Inhibition of T-cell receptor beta-chain gene rearrangement by overexpression of the non-receptor protein tyrosine kinase p56lck.
作者： S.J. Anderson , K.M. Abraham , T. Nakayama , A. Singer , R.M. Perlmutter
DOI: 10.1002/J.1460-2075.1992.TB05594.X
关键词:
摘要: The variable region genes of the T cell receptor (TCR) alpha and beta chains are assembled by somatic recombination separate germline elements. During thymocyte development, gene rearrangements display both an ordered progression, with chain formation preceding chain, allelic exclusion, each containing a single functional rearrangement. Although considerable evidence supports view that individual loci regulated independently, signaling molecules may participate in controlling TCR remain unidentified. Here we report lymphocyte-specific protein tyrosine kinase p56lck, when overexpressed developing thymocytes, provokes reduction V beta--D rearrangement while permitting normal juxtaposition other segments. Our data support model which p56lck activity impinges upon process ordinarily permits exclusion at beta-chain locus.
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