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pubmed-article:18597688pubmed:abstractTextSignaling downstream of Ras is mediated by three major pathways, Raf/ERK, phosphatidylinositol 3 kinase (PI3K), and Ral guanine nucleotide exchange factor (RalGEF). Ras signal transduction pathways play an important role in breast cancer progression, as evidenced by the frequent over-expression of the Ras-activating epidermal growth factor receptors EGFR and ErbB2. Here we investigated which signal transduction pathways downstream of Ras contribute to EGFR-dependent transformation of telomerase-immortalized mammary epithelial cells HME16C. Furthermore, we examined whether a highly transcriptionally regulated ERK pathway target, PHLDA1 (TDAG51), suggested to be a tumor suppressor in breast cancer and melanoma, might modulate the transformation process.lld:pubmed
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pubmed-article:18597688pubmed:authorpubmed-author:LiuZhaoZlld:pubmed
pubmed-article:18597688pubmed:authorpubmed-author:KellyKathleen...lld:pubmed
pubmed-article:18597688pubmed:authorpubmed-author:OberstMichael...lld:pubmed
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pubmed-article:18597688pubmed:articleTitleTDAG51 is an ERK signaling target that opposes ERK-mediated HME16C mammary epithelial cell transformation.lld:pubmed
pubmed-article:18597688pubmed:affiliationCell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 1066, Bethesda, MD 20892, USA. michaeloberst@gmail.comlld:pubmed
pubmed-article:18597688pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18597688pubmed:publicationTypeResearch Support, N.I.H., Intramurallld:pubmed