Elevated expression of HER3, which interacts with HER2 in breast cancer cells, confers chemoresistance via phosphoinositide 3-kinase (PI-3K)/Akt-dependent upregulation of Survivin. However, the underlying mechanism is not clear. Ectopic expression or specific knockdown of HER3 in HER2-overexpressing breast cancer cells did not alter Survivin mRNA levels and Survivin protein stability, supporting the notion that HER3 signaling may regulate specific miRNAs that target Survivin to alter its protein translation.
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This case report outlines the possibility of accelerated tooth movement with the combination of microosteoperforation and mini-screws. A 14-...
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by Rebekah L. Rogers, Ling Shao, Kevin R. Thornton One common hypothesis to explain the impacts of tandem duplications is that whole gene ...
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