Linked Life Data

17123777

Source:http://linkedlifedata.com/resource/pubmed/id/17123777

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-1-12
pubmed:abstractText
Phosphoinositide lipids generated at the cell membrane are a key component of a variety of signaling pathways. Among several inositol phosphatases that regulate the availability of signaling phosphoinositide lipids, the type II SH2-domain-containing inositol 5-phosphatase (SHIP2; approved gene symbol Inppl1) is believed to have multiple functions, including the regulation of insulin signaling and cytoskeletal functions. To understand the function of SHIP2 in C2C12 muscle cells, we depleted SHIP2 through the use of RNA interference and analyzed the global effect of SHIP2 depletion on gene expression using Affymetrix microarrays containing approximately 45,000 mouse probe sets. Expression of SHIP2-targeting small-hairpin RNA in differentiated C2C12 muscle cells led to >80% decrease in SHIP2 mRNA and 60-80% decrease in SHIP2 protein, which resulted in significant gene expression changes linked to cytoskeletal functions, including altered expression of adducin-alpha, pallidin, stathmin-like-2, and synaptojanin-2 binding protein. Insulin treatment of C2C12 muscle cells caused transcriptional changes associated with known signaling pathways. However, SHIP2 depletion had no discernible effect on insulin-regulated gene expression. Taken together, our results suggest that SHIP2 is involved in the regulation of cytoskeletal functions, but a large reduction of SHIP2 in C2C12 muscle cells is not sufficient to affect insulin-mediated gene expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0888-7543
pubmed:author
pubmed:issnType
Print
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
270-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Transcriptional profiling of C2C12 myotubes in response to SHIP2 depletion and insulin stimulation.
pubmed:affiliation
Biological Technologies, Wyeth Research, 87 Cambridge Park Drive, Cambridge, MA 02140, USA.
pubmed:publicationType
Journal Article