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Neurochem Res. 2008 Sep;33(9):1859-68. doi: 10.1007/s11064-008-9658-0. Epub 2008 Mar 25.

Concomitant transitory up-regulation of X-linked inhibitor of apoptosis protein (XIAP) and the heterogeneous nuclear ribonucleoprotein C1-C2 in surviving cells during neuronal apoptosis.

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  • 1Institute of Cellular and Molecular Anatomy (Anatomie III), Clinic of Johann Wolfgang von Goethe-University, Theodor-Stern-Kai 7, 60590, Franfurt/Main, Germany.


Although cap-dependent translation initiation is the prevalent mode of ribosome binding to mRNAs in eukaryotes, some mRNAs exhibit the ability to bypass the requirement for the cap structure. The translation of X-chromosome-linked inhibitor of apoptosis protein (XIAP) mRNA is controlled by an internal ribosome entry site (IRES) element, which requires the interaction of the heterogeneous nuclear ribonucleoprotein C1-C2 (hnRNP-C1/C2). We analyze, at the protein level, the time course and distribution of XIAP and hnRNP-C1/C2 upon ischemia in mice or staurosporine (STP)-induced apoptosis in HT22 cells. Both ischemia and STP induced a parallel upregulation of XIAP and hnRNP-C1/C2 protein levels in the penumbra and in HT22 cells. These results suggest that the increased levels of hnRNP C1/C2 may modulate XIAP translation, probably by interacting with the XIAP-IRES. The up-regulation of hnRNP-C1/C2 may foster the synthesis of XIAP as a protective pathway by which neurons try to counteract the initial deleterious effects of apoptosis.

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