HIGHLIGHTS
SUMMARY
The authors reported that glucose can function as a mitogen in ESCC but not in EAC, and that it induced the phosphorylation of FAK-His58. The authors showed that expression of FAKH58A in ESCC abrogated glucose-induced proliferation concomitant with decreases in the activation levels of AMPK, 70S6K and AKT. This effect was not dependent on the autophosphorylation site on FAK, Y397, whose phosphorylation by growth factors induces intrinsic tyrosine kinase activity and mitogenic cell signaling. The authors reported that the overexpression of FAKY397F did not attenuate either glucoseincreased FAKpHis levels or glucose-induced . . .
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