Evidence map›Paper›PMID 34018631›Full record

ArticleJournal of clinical laboratory analysis2021

The variations in human orphan G protein-coupled receptor QRFPR affect PI3K-AKT-mTOR signaling.

Huanzheng Li, Ran Lou, Xueqin Xu, Chenyang Xu, Yuan Yu, Yunzhi Xu, Lin Hu, Yanbao Xiang, Xuan Lin, Shaohua Tang

Open access · goldAbstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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 4 institutions in 1 country.

Huanzheng LiWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.
Ran LouDepartment of Acupuncture, Wenzhou Central Hospital, Wenzhou, China.
Xueqin XuWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.
Chenyang XuWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.
Yuan YuWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.
Yunzhi XuWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.
Lin HuDepartment of Blood Transfusion, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Yanbao XiangWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.
Xuan LinWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.
Shaohua TangWenzhou Key Laboratory of Birth Defects, Wenzhou Central Hospital, Dingli Clinical Medical College of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0002-2918-8532
Wenzhou Medical University · CNNanchang University · CNSoochow University · CNWenzhou Central Hospital · CN

Funding

Wenzhou Major Science and Technology Project ZS2017004Zhejiang Provincial Natural Science Foundation of China Q16H200001
6 · The paper itself

Abstract

backgroundQRFPR is a recently identified member of the G protein-coupled receptor and is an orphan receptor for 26Rfa, which plays important role in the regulation of many physiological functions.

methodsHere, we employed whole exome sequencing (WES) to examine the patients with intellectual disability (ID) and difficulty in feeding. We performed SIFT and PolyPhen2 predictions for the variants. The structure model was built from scratch by I-TASSER. Here, results derived from a number of cell-based functional assays, including shRNA experiment, intracellular Ca

resultHere, we identified two QRFPR variants at c.202 T>C (p.Y68H) and c.1111C>T (p.R371W) in 2 unrelated individuals. Structural analysis revealed that p.Y68H and p.R371W variants may affect the side chain structure of adjacent amino acids causing reduced binding of QRFPR to 26Rfa. The results show that QRFPR stimulated by 26Rfa leading to the transient rise of intracellular Ca

conclusionsOur findings suggest that QRFPR acts as important role in neurodevelopment, and the effects of QRFPR are likely to be mediated by the Ca

Indexed as

Genetic VariationSignal TransductionBase SequenceCalcium SignalingChildChild, PreschoolExome SequencingHEK293 CellsHumansIntracellular SpaceMaleModels, MolecularPhenotypePhosphatidylinositol 3-KinasesPhosphorylationProtein StabilityMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktQRFPR protein, humanReceptors, G-Protein-CoupledTOR Serine-Threonine KinasesCa2+G protein-coupled receptor (GPCR)neurodevelopmentPI3K-AKT-mTOR signalingQRFPR

Identifiers

PMID34018631
PMCPMC8275006
OpenAlexW3160853876

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.