Mst1 and Mst2 form heterodimers in cells
Mst1/Mst2 heterodimers have low kinase activity compared to homodimers
Mst1/Mst2 heterodimerization is promoted by H-ras via an Erk-dependent mechanism
Mst1−/− cells, which cannot form Mst1/Mst2 heterodimers, resist transformation by H-ras