Key result
hnRNP A1 regulates cyclin D1 and c-myc IRES activity in an Akt-dependent manner, and its knockdown renders quiescent Akt-containing cells sensitive to rapamycin-induced G1 arrest.
This study provides the first direct link between Akt signaling and the regulation of IRES activity via hnRNP A1 phosphorylation.
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Does not support clinical translation; leaves open whether hnRNP A1 modulation enhances rapamycin efficacy in human disease.
Jo et al. (2008) studied this question. hnRNP A1 modulation and rapamycin was evaluated on IRES activity and translation of cyclin D1 and c-myc. hnRNP A1 regulates cyclin D1 and c-myc IRES activity in an Akt-dependent manner, and its knockdown renders quiescent Akt-containing cells sensitive to rapamycin-induced G1 arrest.
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