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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Abstract Kenaf is a multipurpose crop, but a lack of genetic information hinders genetic and molecular research. In this study, we aimed t...
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As demonstrated by the market reactions to downgrades of various sovereign credit ratings in 2011, the credit rating agencies occupy an impo...
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ORIGINAL ARTICLES Cyclooxygenase-2 and estrogen receptor-β as possible therapeutic targets in desmoid tumors p. 47 Rasha A Khairy DOI :10....
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Umbrella reviews: what they are and why we need them Cystic echinococcosis in unaccompanied minor refugees from Afghanistan and the Middle E...
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Spindle cell/pleomorphic lipoma is an uncommonly encountered benign neoplasm that is usually found in the subcutaneous tissues. Rare cases r...
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Lichtenstein intervention is currently the classic model of the regulated treatment of inguinal hernias by direct local approach. This “tens...
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2016-09-29T05-30-58Z Source: Journal of Applied Pharmaceutical Science Sadhana Nittur Holla, Meena Kumari Kamal Kishore, Mohan Babu Amber...
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Abstract Despite the recent promising results of clinical trials using human pluripotent stem cell (hPSC)-based cell therapies for age-rel...
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