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A Bcl-xL timer sets platelet life span
1Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.
Abstract:
Platelets are cell fragments lacking nuclei that play a key role in blood clotting. Using an impressive genetic screen involving ENU-mutagenesis of whole mice, Mason et al. (2007) report in this issue their identification of mutations in the antiapoptotic protein Bcl-x(L) that cause accelerated death of platelets leading to platelet deficiency.
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