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Phosphatidylserine

Phosphatidylserine
Phosphatidyl-Serine.png
Components of phosphatidylserines:
Blue, green: variable fatty acid groups
Black: glycerol
Red: phosphate
Purple: serine
Identifiers
ChEBI CHEBI:18303 YesY
ECHA InfoCard 100.029.368
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N  (what is YesYN ?)
Infobox references

Phosphatidylserine (abbreviated Ptd-L-Ser or PS) is a phospholipid and is a component of the cell membrane. It plays a key role in cell cycle signaling, specifically in relationship to apoptosis.

Phosphatidylserine is a phospholipid (more specifically a glycerophospholipid). It consists of two fatty acids attached in ester linkage to the first and second carbon of glycerol and serine attached through a phosphodiester linkage to the third carbon of the glycerol.

Phosphatidylserine coming from plants and phosphatidylserine coming from animals differ in fatty acid composition.

Phosphatidylserine(s) are actively held facing the cytosolic (inner) side of the cell membrane by the enzyme flippase. However, when a cell undergoes apoptosis, phosphatidylserine is no longer restricted to the cytosolic side by flippase. Instead scramblase catalyzes the rapid exchange of phosphatidylserine between the two sides. When the phosphatidylserines flip to the extracellular (outer) surface of the cell, they act as a signal for macrophages to engulf the cells.

Phosphatidylserine plays a role in blood coagulation (also known as clotting). When circulating platelets encounter the site of an injury, collagen and thrombin -mediated activation causes externalization of phosphatidylserine (PS) from the inner membrane layer, where it serves as a pro-coagulant surface. This surface acts to orient coagulation proteases, specifically tissue factor (TF) and factor VII (the tenase complex), facilitating further proteolysis, activation of factor X, and ultimately generating thrombin.

In the coagulation disorder Scott syndrome, the mechanism in platelets for transportation of PS from the inner platelet membrane surface to the outer membrane surface is defective. It is characterized as a mild bleeding disorder stemming from the patient's deficiency in thrombin synthesis.


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