作者: Li Wang , Jie Zhang , Karl Herrup
DOI: 10.1007/978-0-387-78887-6_9
关键词:
摘要: Cyclin-dependent kinase 5 (Cdk5) is a non-traditional CDK. It relies on two specific activators––p35 and p39––that are structurally similar to cyclins but genetically distinct. Analysis of the Cdk5 knockout (or double p35/p39 knockout) has led view that primary function in migration maturation embryonic post-mitotic neurons. The literature no reference role normal cell cycle regulation. Recent data from our lab, however, suggest while it may not as traditional CDK facilitate progression, does play crucial suppressor In this chapter, we review evidence unique important for neuronal survival differentiation. action neurons appears have sub-cellular specificity well. We present early nuclear form holding check. found exit nucleus stressed at risk death. shift location accompanied by re-entry This “new” raises cautions design Cdk5-directed drugs therapy neurodegenerative diseases