Linked Life Data

18407419

Source:http://linkedlifedata.com/resource/pubmed/id/18407419

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-5-12
pubmed:abstractText
The signal transduction pathways regulating growth cone motility remain poorly defined. Previously, we have characterized the inhibitory molecule, motuporamine C (MotC), as a robust stimulator of growth cone collapse. Utilizing MotC as a research tool to elucidate pathways involved with collapse, we have previously shown that the Rho-Rho kinase (ROCK) pathway is partially required for collapse. In this study, we report MotC induces a high-amplitude rise in intracellular free Ca(2+) concentration levels in chicks, resulting in the activation of the Ca(2+)-sensitive protease, calpain. Furthermore, we show that while calpain is necessary for collapse, inhibition of calpain only partially attenuates MotC-mediated collapse. Instead, concomitant inhibition of both the Rho-ROCK and calpain pathways has an additive effect in attenuating the collapse response to MotC. To our knowledge, this is the first demonstration of concurrent activation of calpain and Rho-ROCK signaling during growth cone collapse. Our data support a model of growth cone collapse that requires the combinatorial regulation of multiple signal transduction cascades that likely target different cellular mechanisms to induce this motile response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1873-7544
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
153
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
645-53
pubmed:dateRevised
2009-6-23
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Growth cone collapse stimulated by both calpain- and Rho-mediated pathways.
pubmed:affiliation
Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't