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TRAF2 is essential for JNK but not NF-kappa B activation and regulates lymphocyte proliferation and survival
Author(s): Lee SY, Reichlin A, Santana A, Sokol KA, Nussenzweig MC, Choi Y
Source: IMMUNITY    Volume: 7    Issue: 5    Pages: 703-713    Published: NOV 1997  
Times Cited: 311     References: 69     
Abstract: TRAF2 is believed to mediate the activation of NF-kappa B and JNK induced by the tumor necrosis factor receptor (TNFR) superfamily, which elicits pleiotropic responses in lymphocytes. We have investigated the physiological roles of TRAF2 in these processes by expressing a lymphocyte-specific dominant negative form of TRAF2, thereby blocking this protein's effector function. We find that the TNFR superfamily signals require TRAF2 for activation of JNK but not NF-kappa B. In addition, we show that TRAF2 induces NF-kappa B-independent anti-apoptotic pathways during TNF-induced apoptosis. Inhibition of TRAF2 leads to splenomegaly, lymphadenopathy, and an increased number of B cells. These findings indicate that TRAF2 is involved in the regulation of lymphocyte function and growth in vivo.
Document Type: Article
Language: English
Addresses:
1. ROCKEFELLER UNIV, IMMUNOL LAB, NEW YORK, NY 10021 USA
2. ROCKEFELLER UNIV, LAB MOL IMMUNOL, NEW YORK, NY 10021 USA
3. ROCKEFELLER UNIV, LAB ANIM RES CTR, NEW YORK, NY 10021 USA
4. ROCKEFELLER UNIV, HOWARD HUGHES MED INST, NEW YORK, NY 10021 USA
Publisher: CELL PRESS, 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138
Subject Category: Immunology
IDS Number: YH554
ISSN: 1074-7613
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