期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 105, 期 9, 页码 3503-3508出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0707959105
关键词
lymphotoxin-beta receptor; p50; tumor-necrosis factor receptor-associated factor 3 (TRAF3)
资金
- NCI NIH HHS [R01 CA087924, R01 CA87924] Funding Source: Medline
- NIAID NIH HHS [T32 AI007126, AI07126-30, R01 AI056154] Funding Source: Medline
- NIGMS NIH HHS [R01 GM57559, R01 GM057559] Funding Source: Medline
Articles in recent years have described two separate and distinct NF-kappa B activation pathways that result in the differential activation of p50- or p52-containing NF-kappa B complexes. Studies examining tumor-necrosis factor receptor-associated factors (TRAFs) have identified positive roles for TRAF2, TRAF5, and TRAF6, but not TRAF3, in canonical (p50-dependent) NF-kappa B activation. Conversely, it recently was reported that TRAF3 functions as an essential negative regulator of the noncanonical (p52-dependent) NF-kappa B pathway. In this article, we provide evidence that TRAF3 potently suppresses canonical NF-kappa B activation and gene expression in vitro and in vivo. We also demonstrate that deregulation of the canonical NF-kappa B pathway in TRAF3-deficient cells results from accumulation of NF-kappa B-inducing kinase (NIK), the essential kinase mediating noncanonical NF-kappa B activation. Thus, our data demonstrate that inhibition of TRAF3 results in coordinated activation of both NF-kappa B activation pathways.
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