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. 2004 Sep 24;279(39):41131-40.
doi: 10.1074/jbc.M402902200. Epub 2004 Jul 22.

"V体育官网入口" Nucling recruits Apaf-1/pro-caspase-9 complex for the induction of stress-induced apoptosis

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Nucling recruits Apaf-1/pro-caspase-9 complex for the induction of stress-induced apoptosis

Takashi Sakai et al. J Biol Chem. .
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Abstract

Nucling is a novel protein isolated from murine embryonal carcinoma cells with an up-regulated expression during cardiac muscle differentiation. We show here that Nucling was up-regulated by proapoptotic stimuli and important for the induction of apoptosis after cytotoxic stress. We further demonstrated that overexpressed Nucling was able to induce apoptosis. In Nucling-deficient cells, the expression levels of Apaf-1 and cytochrome c, which are the major components of an apoptosis-promoting complex named apoptosome, were both down-regulated under cellular stress. A deficiency of Nucling also conferred resistance to apoptotic stress on the cell VSports手机版. After UV irradiation, Nucling was shown to reside in an Apaf-1/pro-caspase-9 complex, suggesting that Nucling might be a key molecule for the formation and maintenance of this complex. Nucling induced translocation of Apaf-1 to the nucleus, thereby distributing the Nucling/Apaf-1/pro-caspase-9 complex to the nuclear fraction. These findings suggest that Nucling recruits and transports the apoptosome complex during stress-induced apoptosis. .

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