期刊论文详细信息
FEBS Letters
Identification of interaction partners of the cytosolic polyproline region of CD95 ligand (CD178) 1
Borkhardt, Arndt4  Thiede, Bernd1  Janssen, Ottmar2  Kabelitz, Dieter2  Plomann, Markus3  Wenzel, Jennifer2  Jing, Qian2  Sanzenbacher, Ralf2  Ghadimi, Markus Philipp2 
[1] Molecular Biology Department, Max-Planck-Institute for Infection Biology, Schumannstraße 21/22, 10117 Berlin, Germany;Institute of Immunology, University Hospital Kiel, Michaelisstr. 5, 24105 Kiel, Germany;Institute for Biochemistry II, University of Cologne, Joseph-Stelzmann-Str. 52, 50931 Cologne, Germany;Hematology and Oncology, Children's University Hospital Giessen, Feulgenstrasse 12, 35392 Giessen, Germany
关键词: CD95L;    CD178;    Signal transduction;    Src homology 3 domain;    T lymphocyte;    aa;    amino acids;    AICD;    activation-induced cell death;    CD95L;    CD95 ligand;    FBP;    formin binding protein;    FCH;    Fes/Fer/CIP4 homology;    GST;    glutathione S-transferase;    MALDI;    matrix-assisted laser desorption ionization;    SH;    Src homology;    TNF;    tumor necrosis factor;   
DOI  :  10.1016/S0014-5793(02)02709-6
学科分类:生物化学/生物物理
来源: John Wiley & Sons Ltd.
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【 摘 要 】

The CD95/Fas/Apo-1 ligand (CD95L, CD178) induces apoptosis through the death receptor CD95. CD95L was also described as a co-stimulatory receptor for T-cell activation in mice in vivo. The molecular basis for the bidirectional signaling capacity and directed expression of CD95L is unknown. In the present study we identify proteins that precipitate from T-cell lysates with constructs containing fragments of the CD95L cytosolic tail. The determined peptide mass fingerprints correspond to Grb2, actin, β-tubulin, formin binding protein 17 (FBP17) and PACSIN2. Grb2 had been identified as a putative mediator of T-cell receptor-to-CD95L signaling before. FBP17 and PACSIN2 may be associated with expression and trafficking of CD95L. When overexpressed, CD95L co-precipitates with FBP17 and PACSIN. Protein–protein interactions are mediated via Src homology 3 (SH3) domain binding to the polyproline region of CD95L and can be abolished by mutation or deletion of the respective SH3 domain.

【 授权许可】

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