CRG Symposium 2014“CEP63 deficiency promote p53 dependent microcephaly and reveals a role for the centrosome in meiotic recombination”. Travis H.Stracker
Mutations in human CEP63 centrosome protein cause Seckel syndrome, characterized by growth retardation and microencephaly. In mice deficient for CEP63, which recapitulate the human pathology, cell death seems to be due to the centrosome-based mitotic errors during brain development and microencephaly is completely rescued by p53 deletion.
Social Media
