AAMP (Angio-associated migratory cell protein) binds to both the TP-alpha and TP-beta isoforms which arise due to differential splicing of a primary RNA transcript encoded by the TBXA2R (thromboxane A2 receptor) gene. Their association with AAMP is dependent on common (residues 312-328) and unique (residues 366-392 of TP-beta) sequences within the variant carboxyl-terminal domains of TP-alpha and TP-beta. Stimulation of the TPs with U46619, a stable mimetic of thromboxane (TX) A2, leads to a transient dissociation of AAMP from both the TP-alpha nad TP-beta isoforms, coinciding with a transient redistribution of AAMP from its localization in an intracellular fibrous network. Down-regulation of AAMP reduces coronary artery smooth muscle migration, an effect that is further enhanced in the presence of U46619, while VEGF-mediated migration is not affected. AAMP and TXA2 can independently activate RHOA signaling. (Reid et al. 2011).