| First Author | Anderson SJ | Year | 1993 |
| Journal | Nature | Volume | 365 |
| Issue | 6446 | Pages | 552-4 |
| PubMed ID | 8413611 | Mgi Jnum | J:76888 |
| Mgi Id | MGI:2180495 | Doi | 10.1038/365552a0 |
| Citation | Anderson SJ, et al. (1993) Protein tyrosine kinase p56lck controls allelic exclusion of T-cell receptor beta-chain genes. Nature 365(6446):552-4 |
| abstractText | During T-cell development, site-specific DNA rearrangements mediating assembly of beta- and alpha-chain genes of the T-cell receptor (TCR) are developmentally ordered. In particular, assembly and expression of a complete beta-chain gene blocks further rearrangements at the beta-locus (a process referred to as allelic exclusion) and drives the generation and expansion of CD4+8+ cells. Although the mechanism used by TCR beta chains to deliver such signals is unknown, studies in transgenic animals have suggested that the lymphocyte-specific protein tyrosine kinase p56lck may impinge on a similar signalling pathway. The hypothesis that TCR beta chains deliver intracellular signals via p56lck makes an explicit prediction: that interference with p56lck function will mitigate the effects of a simultaneously expressed TCR beta chain. Here we confirm this prediction through examination of allelic exclusion in mice expressing both a functional TCR beta chain transgene and a catalytically inactive form of p56lck. |
