Evidence map›Paper›PMID 26399640›Full record

ArticleMolecular neurobiology2016

Evolution of GLUD2 Glutamate Dehydrogenase Allows Expression in Human Cortical Neurons.

Cleanthe Spanaki, Dimitra Kotzamani, Kleopas Kleopa, Andreas Plaitakis

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Evolution of Glutamate Metabolism viaInternational journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Glutamate dehydrogenase is essential to sustain neuronal oxidative energy metabolism during stimulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
  10. Review
  11. Article
  12. Article
  13. 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

4 authors at 2 institutions in 2 countries.

Cleanthe SpanakiDepartment of Neurology, Faculty of Medicine, School of Health Sciences, University of Crete, Heraklion, Crete, Greece. kliospanaki@gmail.com.
Dimitra KotzamaniDepartment of Neurology, Faculty of Medicine, School of Health Sciences, University of Crete, Heraklion, Crete, Greece.
Kleopas KleopaNeuroscience Laboratory and Neurology Clinics, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus.
Andreas PlaitakisDepartment of Neurology, Faculty of Medicine, School of Health Sciences, University of Crete, Heraklion, Crete, Greece.
University of Crete · GRCyprus Institute of Neurology and Genetics · CY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human hGDH2 arose via duplication in the apes and driven by positive selection acquired enhanced catalytic ability under conditions inhibitory to its precursor hGDH1 (common to all mammals). To explore the biological advantage provided by the novel enzyme, we studied, by immunohistochemistry (IHC) and immunofluorescence (IF), hGDH1 and hGDH2 expression in the human brain. Studies on human cortical tissue using anti-hGDH1-specific antibody revealed that hGDH1 was expressed in glial cells (astrocytes, oligodendrocytes, and oligodendrocyte precursors) with neurons being devoid of hGDH1 staining. In contrast, an hGDH2-specific antiserum labeled both astrocytes and neurons. Specifically, hGDH2 immunoreactivity was found in the cytoplasm of large neuronal cells within coarse structures resembling mitochondria. These were distributed either in the perikaryon or in the cell periphery. Double immunofluorescence (IF) suggested that the latter represented hGDH2-labeled mitochondria of presynaptic nerve terminals. Hence, hGDH2 evolution bestowed large human neurons with enhanced glutamate metabolizing capacity, thus strengthening cortical excitatory transmission.

Indexed as

Evolution, MolecularAdultAgedAged, 80 and overAntibody SpecificityAstrocytesCalnexinCell NucleusCerebral CortexGlutamate DehydrogenaseHumansMiddle AgedNeuronsCalnexinGLUD1 protein, humanGLUD2 protein, humanGlutamate DehydrogenasehGDH1hGDH2Human brainNeuron glial cells

Identifiers

PMID26399640
OpenAlexW1684949463

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.