Involved in the negative regulation of lymphocyte motility. It mediates the migration-inhibitory effects of IL6. Serves as a positive regulator of the RhoA signaling pathway. Enhancement of RhoA activation results in inhibition of lymphocyte and lymphoma cell motility by activation of its downstream effector ROCK. Is a regulator of B-cell receptor signaling, that acts through SYK kinase activation. Interacts with ACTB and MYH2; the interaction with MYH2 is increased by IL6-induced phosphorylation. Interacts (via C-terminus) with ARHGEF11 (via DH domain). Interacts with ARHGEF12. Interacts with SYK; the interaction increases after B-cell receptor stimulation, resulting in enhanced SYK autophosphorylation and activity. It relocalizes from the cytoplasm to podosome-like structures upon cell treatment with IL6. Highly expressed in normal germinal center (GC) B-cells. Expressed in spleen and, to a lesser extent, bone marrow. Phosphorylation on tyrosine residues can be induced by IL6. Phosphorylation is mediated by LYN. GCSAM transgenic mice develop B-cell lymphoid hyperplasia, hypergammaglobulinemia and systemic reactive amyloid A (AA) amyloidosis strating from 12 months of age.