Source:http://linkedlifedata.com/resource/pubmed/id/21697469
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
17
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pubmed:dateCreated |
2011-8-9
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pubmed:abstractText |
v-Abl protein tyrosine kinase encoded by Abelson murine leukemia virus (Ab-MLV) transforms pre-B cells. Transformation requires the phosphatidylinositol 3-kinase (PI3K) pathway. This pathway is antagonized by SH2-containing inositol 5'-phosphatase (SHIP), raising the possibility that v-Abl modulates PI3K signaling through SHIP. Consistent with this, we show that v-Abl expression reduces levels of full-length p145 SHIP in a v-Abl kinase activity-dependent fashion. This event requires signals from the Abl SH2 domain but not the carboxyl terminus. Forced expression of full-length SHIP significantly reduces Ab-MLV pre-B-cell transformation. Therefore, reduction of SHIP protein by v-Abl is a critical component in Ab-MLV transformation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1098-5514
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
9239-42
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pubmed:meshHeading |
pubmed-meshheading:21697469-Abelson murine leukemia virus,
pubmed-meshheading:21697469-Animals,
pubmed-meshheading:21697469-Cell Transformation, Viral,
pubmed-meshheading:21697469-Host-Pathogen Interactions,
pubmed-meshheading:21697469-Mice,
pubmed-meshheading:21697469-Oncogene Proteins v-abl,
pubmed-meshheading:21697469-Phosphoric Monoester Hydrolases,
pubmed-meshheading:21697469-Precursor Cells, B-Lymphoid,
pubmed-meshheading:21697469-Protein Interaction Mapping
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pubmed:year |
2011
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pubmed:articleTitle |
SH2-containing inositol 5'-phosphatase inhibits transformation of Abelson murine leukemia virus.
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pubmed:affiliation |
Immunology Graduate Program, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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