Key result
Overexpression of heterogeneous nuclear ribonucleoproteins C1 and C2 specifically enhanced translation of the antiapoptotic protein XIAP via its internal ribosome entry site by approximately 3.5-fold.
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The study demonstrates that hnRNPC1 and -C2 bind specifically to the XIAP IRES element and positively modulate its translation, providing insight into the regulation of apoptosis.
The X-chromosome-linked inhibitor of apoptosis, XIAP, is the most powerful and ubiquitous intrinsic inhibitor of apoptosis. We have shown previously that the translation of XIAP is controlled by a potent internal ribosome entry site (IRES) element. IRES-mediated translation of XIAP is increased in response to cellular stress, suggesting the critical role for IRES translation during cellular stress. Here, we demonstrate that heterogeneous nuclear ribonucleoproteins C1 and C2 (hnRNPC1 and -C2) are part of the RNP complex that forms on XIAP IRES. Furthermore, the cellular levels of hnRNPC1 and -C2 parallel the activity of XIAP IRES and the overexpression of hnRNPC1 and -C2 specifically enhanced translation of XIAP IRES, suggesting that hnRNPC1 and -C2 may modulate XIAP expression. Given the central role of XIAP in the regulation of apoptosis these results are important for our understanding of the control of apoptosis.
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Holčı́k et al. (2002) studied Apoptosis. hnRNPC1 and -C2 overexpression vs. Control vector was evaluated on XIAP IRES translation activity. Overexpression of heterogeneous nuclear ribonucleoproteins C1 and C2 specifically enhanced translation of the antiapoptotic protein XIAP via its internal ribosome entry site by approximately 3.5-fold.
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