Figure 7.

Schematic diagram of the biological effects attributed to the interaction between HGAL and Grb2 proteins. Grb2 is known to interact with Syk and attenuates its activation by Lyn, leading to decreased BCR-induced intracellular signaling, while promoting cSMAC and immunological synapse formation (left). HGAL directly binds to Syk and increases its kinase activity, leading to enhanced BCR signaling (right). Further, HGAL contributes to faster dynamics of cSMAC formation and increases BCR accumulation in cSMACs. Grb2-HGAL binding counteracts the effects of individual proteins on BCR-induced biochemical signaling while cooperating to regulate cSMAC formation (middle).