06 04:00:00 EDT 2008 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/j.bbrc.2008.03.136· OSTI ID:21143714

Chae, Myounghee; Kim, Kwangsoo ^[1]; Park, Sun-Mi ^[1]; Jang, Ik-Soon ^[1]; Seo, Taegun ^[2]; Kim, Dong-Min; Kim, Il-Chul ^[3]; Lee, Je-Ho ^[4]; Park, Junsoo ^[1]

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1. Korea Basic Science Institute, Gwangju Center, 300, Yongbong-Dong, Book-Ku, Gwangju 500-757 (Korea, Republic of)
2. Department of Life Science, Dongguk University, Seoul 100-715 (Korea, Republic of)
3. 21 Higher Education Center for Bioregulator Research, Chonnam National University, Gwangju 500-757 (Korea, Republic of)
4. Molecular Therapy Research Center, Sungkyunkwan University, Seoul 135-710 (Korea, Republic of)

Nuclear Factor-kappa B (NF-{kappa}B) is a transcription factor essential to the control of cell proliferation, survival, differentiation, immune response, and inflammation. Constitutive NF-{kappa}B activation has been observed in a broad variety of solid tumors and hematological malignancies, which suggests that NF-{kappa}B signaling may perform a critical role in the development of human cancers. Interferon regulatory factor-2 (IRF-2), an antagonistic transcriptional repressor of IRF-1, evidences oncogenic potential, but little is currently known regarding the mechanism underlying the oncogenic activities of IRF-2. In this study, we report that IRF-2 recruits RelA/p65 transcription factors into the nucleus via physical interaction. While the nuclear recruitment of RelA by IRF-2 augments TNF{alpha}-induced NF-{kappa}B dependent transcription, the N-terminal truncated mutant form of IRF-2 inhibits the nuclear localization of RelA, and thus interferes with NF-{kappa}B activation. Furthermore, the knockdown of IRF-2 by IRF-2 siRNA attenuates TNF{alpha}-induced NF-{kappa}B dependent transcription by inhibiting the nuclear localization of RelA. Thus, these results show that IRF-2 regulates NF-{kappa}B activity via the modulation of NF-{kappa}B subcellular localization.

• OSTI ID: 21143714
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 3 Vol. 370; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
CELL PROLIFERATION
INFLAMMATION
INTERFERON
MUTANTS
NEOPLASMS
TRANSCRIPTION
TRANSCRIPTION FACTORS