Journal article
The Src kinase Lyn is a negative regulator of mast cell proliferation
Journal of Leukocyte Biology, Vol.75(1), pp.143-151
2004
PMID: 14525964
Abstract
Previous investigators have reported that deletion of the protein tyrosine kinase Lyn alters mast cell (MC) signaling responses but does not affect or reduces the cytokine-mediated proliferation of mouse bone marrow-derived MC (BMMC) precursors and of mature MC. We observed that Lyn-deficient mice have more peritoneal MC than wild-type (WT) mice. Studies to explore this unexpected result showed that Lyn(-/-) BM cells expand faster than WT cells in response to interleukin (IL)-3 and stem-cell factor over the 4-5 weeks required to produce a >95% pure population of granular, receptor with high affinity for immunoglobulin E-positive BMMC. Furthermore, differentiated Lyn(-/-) BMMC continue to proliferate more rapidly than WT BMMC and undergo less apoptosis in response to cytokine withdrawal. Additionally, Lyn(-/-) BMMC support greater IL-3-mediated phosphorylation of the prosurvival kinase, Akt, and the proliferative kinase, extracellular-regulated kinase 1/2. These results identify Lyn as a negative regulator of murine MC survival and proliferation.
Details
- Title
- The Src kinase Lyn is a negative regulator of mast cell proliferation
- Authors
- Valerie Hernandez-Hansen (Author) - University of New MexicoGraham A Mackay (Author) - University of New MexicoClifford A Lowell (Author) - University of California, San FranciscoBridget S Wilson (Author) - University of New MexicoJanet M Oliver (Author) - University of New Mexico
- Publication details
- Journal of Leukocyte Biology, Vol.75(1), pp.143-151
- Publisher
- John Wiley & Sons Ltd.
- DOI
- 10.1189/jlb.0503224
- ISSN
- 1938-3673
- PMID
- 14525964
- Organisation Unit
- University of the Sunshine Coast, Queensland
- Language
- English
- Record Identifier
- 99522303502621
- Output Type
- Journal article
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- Domestic collaboration
- Web Of Science research areas
- Cell Biology
- Hematology
- Immunology
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Source: InCites