Evidence map›Paper›PMID 17224065›Full record

ArticleBMC biochemistry2007

Effect of polyamines and synthetic polyamine-analogues on the expression of antizyme (AtoC) and its regulatory genes.

Panagiota S Filippou, Efthimia E Lioliou, Christos A Panagiotidis, Constantinos M Athanassopoulos, Thomas Garnelis, Dionyssios Papaioannou, Dimitrios A Kyriakidis

Abstract read
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Article in BMC biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Frontiers in microbiology · 2017
    Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Panagiota S FilippouLaboratory of Biochemistry, Department of Chemistry, Aristotle University of Thessaloniki, Thessaloniki, 54124, Greece. filippouyiota@yahoo.gr <filippouyiota@yahoo.gr>
Efthimia E Lioliou
Christos A Panagiotidis
Constantinos M Athanassopoulos
Thomas Garnelis
Dionyssios Papaioannou
Dimitrios A Kyriakidis

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn bacteria, the biosynthesis of polyamines is modulated at the level of transcription as well as post-translationally. Antizyme (Az) has long been identified as a non-competitive protein inhibitor of polyamine biosynthesis in E. coli. Az was also revealed to be the product of the atoC gene. AtoC is the response regulator of the AtoS-AtoC two-component system and it functions as the positive transcriptional regulator of the atoDAEB operon genes, encoding enzymes involved in short chain fatty acid metabolism. The antizyme is referred to as AtoC/Az, to indicate its dual function as both a transcriptional and post-translational regulator.

resultsThe roles of polyamines on the transcription of atoS and atoC genes as well as that of atoDAEB(ato) operon were studied. Polyamine-mediated induction was tested both in atoSC positive and negative E. coli backgrounds by using beta-galactosidase reporter constructs carrying the appropriate promoters patoDAEB, patoS, patoC. In addition, a selection of synthetic polyamine analogues have been synthesized and tested for their effectiveness in inducing the expression of atoC/Az, the product of which plays a pivotal role in the feedback inhibition of putrescine biosynthesis and the transcriptional regulation of the ato operon. The effects of these compounds were also determined on the ato operon expression. The polyamine analogues were also tested for their effect on the activity of ornithine decarboxylase (ODC), the key enzyme of polyamine biosynthesis and on the growth of polyamine-deficient E. coli.

conclusionPolyamines, which have been reported to induce the protein levels of AtoC/Az in E. coli, act at the transcriptional level, since they cause activation of the atoC transcription. In addition, a series of polyamine analogues were studied on the transcription of atoC gene and ODC activity.

Indexed as

Genes, RegulatorBiogenic PolyaminesDNA-Binding ProteinsEscherichia coliEscherichia coli ProteinsOperonOrnithine DecarboxylaseProtein Processing, Post-TranslationalTranscription, GeneticAtoC protein, E coliBiogenic PolyaminesDNA-Binding ProteinsEscherichia coli ProteinsOrnithine Decarboxylase

Identifiers

PMID17224065
PMCPMC1784093

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.