An interaction between two brain proteins that leads to abnormal brain development has been identified by researchers at the University of California, San Diego (UCSD) School of Medicine in a study published in the January 22, 2004 issue of the journal Neuron.
The studies in mice, conducted in the lab of Joseph G. Gleeson, M.D., UCSD assistant professor of neurosciences, combines work in both humans and mice to identify a protein kinase called Cdk5 as the “off” switch for a crucial neuronal migration protein called doublecortin. When Cdk5 adds a phosphate molecule to doublecortin, the doublecortin is inactivated and neuronal migration is arrested.
In the normal brain, neurons are born deep within fluid filled cavities of the brain during the third and fourth month of gestation. Then, they must migrate hundreds of cell-body distances to reach their proper position within the six-layered cortex. When this migration is defective and neurons are stopped short of their destination, there is an absence of the normal grooves and ridges that characterize the brain in higher mammals.
Sue Pondrom | UCSD
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