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. 2018 Feb 14;8(2):170253. doi: 10.1098/rsob.170253

Figure 7.

Figure 7.

A proposed network controlling STIL abundance. According to this model, cytoplasmic STIL is degraded by SCF-βTrCP throughout interphase, while centrosome-associated STIL is protected, possibly through CPAP. CDK2 activity antagonizes SCF-βTrCP-mediated STIL degradation and additionally, may cooperate with PLK4 to enhance STIL recruitment to centrioles. During progression through M phase, the combined action of CDK1 and APC/C then results in STIL release from centrioles and cytoplasmic degradation, respectively [39].