| First Author | Fox JA | Year | 2002 |
| Journal | J Immunol | Volume | 169 |
| Issue | 1 | Pages | 49-54 |
| PubMed ID | 12077227 | Mgi Jnum | J:77240 |
| Mgi Id | MGI:2181237 | Doi | 10.4049/jimmunol.169.1.49 |
| Citation | Fox JA, et al. (2002) Disruption of a single Pten allele augments the chemotactic response of B lymphocytes to stromal cell-derived factor-1. J Immunol 169(1):49-54 |
| abstractText | The tumor suppressor, Pten, has emerged as a critical negative regulator of phosphatidylinositol-3-kinase-dependent intracellular signaling pathways responsible for phenomena such as cellular adhesion, proliferation, and apoptosis. Herein, we present evidence that Pten regulates chemokine-dependent events in B lymphocytes. Primary B cells isolated from Pten(+/-) mice demonstrated increased responsiveness to stromal cell-derived factor-1-induced chemotaxis. This was accompanied by an elevated level of protein kinase B phosphorylation on Ser(473). Our results suggest not only that Pten may be an important regulator of stromal cell-derived factor-1-directed chemotaxis, but also that Pten heterozygosity is associated with increased cellular sensitivity to this chemokine, likely via dysregulation of events lying downstream of phosphatidylinositol-3-kinase. These observations suggest a mechanism by which loss of a single Pten allele may confer a selective advantage on cells during multistep tumor progression. |
