Evidence map›Paper›PMID 35460606›Full record

ArticleAmerican journal of human genetics2022

Powerful and robust inference of complex phenotypes' causal genes with dependent expression quantitative loci by a median-based Mendelian randomization.

Lin Jiang, Lin Miao, Guorong Yi, Xiangyi Li, Chao Xue, Mulin Jun Li, Hailiang Huang, Miaoxin Li

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Article in American journal of human genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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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

8 authors.

Lin JiangResearch Center of Medical Sciences, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China. Electronic address: jianglin@gdph.org.cn.
Lin MiaoResearch Center of Medical Sciences, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, China.
Guorong YiZhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Beijing Institute of Technology, Zhuhai 519088, China.
Xiangyi LiZhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Chao XueZhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Mulin Jun LiMedical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin 300070, China; The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin 300070, China.
Hailiang HuangMassachusetts General Hospital, 185 Cambridge Street, Boston, MA 02114, USA.
Miaoxin LiZhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China; Center for Precision Medicine, Sun Yat-sen University, Guangzhou 510080, China. Electronic address: limiaoxin@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Isolating the causal genes from numerous genetic association signals in genome-wide association studies (GWASs) of complex phenotypes remains an open and challenging question. In the present study, we proposed a statistical approach, the effective-median-based Mendelian randomization (MR) framework, for inferring the causal genes of complex phenotypes with the GWAS summary statistics (named EMIC). The effective-median method solved the high false-positive issue in the existing MR methods due to either correlation among instrumental variables or noises in approximated linkage disequilibrium (LD). EMIC can further perform a pleiotropy fine-mapping analysis to remove possible false-positive estimates. With the usage of multiple cis-expression quantitative trait loci (eQTLs), EMIC was also more powerful than the alternative methods for the causal gene inference in the simulated datasets. Furthermore, EMIC rediscovered many known causal genes of complex phenotypes (schizophrenia, bipolar disorder, and total cholesterol) and reported many new and promising candidate causal genes. In sum, this study provided an efficient solution to discriminate the candidate causal genes from vast amounts of GWAS signals with eQTLs. EMIC has been implemented in our integrative software platform KGGSEE.

Indexed as

Genome-Wide Association StudyMendelian Randomization AnalysisHumansLinkage DisequilibriumPhenotypePolymorphism, Single NucleotideQuantitative Trait Locicausal geneexpression quantitative trait locusgenome-wide association studyMendelian randomization

Identifiers

PMID35460606
PMCPMC9118119

What Socratic holds

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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 Socratic graph.