Comparison of p56lck and p59fyn protein expression in thymocyte subsets, peripheral T cells, NK cells, and lymphoid cell lines
Autor: | M W, Olszowy, P L, Leuchtmann, A, Veillette, A S, Shaw |
---|---|
Rok vydání: | 1995 |
Předmět: |
CD4-Positive T-Lymphocytes
Mice Inbred BALB C Mice SCID CD8-Positive T-Lymphocytes Protein-Tyrosine Kinases Proto-Oncogene Proteins c-fyn Cell Line Killer Cells Natural Mice src-Family Kinases Lymphocyte Specific Protein Tyrosine Kinase p56(lck) T-Lymphocyte Subsets Proto-Oncogene Proteins Tumor Cells Cultured Animals Humans Interleukin-2 Female |
Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 155(9) |
ISSN: | 0022-1767 |
Popis: | The expression of the src-family kinases, p56lck and p59fyn, is critical for thymocyte development and TCR-mediated signal transduction, and may be important for signaling through other lymphoid receptors as well. Overexpression studies have demonstrated that the levels of p56lck and p59fyn expression can affect T cell development and signaling through the TCR. Therefore, it is likely that their exact expression levels play an important role in modulating signaling in thymocytes, mature T cells, and other lymphocytes. Here, we used quantitative immunoblotting to measure p56lck and p59fyn protein expression levels in thymocyte subsets, peripheral T cells, NK cells, and lymphoid cell lines. p59fyn expression levels were similar to p56lck in most cells that were examined demonstrating that p59fyn is abundantly expressed in T cells. In addition, we found that p56lck protein expression is equivalent in CD4 and CD8 double-negative, double-positive, and single-positive thymocytes. In contrast, p59fyn expression levels were significantly lower in double-positive thymocytes than in the other thymocyte subpopulations. Finally, we demonstrate that p56lck and p59fyn expression varies greatly in a number of cell lines used to study T cell activation and that IL-2 treatment can dynamically regulate p56lck and p59fyn expression in some cells. |
Databáze: | OpenAIRE |
Externí odkaz: |