Practice question

Phosphatidylserine externalization is tightly regulated apoptotic signature converting silent inner lipid into eat me signal for phagocytes and coagulation cofactor. In viable cells phosphatidylserine restricted inside by flippase ATP11C ATP11A requiring CDC50A chaperone maintaining aminophospholipid gradient preventing thrombin generation and immune recognition. Apoptotic executioner caspases three and seven cleave ATP11C at conserved DEVD site inactivating inward pumping and cleave Xkr8 at C terminus unmasking scramblase activity requiring binding to basigin neuroplastin heterodimer. External PS binds Annexin V calcium dependent manner enabling flow cytometric detection of apoptosis, bridges MFG E8 to integrin alphaVbeta3, engages Tim4 stabilin two and BAI1 receptors initiating engulfment without inflammation. Procoagulant platelets also expose PS via TMEM16F providing scaffold for factors Va Xa tenase prothrombinase amplifying clot formation. Other lipids PC SM remain outside constitutively without signaling role. Mutations causing Scott syndrome impair TMEM16F leading to bleeding diathesis linking lipid topology to immunity hemostasis and therapeutic annexin imaging applications.