Potential tumor suppressor. Seems to be involved in lymphocyte adhesion by linking RAP1A activation upon T-cell receptor or chemokine stimulation to integrin activation. Stimulates lymphocyte polarization and the patch-like distribution of ITGAL/LFA-1, resulting in an enhanced adhesion to ICAM1. Together with RAP1A may participate in regulation of microtubule growth. The association with activated RAP1A is required for directional movement of endothelial cells during wound healing. May be involved in regulation of Ras apoptotic function. The RASSF5-STK4/MST1 complex may mediate HRAS and KRAS induced apoptosis (By similarity). Interacts directly with activated HRAS; a RASSF5-STK4/MST1 complex probably associates with activated HRAS. Interacts with KRAS. Probably interacts with Ras-like GTPases RRAS, MRAS, RAP1B, RAP2A and RALA (By similarity). Interacts with RRAS2 (By similarity). Can self-associate. Interacts with RSSF1 isoform A. The RSSF1 isoform A-RSSF5 heterodimer probably mediates the association of RSSF1 with HRAS (By similarity). Isoform 2 interacts with activated RAP1A and ITGAL/LFA-1. Binds STK4/MST1, inhibiting STK4/MST1 autoactivation (By similarity). Mainly located in the perinuclear region of unstimulated primary T-cells; upon stimulation translocates to the leading edge and colocalizes with ITGAL/LFA-1 in the peripheral zone of the immunological synapse. Localized to growing microtubules in vascular endothelial cells and is dissociated from microtubules by activated RAP1A (By similarity).