| pubmed-article:11073970 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11073970 | lifeskim:mentions | umls-concept:C0086661 | lld:lifeskim |
| pubmed-article:11073970 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:11073970 | lifeskim:mentions | umls-concept:C0035143 | lld:lifeskim |
| pubmed-article:11073970 | lifeskim:mentions | umls-concept:C2752630 | lld:lifeskim |
| pubmed-article:11073970 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:11073970 | lifeskim:mentions | umls-concept:C0205410 | lld:lifeskim |
| pubmed-article:11073970 | pubmed:issue | 23 | lld:pubmed |
| pubmed-article:11073970 | pubmed:dateCreated | 2000-12-19 | lld:pubmed |
| pubmed-article:11073970 | pubmed:abstractText | The importance of c-myc as a target of the Blimp-1 repressor has been studied in BCL-1 cells, in which Blimp-1 is sufficient to trigger terminal B-cell differentiation. Our data show that Blimp-1-dependent repression of c-myc is required for BCL-1 differentiation, since constitutive expression of c-Myc blocked differentiation. Furthermore, ectopic expression of cyclin E mimicked the effects of c-Myc on both proliferation and differentiation, indicating that the ability of c-Myc to drive proliferation is responsible for blocking BCL-1 differentiation. However, inhibition of c-Myc by a dominant negative form was not sufficient to drive BCL-1 differentiation. Thus, during Blimp-1-dependent plasma cell differentiation, repression of c-myc is necessary but not sufficient, demonstrating the existence of additional Blimp-1 target genes. | lld:pubmed |
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| pubmed-article:11073970 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11073970 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11073970 | pubmed:status | MEDLINE | lld:pubmed |
