TRAF2 plays a key, nonredundant role in LIGHT-lymphotoxin beta receptor signalingстатья

Статья опубликована в высокорейтинговом журнале

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Дата последнего поиска статьи во внешних источниках: 14 сентября 2013 г.

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[1] YS K., SA N., ZG L. Traf2 plays a key, nonredundant role in light-lymphotoxin beta receptor signaling // Molecular and Cellular Biology. — 2005. — Vol. 25, no. 6. — P. 2130–2137. LIGHT is a member of the tumor necrosis factor (TNF) superfamily, and its function is mediated by at least two receptors, including lymphotoxin ���� receptor (LT����R) and herpes simplex virus entry mediator. However, the molecular mechanism of LIGHT signaling mediated by LT����R has not been clearly defined. In this report, we demonstrate that TRAF2 is critical for LIGHT- and LT����R-mediated activation of both the transcription factor NF-����B and the mitogen-activated protein kinase JNK. In HeLa cells, LIGHT induces NF-����B and JNK activation, which can be blocked by the dominant negative mutant of TRAF2. In these cells, LIGHT causes the recruitment of TRAF2, TRAF3, and I����B kinase into the LT����R complex. Importantly, while both NF-����B and JNK are activated by LIGHT in wild-type mouse embryonic fibroblasts, no activation of either of these two pathways is observed in TRAF2 null fibroblasts. However, LIGHT-induced NF-����B and JNK activation can be restored by ectopic expression of TRAF2 in TRAF2����/���� cells. Interestingly, in contrast to TNF signaling, the activation of both NF-����B and JNK by LIGHT was normal in RIP����/���� and TRAF5����/���� cells. Taken together, our data demonstrate that TRAF2, an important effector molecule of TNF signaling, plays a critical, nonredundant role in LIGHT-LT����R signaling.

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