The origin of isocortical development [1]

Trends in Neurosciences

Volumn 24, Issue 4, 2001, Pages 202-203

  Aboitiz, Francisco ^a  

^a UNIVERSITY OF CHILE   (Chile)

Author keywords

[No Author keywords available]

Indexed keywords

BRAIN DEVELOPMENT; CELL MIGRATION; LETTER; NERVE CELL; PRIORITY JOURNAL; REGULATORY MECHANISM; SIGNAL TRANSDUCTION;

EID: 0035313972     PISSN: 01662236     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0166-2236(00)01771-9     Document Type: Letter

References (14)

1. The evolution of cortical development. An hypothesis based on the role of the Reelin signaling pathway
2. Cajal-Retzius cells, reelin and the formation of layers
3. Reelin binds α3β1 integrin and inhibits neuronal migration
4. The reeler malformation. Implications for neocortical histogenesis
5. Evolution of isocortical organization. A tentative scenario including roles of reelin, p35/cdk5 and the subplate zone
6. Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death
7. Mice lacking p35, a neuronal specific activator of cdk5, display cortical lamination defects, seizures, and adult lethality
8. Cyclin-dependent kinase 5-deficient mice demonstrate novel developmental arrest in cerebral cortex
9. A novel disruption of cortical development in p35(-/-) mice distinct from reeler
10. Potential mechanism of mutations that affect neuronal migration in man and mouse
11. Evidence for the participation of the neuron-specific cdk5 activator p35 during laminin-enhanced axonal growth
12. Callosalaxon guidance defects in p35(-/-) mice
13. The p35/cdk5 kinase is a neuron-specific Rac effector that inhibits Pak1 activity
14. Regulation of N-cadherin-mediated adhesion by the p35-Cdk5 kinase