These findings demonstrate that Cep131 is a novel substrate of Plk4 and that phosphorylation or dysregulated Cep131 overexpression promotes Plk4 stabilization and therefore centrosome amplification establishing a perspective in understanding a relationship between centrosome amplification and cancer development.
Analysis of the data suggested that SP1 is a pivotal transcription factor for the regulation of CEP131 expression consequently leading the control of centrosome functions.
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