pubmed-article:15509516 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15509516 | lifeskim:mentions | umls-concept:C0006142 | lld:lifeskim |
pubmed-article:15509516 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:15509516 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:15509516 | lifeskim:mentions | umls-concept:C0015576 | lld:lifeskim |
pubmed-article:15509516 | lifeskim:mentions | umls-concept:C0040648 | lld:lifeskim |
pubmed-article:15509516 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:15509516 | lifeskim:mentions | umls-concept:C0205548 | lld:lifeskim |
pubmed-article:15509516 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:15509516 | pubmed:dateCreated | 2004-10-28 | lld:pubmed |
pubmed-article:15509516 | pubmed:abstractText | Stats (for signal transducers and activators of transcription) are a family of transcription factors that regulate cell growth and differentiation. Their activity is latent until phosphorylation by receptor-associated kinases. A sizable body of data from cell lines, mouse models, and human tissues now implicates these transcription factors in the oncogenesis of breast cancer. Because Stat activity is modulated by several posttranslational modifications and protein-protein interactions, these transcription factors are capable of integrating inputs from multiple signaling networks. Given this, the future utilization of Stats as prognostic markers and therapeutic targets in human breast cancer appears likely. | lld:pubmed |
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