論文がアクセプトされました

On 2008/4/17 木曜日, in hypoxia reseacrh, by bodyhacker

研究室で一緒にやっていたO田先生の論文がPLoS ONEにアクセプトされました。
おめでとうございました。もちろんぼくもとってもうれしいです。

Macrophage migration inhibitory factor activates hypoxia-inducible factor in a p53-dependent manner

結構面白い論文だと思います。
ここ数年やっている炎症-酸素分圧-HIFの流れにそった内容になっています。
これにK野先生の論文が加われば一応このラインの仕事の在庫は一掃ということになります。

Abstract

Background Macrophage migration inhibitory factor (MIF) is not only a cytokine which has a critical role in several inflammatory conditions but also has endocrine and enzymatic functions. MIF is identified as an intracellular signaling molecule and is implicated in the process of tumor progression, and also strongly enhances neovascularization. Overexpression of MIF has been observed in tumors from various organs. MIF is one of the genes induced by hypoxia in an hypoxia-inducible factor 1 (HIF-1)-dependent manner. Methods/Principle Findings The effect of MIF on HIF-1 activity was investigated in human braest cancer MCF-7 and MDA-MB-231 cells, and osteosarcoma Saos-2 cells. We demonstrate that intracellular overexpression or extracellular administration of MIF enhances activation of HIF-1 under hypoxic conditions in MCF-7 cells. Mutagenesis analysis of MIF and knockdown pf 53 demonstrates that the activation is not dependent on redox activity of MIF but on wild-type p53. We also indicate that the MIF receptor CD74 is involved in HIF-1 activation by MIF at least when MIF is administrated extracellularly. Conclusion/significance MIF regulates HIF-1 activity in a p53-dependent manner. In addition to MIF’s potent effects on the immune system, MIF is linked to fundamental processes conferring cell proliferation, cell survival, angiogenesis, and tumor invasiveness. This functional interdependence between MIF and HIF-1α protein stabilization and transactivation activity provide a molecular mechanism for promotion of tumorigenesis by MIF.

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