Linked Life Data

21050850

Source:http://linkedlifedata.com/resource/pubmed/id/21050850

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
23
pubmed:dateCreated
2010-12-3
pubmed:abstractText
The phosphatidylinositol 3-kinase/Akt pathway is responsible for key aspects of tumor progression, and is frequently hyperactivated in cancer. We have recently identified palladin, an actin-bundling protein that functions to control the actin cytoskeleton, as an Akt1-specific substrate that inhibits breast cancer cell migration. Here we have identified a role for Akt isoforms in the regulation of palladin expression. Akt2, but not Akt1, enhances palladin expression by maintaining protein stability and upregulating transcription. These data reveal that Akt signaling regulates the stability of palladin, and further supports the notion that Akt isoforms have distinct and specific roles in tumorigenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1873-3468
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
584
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4769-74
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Akt2 regulates expression of the actin-bundling protein palladin.
pubmed:affiliation
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. rchin1@bidmc.harvard.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural