Crosstalk between transforming growth factor beta (TGF-β) signaling and p53 has a critical role in cancer progression. TGF-β signals via Smad and non-Smad pathways. Under normal conditions, wild-type p53 forms a complex with Smad2/3 and co-activates transcription of a variety of tumor suppressor genes, resulting in tumor suppressive effects. Thus, p53 stability is essential in progression of tumor suppressive responses mediated by TGF-β signaling. However, it remains unknown whether p53 stability is regulated by TGF-β. In the current study, we identify that USP15 binds to and stabilizes p53 through deubiquitination in U2OS and HEK293 cells. TGF-β promotes the translation of USP15 through activation of mammalian target of rapamycin by the phosphoinositide 3-kinase/AKT pathway. Upregulation of USP15 translation links the crosstalk between TGF-β signaling and p53 stability, allowing this cytokine to have a critical role in cancer progression.

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Abstract. We study numerically the collapse behavior of self-generated magnetic fields described by the nonlinear coupling equations in laser-produced plasmas. The results show that magnetic fields self-generated by transverse pumping plasmons near critical points may collapse, leading to the enhancement of magnetic fields about up to 0.18 MG and 1.8 MG at laser irradiances of 1012 W cm−2 and 1016 W cm−2 respectively, which are similar to the experimental results.

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