Young et al, ErbB3 loss delays PIK3CA mammary hyperplasia, pg. 1 Conditional loss of ErbB3 delays mammary gland hyperplasia induced by mutant PIK3CA without affecting mammary tumor latency, gene expression or signaling
نویسندگان
چکیده
1. Department of Medicine, Vanderbilt University, Nashville, TN 37232, USA. 2. Department of Cancer Biology, Vanderbilt University, Nashville, TN 37232, USA 3. Department of Pathology, Vanderbilt University, Nashville, TN 37232, USA. 4. Breast Cancer Research Program, Vanderbilt-Ingram Cancer Center, Nashville, TN 37232, USA. 5. Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA. 6. Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA. 7. Department of Genetics, University of North Carolina, Chapel Hill, NC 27599, USA. 8. Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. # Contributed equally
منابع مشابه
Conditional loss of ErbB3 delays mammary gland hyperplasia induced by mutant PIK3CA without affecting mammary tumor latency, gene expression, or signaling.
Mutations in PIK3CA, the gene encoding the p110α catalytic subunit of phosphoinositide 3-kinase (PI3K), have been shown to transform mammary epithelial cells (MEC). Studies suggest this transforming activity requires binding of mutant p110α via p85 to phosphorylated YXXM motifs in activated receptor tyrosine kinases (RTK) or adaptors. Using transgenic mice, we examined if ErbB3, a potent activa...
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The formation of ErbB2/ErbB3 heterodimers plays a critical role in ErbB2-mediated signaling in both normal mammary development and mammary tumor progression. Through 7 phosphoinositide 3-kinase (PI3K) phosphotyrosine-binding sites, ErbB3 is able to recruit PI3K and initiate the PI3K/AKT signaling pathway. To directly explore the importance of the ErbB3/PI3K pathway in mammary development and tu...
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