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

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 intern...

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Bibliographic Details
Published in:Neurochemical research 2008-09, Vol.33 (9), p.1859-1868
Main Authors: Spahn, A., Blondeau, N., Heurteaux, C., Dehghani, F., Rami, A.
Format: Article
Language:English
Subjects:
Animals
Apoptosis - physiology
Biochemistry
Biochemistry, Molecular Biology
Biomedical and Life Sciences
Biomedicine
Brain Ischemia - metabolism
Caspase 3 - metabolism
Cell Biology
Cell Line
Cell Survival
Cellular Biology
Cytochromes c - metabolism
Enzyme Inhibitors - metabolism
Gene Expression Regulation
Heterogeneous-Nuclear Ribonucleoprotein Group C - genetics
Heterogeneous-Nuclear Ribonucleoprotein Group C - metabolism
Human health and pathology
Life Sciences
Male
Mice
Mice, Inbred C57BL
Neurochemistry
Neurology
Neurons - cytology
Neurons - physiology
Neurons and Cognition
Neurosciences
Original Paper
Staurosporine - metabolism
X-Linked Inhibitor of Apoptosis Protein - genetics
X-Linked Inhibitor of Apoptosis Protein - metabolism
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Summary: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.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-008-9658-0