Linked Life Data

16930532

Source:http://linkedlifedata.com/resource/pubmed/id/16930532

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-9-11
pubmed:abstractText
We have shown that protein kinase C (PKC)epsilon, independently of the catalytic domain, induces outgrowth of cellular processes via its regulatory domain in both neural cells and fibroblasts. This was accompanied by stress fibre loss. Here, we have examined the role of the small GTPases, Rac1, and Cdc42, in these PKC-mediated morphological and cytoskeletal changes. Both constitutively active and dominant negative Rac1 and Cdc42 attenuated the PKC-mediated outgrowth of processes. The suppression was larger for Cdc42 than for Rac1. The PKC-mediated dismantling of the stress fibres in both HiB5 and fibroblasts was inhibited by the expression of the Cdc42 mutants whereas they had smaller effects on the stress fibre dismantling induced by the ROCK inhibitor, Y-27632, indicating a more crucial role for Cdc42 in the PKC-mediated pathway. We conclude that Cdc42 is an important downstream factor in the pathway through which PKC mediates morphological and cytoskeletal effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
349
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Cdc42 is involved in PKCepsilon- and delta-induced neurite outgrowth and stress fibre dismantling.
pubmed:affiliation
Lund University, Department of Laboratory Medicine, Molecular Medicine, Entrance 78, 3rd floor, Malmö University Hospital, SE-205 02 Malmö, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't