Evidence map›Paper›PMID 26147511›Full record

SynthesisPloS one2015

The C825T Polymorphism of the G-Protein β3 Gene as a Risk Factor for Depression: A Meta-Analysis.

Liang Fang, Chanjuan Zhou, Shunjie Bai, Chenglong Huang, Junxi Pan, Ling Wang, Xinfa Wang, Qiang Mao, Lu Sun, Peng Xie

Open access · goldAbstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. G protein beta 3(Oncotarget · 2018
    Article
  5. Article
  6. Review
  7. 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

10 authors at 2 institutions in 1 country.

Liang FangDepartment of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Institute of Neuroscience, Chongqing Medical University, Chongqing, China.
Chanjuan ZhouDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Institute of Neuroscience, Chongqing Medical University, Chongqing, China.
Shunjie BaiDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Chenglong HuangDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Junxi PanDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Ling WangDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Institute of Neuroscience, Chongqing Medical University, Chongqing, China.
Xinfa WangDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Institute of Neuroscience, Chongqing Medical University, Chongqing, China.
Qiang MaoDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China.
Lu SunDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing, China.
Peng XieDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurobiology, Chongqing, China; Institute of Neuroscience, Chongqing Medical University, Chongqing, China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTheG-protein β3 gene (GNβ3) has been implicated in psychiatric illness through its effects upon intracellular transduction of several neurotransmitter receptors. Multiple studies have investigated the relationship of the C825T polymorphism of the GNβ3 gene (GNβ3 C825T) to depression and antidepressant response. However, the relationship between GNβ3 C825T and depression remains inconsistent. Therefore, here we performed a meta-analysis to investigate the role of GNβ3 C825Tin depression risk.

methodsPublished case-control studies examining the association between GNβ3 C825T and depression were systematically searched for through several electronic databases (PubMed, Scopus, Science Direct, Springer, Embase, psyINFO, and CNKI). The association between GNβ3 C825T and depression risk were assessed by odd ratios (ORs) and their 95% confidence intervals (CIs) for each study. Pooled ORs were constructed for allele contrast (C versus T), homozygote (CC versus TT) model, heterozygote (CC versus CT) model, dominant model (CC + CT versus TT), and recessive (CC versus TT+CT) model. In order to evaluate possible biases, a sensitivity analysis was conducted by sequential deletion of individual studies in an attempt to assess the contribution of each individual dataset to the pooled OR.

resultsNine studies, including 1055 depressed patients and 1325 healthy controls, were included. A significant association between GNβ3 C825Tand depression was found to exist, suggesting that the T-allele of GNβ3 C825Tcan increase susceptibility to depression. After stratification by ethnicity, the same association was found in the Asian subpopulation, but not the Caucasian subpopulation.

conclusionsThis is the first meta-analysis to reveal a relationship between GNβ3 C825T and depression. Asian T-allele carriers of GNβ3 C825T appear to be more susceptible to depression.

Indexed as

Polymorphism, Single NucleotideAllelesAmino Acid SubstitutionAsian PeopleCase-Control StudiesDepressive DisorderGenotypeHeterotrimeric GTP-Binding ProteinsHumansPublication BiasRisk FactorsWhite PeopleGNB3 protein, humanHeterotrimeric GTP-Binding Proteins

Identifiers

PMID26147511
PMCPMC4493085
OpenAlexW803946862

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.