Evidence map›Paper›PMID 28478509›Full record

ArticleMolecular neurobiology2018

p73 Regulates Primary Cortical Neuron Metabolism: a Global Metabolic Profile.

Massimiliano Agostini, Maria Victoria Niklison-Chirou, Margherita Maria Annicchiarico-Petruzzelli, Sandro Grelli, Nicola Di Daniele, Ilias Pestlikis, Richard A Knight, Gerry Melino, Alessandro Rufini

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Metabolomic Analysis Identifies Betaine as a Key Mediator ofInternational journal of molecular sciences · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Observational
  7. Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Review
  10. Review
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

9 authors at 3 institutions in 2 countries.

Massimiliano AgostiniMedical Research Council, Toxicology Unit, Leicester University, Leicester, LE1 9HN, UK.
Maria Victoria Niklison-ChirouMedical Research Council, Toxicology Unit, Leicester University, Leicester, LE1 9HN, UK.
Margherita Maria Annicchiarico-PetruzzelliBiochemistry Laboratory IDI-IRCC, c/o Department of Experimental Medicine and Surgery, "Tor Vergata" University Hospital, Rome, Italy.
Sandro GrelliDepartment of Experimental Medicine and Surgery, University of Rome "Tor Vergata", 00133, Rome, Italy.
Nicola Di DanieleDepartment of Systems Medicine, Nephrology and Hypertension Unit, "Tor Vergata" University Hospital, Rome, Italy.
Ilias PestlikisDepartment of Experimental Medicine and Surgery, University of Rome "Tor Vergata", 00133, Rome, Italy.
Richard A KnightMedical Research Council, Toxicology Unit, Leicester University, Leicester, LE1 9HN, UK.
Gerry MelinoMedical Research Council, Toxicology Unit, Leicester University, Leicester, LE1 9HN, UK. gm89@le.ac.uk.
Alessandro RufiniDepartment of Cancer Studies, University of Leicester, Leicester, LE2 7LX, UK. ar230@le.ac.uk.
University of Rome Tor Vergata · ITMedical Research Council · GBUniversity of Leicester · GB

Funding

AIRC AIRC 2014 IG15653AIRC 5xmille MCO9979Fondazione Roma malattie Non trasmissibili Cronico-Degenerative NCDS-2013-00000334Medical Research Council MC_U132670600
6 · The paper itself

Abstract

The transcription factor p73 has been demonstrated to play a significant role in survival and differentiation of neuronal stem cells. In this report, by employing comprehensive metabolic profile and mitochondrial bioenergetics analysis, we have explored the metabolic alterations in cortical neurons isolated from p73 N-terminal isoform specific knockout animals. We found that loss of the TAp73 or ΔNp73 triggers selective biochemical changes. In particular, p73 isoforms regulate sphingolipid and phospholipid biochemical pathway signaling. Indeed, sphinganine and sphingosine levels were reduced in p73-depleted cortical neurons, and decreased levels of several membrane phospholipids were also observed. Moreover, in line with the complexity associated with p73 functions, loss of the TAp73 seems to increase glycolysis, whereas on the contrary, loss of ΔNp73 isoform reduces glucose metabolism, indicating an isoform-specific differential effect on glycolysis. These changes in glycolytic flux were not reflected by parallel alterations of mitochondrial respiration, as only a slight increase of mitochondrial maximal respiration was observed in p73-depleted cortical neurons. Overall, our findings reinforce the key role of p73 in regulating cellular metabolism and point out that p73 exerts its functions in neuronal biology at least partially through the regulation of metabolic pathways.

Indexed as

MetabolomicsAnimalsCell MembraneCells, CulturedCerebral CortexEnergy MetabolismFatty AcidsGlycolysisMice, KnockoutMitochondriaNeuronsPentose Phosphate PathwayProtein IsoformsSphingolipidsTumor Protein p73Fatty AcidsProtein IsoformsSphingolipidsTumor Protein p73MetabolismNeuronsp53 familyp73Sphingolipids

Identifiers

PMID28478509
OpenAlexW2610243742

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.