Evidence map›Paper›PMID 28797121›Full record

ArticlePloS one2017

Non-alcoholic fatty liver disease in mice with heterozygous mutation in TMED2.

Wenyang Hou, Swati Gupta, Marie-Claude Beauchamp, Libin Yuan, Loydie A Jerome-Majewska

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. TMED family genes and their roles in human diseases.International journal of medical sciences · 2023
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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.

Wenyang HouDepartment of Human Genetics, McGill University, Montreal, Québec, Canada.
Swati GuptaDepartment of Human Genetics, McGill University, Montreal, Québec, Canada.
Marie-Claude BeauchampDepartment of Human Genetics, McGill University, Montreal, Québec, Canada.
Libin YuanDepartment of Human Genetics, McGill University, Montreal, Québec, Canada.
Loydie A Jerome-MajewskaDepartment of Human Genetics, McGill University, Montreal, Québec, Canada.ORCID http://orcid.org/0000-0002-5047-4058
McGill University · CAMcGill University Health Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transmembrane emp24 domain/p24 (TMED) family are essential components of the vesicular transport machinery. Members of the TMED family serve as cargo receptors implicated in selection and packaging of endoplasmic reticulum (ER) luminal proteins into coatomer (COP) II coated vesicles for anterograde transport to the Golgi. Deletion or mutations of Tmed genes in yeast and Drosophila results in ER-stress and activation of the unfolded protein response (UPR). The UPR leads to expression of genes and proteins important for expanding the folding capacity of the ER, degrading misfolded proteins, and reducing the load of new proteins entering the ER. The UPR is activated in non-alcoholic fatty liver disease (NAFLD) in human and mouse and may contribute to the development and the progression of NAFLD. Tmed2, the sole member of the vertebrate Tmed β subfamily, exhibits tissue and temporal specific patterns of expression in embryos and developing placenta but is ubiquitously expressed in all adult organs. We previously identified a single point mutation, the 99J mutation, in the signal sequence of Tmed2 in an N-ethyl-N-nitrosourea (ENU) mutagenesis screen. Histological and molecular analysis of livers from heterozygous mice carrying the 99J mutation, Tmed299J/+, revealed a requirement for TMED2 in liver health. We show that Tmed299J/+ mice had decreased levels of TMED2 and TMED10, dilated endoplasmic reticulum membrane, and increased phosphorylation of eIF2α, indicating ER-stress and activation of the UPR. Increased expression of Srebp1a and 2 at the newborn stage and increased incidence of NAFLD were also found in Tmed299J/+ mice. Our data establishes Tmed299J/+ mice as a novel mouse model for NAFLD and supports a role for TMED2 in liver health.

Indexed as

Point MutationAnimalsEndoplasmic Reticulum StressHep G2 CellsHeterozygoteHumansLiverMembrane ProteinsMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSterol Regulatory Element Binding Protein 1Sterol Regulatory Element Binding Protein 2Unfolded Protein ResponseUp-RegulationVesicular Transport ProteinsMembrane ProteinsSrebf1 protein, mouseSrebf2 protein, mouseSterol Regulatory Element Binding Protein 1Sterol Regulatory Element Binding Protein 2Tmed10 protein, mouseTmed2 protein, mouseVesicular Transport Proteins

Identifiers

PMID28797121
PMCPMC5552249
OpenAlexW2743399307

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.