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  Multiple mechanisms repress N-Bak mRNA translation in the healthy and apoptotic neurons

Jakobson, M., Jakobson, M., Llano, O., Palgi, J., & Arumae, U. (2013). Multiple mechanisms repress N-Bak mRNA translation in the healthy and apoptotic neurons. CELL DEATH & DISEASE, 4: e777. doi:10.1038/cddis.2013.297.

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Jakobson, M.1, Author
Jakobson, M.2, Author           
Llano, O.1, Author
Palgi, J.1, Author
Arumae, U.1, Author
Affiliations:
1external, ou_persistent22              
2Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565147              

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Free keywords: DEPRIVED SYMPATHETIC NEURONS; OPEN READING FRAMES; STRESS GRANULES; CYTOCHROME-C; P-BODIES; BH3-ONLY PROTEINS; GENE-EXPRESSION; CELL-DEATH; MITOCHONDRIA; INITIATIONN-Bak; translational repression; PTC; uORF; UTR; NMTR;
 Abstract: N-Bak is a neuron-specific BH3-only splice variant of pro-apoptotic Bcl-2 family member Bak. We have shown that its mRNA is stable in the neurons, whereas the protein cannot be detected by antibodies, suggesting a strong translational arrest of the mRNA. Here we identify two regulatory elements in the N-Bak mRNA that significantly repress translation in the luciferase reporter assay: an upstream open reading frame in the 5'-untranslated region (UTR) and naturally spliced exon-exon junction downstream of the premature translation termination codon in the 3'UTR. We also show that N-Bak mRNA is stored in granular structures in the sympathetic neurons and stays in these granules during intrinsic apoptosis. Finally, we confirm the absence of N-Bak protein by quantitative mass spectrometry analysis in the healthy, apoptotic or stressed sympathetic and cortical neurons. We conclude that N-Bak mRNA is translationally repressed by multiple mechanisms, and the protein does not participate in the classical apoptosis or cellular stress response.

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Language(s): eng - English
 Dates: 2013-08
 Publication Status: Published online
 Pages: 10
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: ISI: 000324146000034
DOI: 10.1038/cddis.2013.297
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Title: CELL DEATH & DISEASE
Source Genre: Journal
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Publ. Info: MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND : NATURE PUBLISHING GROUP
Pages: - Volume / Issue: 4 Sequence Number: e777 Start / End Page: - Identifier: ISSN: 2041-4889