| First Author | Molina TJ | Year | 1992 |
| Journal | Nature | Volume | 357 |
| Issue | 6374 | Pages | 161-4 |
| PubMed ID | 1579166 | Mgi Jnum | J:1119 |
| Mgi Id | MGI:49651 | Doi | 10.1038/357161a0 |
| Citation | Molina TJ, et al. (1992) Profound block in thymocyte development in mice lacking p56lck [see comments]. Nature 357(6374):161-4 |
| abstractText | The protein Lck (p56lck) has a relative molecular mass of 56,000 and belongs to the Src family of tyrosine kinases. It is expressed exclusively in lymphoid cells, predominantly in thymocytes and peripheral T cells. Lck associates specifically with the cytoplasmic domains of both CD4 and CD8 T-cell surface glycoproteins and interacts with the beta-chain of the interleukin-2 receptor, which implicates Lck activity in signal transduction during thymocyte ontogeny and activation of mature T cells. Here we generate an lck null mutation by homologous recombination in embryonic stem cells to evaluate the role of p56lck in T-cell development and activation. Lck-deficient mice show a pronounced thymic atrophy, with a dramatic reduction in the double-positive (CD4+CD8+) thymocyte population. Mature, single-positive thymocytes are not detectable in these mice and there are only very few peripheral T cells. These results illustrate the crucial role of this T-cell-specific tyrosine kinase in the thymocyte development. |
