Abnormal expression of cdk5 in focal cortical dysplasia in humans.
Focal cortical dysplasia (FCD) is an important cause of refractory epilepsy in humans. The origin of its pathognomonic abnormal cell types and the links between abnormal cell morphology and epileptogenicity remain unknown. The developmentally-regulated kinase cdk5 and its neuronal activator p35 are known to be central to a number of key components in neuronal development, cellular morphology, cytoskeletal function, synaptic plasticity and neurodegeneration. Here we examine eight cases of human FCD for expression of cdk5. We show abnormal cdk5 immunoreactivity and aggregation of protein suggesting alterations in cdk5 may also be involved in this important epileptogenic human pathology.
Sisodiya
Sanjay M
SM
Department of Clinical and Experimental Epilepsy, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK. sisodiya@ion.ucl.ac.uk
Thom
Maria
M
Lin
Woan Ru
WR
Bajaj
Narinder P S
NP
Cross
J Helen
JH
Harding
Brian N
BN
D002540:Cerebral Cortex / Q000002:abnormalities* / Q000201:enzymology*; D000013:Congenital Abnormalities / Q000201:enzymology; D051360:Cyclin-Dependent Kinase 5; D018844:Cyclin-Dependent Kinases / Q000378:metabolism*; D006801:Humans; D009474:Neurons / Q000201:enzymology
D051360:Cyclin-Dependent Kinase 5; C495905:CDK5 protein, human; D018844:Cyclin-Dependent Kinases