A Bcl-xL Timer Sets Platelet Life Span

Bing Qi; J. Marie Hardwick

doi:10.1016/j.cell.2007.03.002

A Bcl-x_L Timer Sets Platelet Life Span

Bing Qi, J. Marie Hardwick

Bloomberg School of Public Health

Research output: Contribution to journal › Short survey › peer-review

21 Scopus citations

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.

Original language	English (US)
Pages (from-to)	1035-1036
Number of pages	2
Journal	Cell
Volume	128
Issue number	6
DOIs	https://doi.org/10.1016/j.cell.2007.03.002
State	Published - Mar 23 2007

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

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10.1016/j.cell.2007.03.002

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title = "A Bcl-xL Timer Sets Platelet Life Span",

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-xL that cause accelerated death of platelets leading to platelet deficiency.",

author = "Bing Qi and Hardwick, {J. Marie}",

year = "2007",

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AU - Qi, Bing

AU - Hardwick, J. Marie

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N2 - 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-xL that cause accelerated death of platelets leading to platelet deficiency.

AB - 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-xL that cause accelerated death of platelets leading to platelet deficiency.

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M3 - Short survey

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VL - 128

SP - 1035

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JO - Cell

JF - Cell

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A Bcl-x_L Timer Sets Platelet Life Span

Abstract

ASJC Scopus subject areas

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