| http://purl.uniprot.org/citations/16051621 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16051621 | http://www.w3.org/2000/01/rdf-schema#comment | "It has been shown that mice with a targeted mutation in the Ets-1 gene exhibit increased B cell terminal differentiation to IgM-secreting plasma cells. Here, we show that mice, formerly described to lack Ets-1 protein, actually express low levels of an internally deleted Ets-1 protein. Mice harboring this Ets-1 hypomorphic allele possess very few marginal zone B cells and have increased expression of activation markers on follicular B cells. Adoptive transfer experiments indicate that this activated phenotype can be reversed upon transfer of Ets-1-deficient B cells to a wild-type host, suggesting a role for B cell-extrinsic factors in regulating the activated state. Supporting this observation, the reverse transfer experiment of wild-type B cells into an Ets-1-deficient host resulted in increased expression of activation markers on the transferred B cells. However, there are also cell-intrinsic changes in Ets-1-deficient B cells as demonstrated by their increased differentiation to plasma cells in vitro in response to stimulation with cytosine-phosphate-guanine DNA sequence-containing oligodeoxynucleotide [CpG DNA, a Toll-like receptor (TLR) 9 ligand]. Consistent with the activated phenotype and increased terminal differentiation of Ets-1-deficient B cells, Ets-1 mutant mice develop autoimmune disease. Hence, our studies establish Ets-1 as an important regulator of peripheral B cell differentiation and B cell responses to TLR9 activation."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.org/dc/terms/identifier | "doi:10.1093/intimm/dxh295"xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/author | "Wang D."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/author | "John S.A."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/author | "Garrett-Sinha L.A."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/author | "Barton K.P."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/author | "Clements J.L."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/author | "Percy D.H."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/name | "Int Immunol"xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/pages | "1179-1191"xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/title | "Ets-1 deficiency leads to altered B cell differentiation, hyperresponsiveness to TLR9 and autoimmune disease."xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://purl.uniprot.org/core/volume | "17"xsd:string |
| http://purl.uniprot.org/citations/16051621 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16051621 |
| http://purl.uniprot.org/citations/16051621 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16051621 |
| http://purl.uniprot.org/uniprot/#_A0A5F8MPR7-mappedCitation-16051621 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16051621 |
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| http://purl.uniprot.org/uniprot/#_Q6R5C9-mappedCitation-16051621 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16051621 |
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| http://purl.uniprot.org/uniprot/#_Q8K3Q9-mappedCitation-16051621 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16051621 |
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