Evidence map›Paper›PMID 23859490›Full record

ArticleJournal of neurochemistry2013

Purine metabolism during neuronal differentiation: the relevance of purine synthesis and recycling.

Martin Göttle, Heike Burhenne, Diane Sutcliffe, H A Jinnah

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

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  18. Systematic Tracking of Disrupted Modules Identifies Altered Pathways Associated with Congenital Heart Defects in Down Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2015
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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

4 authors at 2 institutions in 2 countries.

Martin GöttleDepartment of Neurology, Emory University, Atlanta, Georgia, USA.
Heike Burhenne
Diane Sutcliffe
H A Jinnah
Emory University · USMedizinische Hochschule Hannover · DE

Funding

Lesch-Nyhan Disease: A Model for Complex Genetic, Proteomic & Metabolic PathwaysR24DK082840 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FRIEDMANN, THEODORE · 2008 to 2012
$7.3M
NEUROBIOLOGY OF DYSTONIAR01NS040470 · NINDS · JOHNS HOPKINS UNIVERSITY · PI JINNAH, HYDER A · 2000 to 2008
$2.5M
NIDDK NIH HHS R24 DK082840NINDS NIH HHS R01 NS040470
6 · The paper itself

Abstract

Purines are a class of small organic molecules that are essential for all cells. They play critical roles in neuronal differentiation and function. Their importance is highlighted by several inherited disorders of purine metabolism, such as Lesch-Nyhan disease, which is caused by a deficiency of the purine salvage enzyme, hypoxanthine-guanine phosphoribosyltransferase (HGprt). Despite the known importance of purines in the nervous system, knowledge regarding their metabolism in neurons is limited. In the current studies, purine pools and their metabolism were examined in rat PC6-3 cells, a PC12 pheochromocytoma subclone that undergoes robust differentiation with nerve growth factor. The results were compared with five new independent PC6-3 subclones with defective purine recycling because of different mutations affecting HGprt enzyme activity. The results demonstrate an increase in most purines and in energy state following neuronal differentiation, as well as specific abnormalities when purine recycling is lost. The loss of HGprt-mediated purine recycling also is associated with significant loss of dopamine and related metabolites in the mutant PC6-3 lines, suggesting an important connection between purine and dopamine pathways. These results provide insights into how purine pools and metabolism change with neuronal differentiation, and how specific enzyme defects may cause neuronal dysfunction. Differentiation of dopaminergic PC6-3 cells is accompanied by increased purine pools and energy state. The lack of a functional purine recycling pathway causes purine limitation in both undifferentiated and differentiated cells, as well as profound loss of dopamine content. The results imply an unknown mechanism by which intracellular purine levels regulate dopamine levels.

Indexed as

AnimalsCell DifferentiationCell ProliferationDopamineHypoxanthine PhosphoribosyltransferaseMutationNerve Growth FactorNeuronsNeurotransmitter Transport ProteinsPC12 CellsPurinesRatsDopamineHypoxanthine PhosphoribosyltransferaseNerve Growth FactorNeurotransmitter Transport ProteinsPurinesdopamine neuronshypoxanthine-guanine phosphoribosyltransferaseLesch-Nyhan diseasepurine nucleotide

Identifiers

PMID23859490
PMCPMC3859826
OpenAlexW2020294802

What OpenQuestion holds

Textmetadata
LicenceTDM
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.