protein
| interacting with SAV1 (SAV1 can bind to, and be phosphorylated by STK3, and the stabilizing effect of STK3 on SAV1 requires its interaction with SAV1 but is probably not due to phosphorylation of SAV1 by STK3) |
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binding partner of RASSF2 (STK3 and RASSF2 form an active complex, in which RASSF2 is maintained in a phosphorylated state and protects STK3 from degradation and turnover) |
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STK3 and the scaffold protein Salvador (SAV1), directly interact with NEK2 and regulate its ability to localize to centrosomes, and phosphorylate CEP250 and rootletin |
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RASSF1 interacts with and activates STK3/STK4 kinases by preventing their dephosphorylation |
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MST2-mediated phosphorylation of four residues within SAV1 may be important in the induction of cell death by the MST pathway |
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STK3/STK4 timulated the binding of SAV1 to PPARG, a transcription factor that plays a key role in adipogenesis |
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ABL1 is a novel upstream activator of STK3 suggesting that the conserved ABL1-MST signaling cascade plays an important role in oxidative stress-induced neuronal cell death |
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ADRBK1 plays a central role in mitogen-promoted centrosome separation most likely via its ability to phosphorylate STK3 |
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RASSF5 can act as an inhibitor or a potential positive regulator of STK3, depending on whether it binds to STK3 before or after activation-loop phosphorylation |
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physical interaction of BCL2 with SAV1 was correlated with proteasomal degradation of SAV1 and STK3 proteins |