| http://purl.uniprot.org/citations/21044800 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21044800 | http://www.w3.org/2000/01/rdf-schema#comment | "SHP-1 plays an important role for the regulation of signaling from various hematopoietic cell receptors. In this study, we examined IL-3-induced cell proliferation and IL-3 depletion-induced apoptosis in bone marrow-derived mast cells (BMMC) established from motheaten (me) that lack SHP-1 expression, viable motheaten (me(v)) expressing phosphatase-deficient SHP-1, and wild-type (WT) mice. When BMMC were stimulated with IL-3, increased ERK activation was evident in resting state and sustained in me-BMMC relative to WT-BMMC. ERK is known to be involved in the regulation of cell proliferation and apoptosis in some cells. In accordance with sustained ERK activation, apoptosis was decreased in me- and me(v)-BMMC compared with WT-BMMC. In contrast to the predicted role of ERK as a pro-survival molecule, IL-3-induced cell proliferation was much lower in me- and me(v)-BMMC than WT-BMMC. Stimulation with lower concentration of IL-3 or addition of PD98059, a MEK inhibitor, to the culture resulted in the suppression of decreased apoptosis and cell proliferation in me- and me(v)-BMMC. Collectively, these results suggest that SHP-1 positively regulates IL-3-dependent mast cell proliferation and apoptosis by inhibiting ERK activity through its phosphatase activity. Furthermore, our results indicate that ERK would act as a negative regulator for cell proliferation and induce apoptosis when its activity is highly increased."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.molimm.2010.10.001"xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/author | "Inoue T."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/author | "Mizuno K."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/author | "Suzuki Y."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/author | "Nakata K."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/author | "Yakura H."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/author | "Ra C."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/name | "Mol Immunol"xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/pages | "472-480"xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/title | "Deficiency of SHP1 leads to sustained and increased ERK activation in mast cells, thereby inhibiting IL-3-dependent proliferation and cell death."xsd:string |
| http://purl.uniprot.org/citations/21044800 | http://purl.uniprot.org/core/volume | "48"xsd:string |
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