LPCAT3 incorporates arachidonic acid into membrane phospholipids, which promotes lipoprotein assembly by enabling triacylgylcerols to cluster in the membrane.
The asymmetric combination of saturated and polyunsaturated acyl chains in phospholipids as typically observed in synapses makes membranes prone to deformation and fission without compromising their impermeability.
Signaling by TAM receptor tyrosine kinases requires the coincident engagement of a TAM ligand with both its receptor and the phospholipid phosphatidylserine.
Inhibition of C. elegans FLD-1 or Human TLCD1/2 prevents saturated fat lipotoxicity by allowing increased levels of membrane phospholipids that contain fluidizing long-chain polyunsaturated fatty acids.
An interaction between the brown fat protein CIDEA and the phospholipid phosphatidic acid is vital for the expansion of intracellular lipid droplets for energy storage.
Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.
Structures of a TMEM16 phospholipid scramblase reveal that its Ca2+-dependent activation entails global conformational changes and how these rearrangements affect the membrane to enable transbilayer lipid transfer.
Unprecedented resolution of the molecular mechanisms of plant membrane protein anchoring involving phospholipids and sterols reveals the control of spatio-temporal segregation into plasma membrane nanodomains.
The amino acids that are necessary for phospholipid scrambling by ANO6/TMEM16F can, via domain swapping, confer scrambling activity to the chloride ion channel ANO1 that normally does not scramble phospholipids.
