Evidence map›Paper›PMID 31954716›Full record

ReviewBiochemical pharmacology2020

Pathway analysis of glutamate-mediated, calcium-related signaling in glioma progression.

Zhe Pei, Kuo-Chieh Lee, Amber Khan, Gabriell Erisnor, Hoau-Yan Wang

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 72 citations in OpenAlex.

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  7. Neuron-glioma synaptic transmission amplified by free 19S proteasome-mediated AMPAR deubiquitination promotes tumor progression.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

5 authors at 2 institutions in 1 country.

Zhe PeiDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, 160 Convent Avenue, New York, NY 10031, USA.
Kuo-Chieh LeeDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, 160 Convent Avenue, New York, NY 10031, USA.
Amber KhanDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, 160 Convent Avenue, New York, NY 10031, USA; Department of Biology, Neuroscience Program, Graduate School of The City University of New York, 365 Fifth Avenue, New York, NY 10061, USA.
Gabriell ErisnorDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, 160 Convent Avenue, New York, NY 10031, USA.
Hoau-Yan WangDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, 160 Convent Avenue, New York, NY 10031, USA; Department of Biology, Neuroscience Program, Graduate School of The City University of New York, 365 Fifth Avenue, New York, NY 10061, USA. Electronic address: hywang@med.cuny.edu.
City University of New York · USCity College of New York · US

Funding

Linking peripheral and brain insulin resistance to AD neuropathology and cognitionRF1AG059621 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI AHIMA, REXFORD S., ARNOLD, STEVEN E · 2018 to 2018
$3.8M
mGluR5 hypoactivity is integral to glutamatergic dysregulation in schizophreniaR01MH116463 · NIMH · THOMAS JEFFERSON UNIVERSITY · PI HAHN, CHANG-GYU · 2019 to 2024
$3.2M
NIA NIH HHS RF1 AG059621NIMH NIH HHS R01 MH116463
6 · The paper itself

Abstract

Brain tumors, particularly high-grade glioblastomas, are a crucial public health issue due to poor prognosis and an extremely low survival rate. The glioblastoma multiforme (GBM) grows rapidly within its unique microenvironment that is characterized by active neural communications. Therefore, diverse neurotransmitters not only maintain normal brain functions but also influence glioma progression. To fully appreciate the relationship between neurotransmitters and glioma progression, we reviewed potential neurotransmitter contributors in human GBM and the much less aggressive Low-grade glioma (LGG) by combining previously published data from gene-mutation/mRNA sequencing databases together with protein-protein interaction (PPI) network analysis results. The summarized results indicate that glutamatergic and calcium signaling may provide positive feedback to promote glioma formation through 1) metabolic reprogramming and genetic switching to accelerate glioma duplication and progression; 2) upregulation of cytoskeleton proteins and elevation of intracellular Ca

Indexed as

Signal TransductionAnimalsBrain NeoplasmsCalciumDisease ProgressionGlioblastomaGlutamic AcidHumansNeuronsNitric OxideCalciumGlutamic AcidNitric OxideCalcium waivesGamma-aminobutyric acid (GABA) receptorGlutamateMetabolic reprogrammingNitric Oxide synthesize (NOS)N-methyl-d-aspartate (NMDA) receptorTransmittersα-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor

Identifiers

PMID31954716
PMCPMC8403340
OpenAlexW2998960573

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.