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Thymic tumorigenesis induced by overexpression of p56lck
Abstract
The lck gene encodes a membrane-associated protein tyrosine kinase (p56lck) that is believed to participate in lymphocyte-specific signal transduction pathways. To investigate the function of this molecule, transgenic mice were generated carrying the wild-type lck gene or a mutated lck gene encoding a constitutively activated form of p56lck (p56lckF505). Transgene expression in thymocytes was achieved in each case using the lck proximal promoter element. Mice expressing high levels of either p56lckF505 or p56lckY505 reproducibly developed thymic tumors. The sensitivity of thymocytes to p56lck-induced transformation suggests that disturbances in lck expression may contribute to the pathogenesis of some human neoplastic diseases.
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“It is known that excessive activation of Lck such as in the constitutively active Lcktg mice suppresses allelic exclusion at the TCRβ gene locus [28, 29]”
From Overexpression of RhoH Permits to Bypass the Pre-TCR Checkpoint (2015) · cites this paper as [28]
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- [16]Amrein, K. E. & Sefton, B. M. (1988) Proc. Natl. Acad. Sci. USA 85, 4247–4251.
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Cited by
Overexpression of RhoH Permits to Bypass the Pre-TCR Checkpoint
Tamehiro, N., Oda, H., Shirai, M., & Suzuki, H. (2015) · PLOS ONE · doi:10.1371/journal.pone.0131047 · Cited by 14
Metadata
- Authors
- Abraham, K. M., Levin, S. D., Marth, J. D., Forbush, K. A., & Perlmutter, R. M.
- Affiliations
- Howard Hughes Medical Institute, University of Washington, Seattle 98195.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1991-05
- Volume
- 88
- Issue
- 9
- Pages
- 3977-3981
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 126
- References
- 0
- Language
- en
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