Grf40, A Novel Grb2 Family Member, Is Involved in T Cell Signaling through Interaction with SLP-76 and LAT

doi:10.1084/jem.189.9.1383

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J. Exp. Med., Volume 189, Number 9, May 3, 1999 1383-1390

Grf40, A Novel Grb2 Family Member, Is Involved in T Cell Signaling through Interaction with SLP-76 and LAT

By Hiroshi Asada,^* Naoto Ishii,^* Yoshiteru Sasaki,^* Kazuhiro Endo,^* Hirotake Kasai,^* Nobuyuki Tanaka,^* Toshikazu Takeshita,^* Shigeru Tsuchiya, Tasuke Konno,^§ and Kazuo Sugamura^*

From the ^* Department of Microbiology and Immunology, Tohoku University School of Medicine, Sendai 980-8575, Japan; the Department of Pediatric Oncology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; the ^§ Research Institute, Miyagi Cancer Center, Natori 981-1293, Japan; and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Tokyo 101-0062, Japan

We molecularly cloned a new Grb2 family member, named Grf40, containing the common SH3-SH2-SH3 motif. Expression of Grf40is predominant in hematopoietic cells, particularly T cells. Grf40binds to the SH2 domain-containing leukocyte protein of 76 kD(SLP-76) via its SH3 domain more tightly than Grb2. Incidentally,Grf40 binds to linker for activation of T cells (LAT) possiblyvia its SH2 domain. Overexpression of wild-type Grf40 in Jurkatcells induced a significant increase of SLP-76-dependent interleukin(IL)-2 promoter and nuclear factor of activated T cell (NF-AT)activation upon T cell receptor (TCR) stimulation, whereas theCOOH-terminal SH3-deleted Grf40 mutant lacked any recognizableincrease in IL-2 promoter activity. Furthermore, the SH2-deletedGrf40 mutant led to a marked inhibition of these regulatory activities,the effect of which is apparently stronger than that of the SH2-deletedGrb2 mutant. Our data suggest that Grf40 is an adaptor moleculeinvolved in TCR-mediated signaling through a more efficient interactionthan Grb2 with SLP-76 andLAT.

Key words: Grb2 family; SLP-76; T cell receptor signaling; nuclear factor of activated T cells

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