Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2000-8-15
pubmed:databankReference
pubmed:abstractText
Cyclin-dependent kinase 5 (Cdk5) is one of a subfamily of Cdks involved in the control of cell differentiation and morphology rather than cell division. Specifically, Cdk5 and its activating subunit, p35, have been implicated in growth cone motility during axon extension. Both Cdk5 and p35 are expressed in post-mitotic neurons and are localized to growth cones [1] [2] [3] [4]. The Cdk5-p35 complex interacts with the Rac GTPase, a protein required for growth cone motility [5]. Studies using cultured neurons have suggested that Cdk5 activity controls the efficiency of neurite extension [3] [4]. Mutant mice lacking p35 exhibit subtle axon-guidance defects [6], but these mice have severe defects in neuronal migration [6] [7] [8], making it difficult to define precisely the role of the Cdk5-p35 complex in vivo. Here, we examined Cdk5 function in axon patterning in the Drosophila embryo. Although our data support the idea that Cdk5-p35 is involved in axonogenesis, they do not support the view that Cdk5 simply promotes growth cone motility. Instead, we found that disrupting Cdk5 function caused widespread errors in axon patterning.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0960-9822
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
599-602
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
The cyclin-dependent kinase Cdk5 controls multiple aspects of axon patterning in vivo.
pubmed:affiliation
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't