1
The breakdown of phosphatidylserine asymmetry is evidenced by annexin binding, a typical feature of apoptotic cells.
2
Consequences include breakdown of phosphatidylserine asymmetry, which depends at least partially on cellular loss of K+.
3
In nucleated cells cellular taurine is released prior to DNA fragmentation and the breakdown of phosphatidylserine asymmetry within the plasma membrane.
4
Similar to what is seen in nucleated cells, phosphatidylserine asymmetry is also abolished in erythrocytes exposed to osmotic shock or oxidative stress.
5
Erythropoietin binds to erythrocytes and inhibits volume-sensitive erythrocyte cation channels and thus the breakdown of phosphatidylserine asymmetry after activation of this channel.
6
Erythrocyte cell volume was estimated from forward scatter and breakdown of phosphatidylserine asymmetry was identified by determination of annexin binding using FACS analysis.