Deficiency of apoptosis-stimulating protein two of p53 promotes liver regeneration in mice by activating mammalian target of rapamycin.

摘要: Although liver regeneration has been intensively studied in various ways, the mechanisms underlying remain elusive. Apoptosis-stimulating protein two of p53 (ASPP2) was discovered as a binding partner and plays an important role regulating cell apoptosis growth. However, ASPP2 hepatocyte proliferation not reported. The expression profile measured mouse model with 70% partial hepatectomy (PHX). Liver were detected wild-type (ASPP2+/+) haploinsufficient (ASPP2+/−) mice PHX. mammalian target rapamycin (mTOR) autophagy pathways analyzed ASPP2+/+ ASPP2+/− After or 3-methyladenine (3-MA) treatment, shown to be upregulated at early stage downregulated late stage. Compared mice, enhanced In addition, compared mTORC1 pathway significantly autophagic ASPP2+/−mice Inhibition suppressed contrast, disruption further deficiency can promote through activating pathway, which regulates downstream molecules, such those related p70S6K post-PHX.