Polyamine-independent Expression of Caenorhabditis elegans Antizyme

Stegehake, Dirk; Kurosinski, Marc-André; Schürmann, Sabine; Daniel, Jens; Lüersen, Kai; Liebau, Eva

doi:10.1074/jbc.m115.644385

Cited by 3 publications

(3 citation statements)

References 56 publications

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“…Agmatine has long been known to affect antizyme frameshifting ( 305 ) and antizyme influences uptake of the nitric oxide synthase inhibitor, agmatine, that has neurological significance ( 306 ). The influence of antizymes, both by direct binding and indirectly, on other pathways and the potential role of factors other than polyamines on antizyme frameshifting, is the subject of several reports and of active investigation ( 291 , 307 , 308 ). The potential for polyamine levels to have specific effects on other cases of frameshifting also needs to be kept in mind especially as a certain combination of the levels of putrescine and spermidine was shown to influence the S. cerevisiae mobile element Ty1 frameshifting and so the rate of its retrotransposition ( 309 ).…”

Section: Free Living Organism Chromosomal Genes Lacking Mobile Predecmentioning

confidence: 99%

Ribosomal frameshifting and transcriptional slippage: From genetic steganography and cryptography to adventitious use

Atkins¹,

Loughran²,

Bhatt³

et al. 2016

Nucleic Acids Res

269

367

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Genetic decoding is not ‘frozen’ as was earlier thought, but dynamic. One facet of this is frameshifting that often results in synthesis of a C-terminal region encoded by a new frame. Ribosomal frameshifting is utilized for the synthesis of additional products, for regulatory purposes and for translational ‘correction’ of problem or ‘savior’ indels. Utilization for synthesis of additional products occurs prominently in the decoding of mobile chromosomal element and viral genomes. One class of regulatory frameshifting of stable chromosomal genes governs cellular polyamine levels from yeasts to humans. In many cases of productively utilized frameshifting, the proportion of ribosomes that frameshift at a shift-prone site is enhanced by specific nascent peptide or mRNA context features. Such mRNA signals, which can be 5′ or 3′ of the shift site or both, can act by pairing with ribosomal RNA or as stem loops or pseudoknots even with one component being 4 kb 3′ from the shift site. Transcriptional realignment at slippage-prone sequences also generates productively utilized products encoded trans-frame with respect to the genomic sequence. This too can be enhanced by nucleic acid structure. Together with dynamic codon redefinition, frameshifting is one of the forms of recoding that enriches gene expression.

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Section: Free Living Organism Chromosomal Genes Lacking Mobile Predecmentioning

confidence: 99%

Ribosomal frameshifting and transcriptional slippage: From genetic steganography and cryptography to adventitious use

Atkins¹,

Loughran²,

Bhatt³

et al. 2016

Nucleic Acids Res

269

367

View full text Add to dashboard Cite

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“…They are essential for cell proliferation, differentiation, and apoptosis [ 1 , 2 ], and function as anti-inflammatories, anti-oxidants, and free radical scavengers [ 3 - 5 ]. During the aging process, polyamines, especially spermidine (SPD), are depleted in the spleen, ovary, liver, stomach, lung, kidney, muscle, and thymus [ 6 , 7 ]. Stegehake, et al reported that cellular polyamine levels decreased in aging post-reproductive Caenorhabditis elegans [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…During the aging process, polyamines, especially spermidine (SPD), are depleted in the spleen, ovary, liver, stomach, lung, kidney, muscle, and thymus [ 6 , 7 ]. Stegehake, et al reported that cellular polyamine levels decreased in aging post-reproductive Caenorhabditis elegans [ 6 ]. Enot, et al found that polyamines are depleted by palmitate, but enhanced by oleate in mouse liver, heart, and skeletal muscle [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Spermine and spermidine reversed age-related cardiac deterioration in rats

Zhang

Wang

et al. 2017

Oncotarget

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Aging is the most important risk factor for cardiovascular disease (CVD). Slowing or reversing the physiological impact of heart aging may reduce morbidity and mortality associated with age-related CVD. The polyamines, spermine (SP) and spermidine (SPD) are essential for cell growth, differentiation and apoptosis, and levels of both decline with age. To explore the effects of these polyamines on heart aging, we administered SP or SPD intraperitoneally to 22- to 24-month-old rats for 6 weeks. Both treatments reversed and inhibited age-related myocardial morphology alterations, myocardial fibrosis, and cell apoptosis. Using combined proteomics and metabolomics analyses, we identified proteins and metabolites up- or downregulated by SP and SPD in aging rat hearts. SP upregulated 51 proteins and 28 metabolites while downregulating 80 proteins and 29 metabolites. SPD upregulated 44 proteins and 24 metabolites and downregulated 84 proteins and 176 metabolites. These molecules were mainly associated with immune responses, blood coagulation, lipid metabolism, and glutathione metabolism pathways. Our study provides novel molecular information on the cardioprotective effects of polyamines in the aging heart, and supports the notion that SP and SPD are potential clinical therapeutics targeting heart disease.

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