Fig. 5: LLPS regulates immune cell alterations during adaptive immunity.
From: Liquid‒liquid phase separation: a potentially fundamental mechanism of sepsis

SLP65 drives tripartite LLPS, forms droplets with CIN85 and SUVs, and activates BCR signalling pathways. Tripartite LLPS requires the interaction between the CIN85 SH3 domain and SLP65 proline-rich motifs and the preference of the lipid-binding domain for high-membrane-curvature SUVs. LAT phosphorylation drives LLPS and forms macromolecule condensates with Grb2 and SOS to trigger TCR signalling pathways. This figure was created with BioRender.com.