Linked Life Data

20942268

Source:http://linkedlifedata.com/resource/pubmed/id/20942268

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2010-10-14
pubmed:abstractText
We previously reported that the disruption of cell spreading by v-Crk was dependent on the activation of the MEK/ERK pathway. Here we demonstrate that the activation of that pathway is sufficient to suppress cell spreading. The MEK/ERK pathway regulates the activity of various proteins including AP-1, which is a transcriptional factor composed of heterodimeric proteins. To examine whether AP-1 activity is required for the suppression of cell spreading by the activation of the MEK/ERK pathway, we expressed BATF, which is a negative regulator of AP-1. The expression of BATF clearly restored cell spreading that was suppressed by the activation of MEK/ERK pathway. In addition, a disrupted formation of stress fibers and focal adhesions by such activation was restored by the suppression of AP-1. Our results define an essential role of the MEK/ERK/AP-1 pathway in the disruption of actin cytoskeleton and cell spreading.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0027-7622
pubmed:author
pubmed:issnType
Print
pubmed:volume
72
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
139-44
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Disruption of cell spreading by the activation of MEK/ERK pathway is dependent on AP-1 activity.
pubmed:affiliation
Department of Cancer Biology, Nagoya University Graduate School of Medicine.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't