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Phosphatidylserine (PS) is a phospholipid component normally confined to the inner leaflet of the plasma membrane in healthy cells due to the action of ATP-dependent flippases[1][3][4]. During apoptosis, caspase-mediated inactivation of flippases and activation of scramblases (such as Xkr8 and TMEM16F) cause PS to translocate to the outer leaflet[2][3][4]. This externalized PS acts as an “eat me” signal recognized by phagocytic cells—including macrophages and dendritic cells—facilitating non-inflammatory clearance of apoptotic cells[2][3][4][5]. Exposed PS is a target for therapies aiming to modulate cell clearance (for example, in cancer), a marker for apoptosis in diagnostics, and also serves as a platform for coagulation on activated platelets[1][4][5]. PS exposure is implicated in diverse diseases, including cancer, infection, and chronic inflammation, where deregulated cell death or defective clearance may occur.
Antibody-dependent cellular cytotoxicity (when targeted by antibodies such as bavituximab) Phagocytosis enhancement (as a recognition signal for clearance by immune cells)
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