A PROTEIN that prevents cell death can switch roles and become an
executioner, says a report in last week’s Science (vol 278, p
1966).
Injured cells commit suicide in a process called apoptosis. Faulty apoptosis
has been implicated in cancer and other diseases.
A membrane protein called Bcl-2 inhibits apoptosis. Marie Hardwick of Johns
Hopkins Medical Institutions in Baltimore decided to investigate what happens
when Bcl-2 is cleaved by caspase, an enzyme that causes apoptosis.
Hardwick thought caspase would merely remove Bcl-2’s inhibitory effect. But
surprisingly, Bcl-2’s cleaved products themselves acted as killers. “The cells
died remarkably quickly,” she says.
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The protein fragments also stimulated more caspase activity, creating a
deadly feedback loop. Hardwick hopes to find out how this interaction kills
cells.
