| pubmed-article:9384581 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9384581 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:9384581 | lifeskim:mentions | umls-concept:C0815089 | lld:lifeskim |
| pubmed-article:9384581 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:9384581 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9384581 | pubmed:issue | 23 | lld:pubmed |
| pubmed-article:9384581 | pubmed:dateCreated | 1998-1-29 | lld:pubmed |
| pubmed-article:9384581 | pubmed:abstractText | Cell fate commitment in a variety of lineages requires signals conveyed via p21ras. To examine the role of p21ras in the development of B lymphocytes, we generated transgenic mice expressing a dominant-negative form of Ras in B lymphocyte progenitors, using a novel transcriptional element consisting of the Emu enhancer and the lck proximal promoter. Expression of dominant-negative Ras arrests B cell development at a very early stage, prior to formation of the pre-B cell receptor. Furthermore, an activated form of Raf expressed in the same experimental system could both drive the maturation of normal pro-B cells and rescue development of progenitors expressing dominant-negative Ras. Hence p21ras normally regulates early development of B lymphocytes by a mechanism that involves activation of the serine/threonine kinase Raf. | lld:pubmed |
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