Evidence map›Paper›PMID 24799716›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Mutation of mouse Samd4 causes leanness, myopathy, uncoupled mitochondrial respiration, and dysregulated mTORC1 signaling.

Zhe Chen, William Holland, John M Shelton, Aktar Ali, Xiaoming Zhan, Sungyong Won, Wataru Tomisato, Chen Liu, Xiaohong Li, Eva Marie Y Moresco and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  6. Review
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  9. Structural basis for binding ofProceedings of the National Academy of Sciences of the United States of America · 2023
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  10. Review
  11. A novel testis-enriched gene,Frontiers in cell and developmental biology · 2022
    Article
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  20. Chronic innate immune activation of TBK1 suppresses mTORC1 activity and dysregulates cellular metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

11 authors at 2 institutions in 1 country.

Zhe ChenCenter for Genetics of Host Defense.
William HollandDepartment of Internal Medicine, Touchstone Diabetes Center.
John M SheltonDepartment of Internal Medicine, Division of Cardiology.
Aktar AliDepartment of Internal Medicine, and.
Xiaoming ZhanCenter for Genetics of Host Defense.
Sungyong WonCenter for Genetics of Host Defense.
Wataru TomisatoCenter for Genetics of Host Defense.
Chen LiuDepartment of Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Xiaohong LiCenter for Genetics of Host Defense.
Eva Marie Y MorescoCenter for Genetics of Host Defense.
Bruce BeutlerCenter for Genetics of Host Defense, bruce.beutler@utsouthwestern.edu.
Center for Human Genetics · USThe University of Texas Southwestern Medical Center · US

Funding

Systems Biology CoreU19AI100627 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI ULEVITCH, RICHARD J · 2012 to 2021
$49.1M
Adiponectin Receptors and S1P Signaling in Beta Cell Survival and ProliferationR00DK094973 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HOLLAND, WILLIAM L · 2014 to 2016
$894k
NIAID NIH HHS U19 AI100627NIDDK NIH HHS R00 DK094973
6 · The paper itself

Abstract

Sterile alpha motif domain containing protein 4 (Samd4) is an RNA binding protein that mediates translational repression. We identified a Samd4 missense mutation, designated supermodel, that caused leanness and kyphosis associated with myopathy and adipocyte defects in C57BL/6J mice. The supermodel mutation protected homozygous mice from high fat diet-induced obesity, likely by promoting enhanced energy expenditure through uncoupled mitochondrial respiration. Glucose tolerance was impaired due to diminished insulin release in homozygous mutant mice. The defects of metabolism in supermodel mice may be explained by dysregulated mechanistic target of rapamycin complex 1 (mTORC1) signaling, evidenced by hypophosphorylation of 4E-BP1 and S6 in muscle and adipose tissues of homozygous mice. Samd4 may interface with mTORC1 signaling through an interaction with 14-3-3 proteins and with Akt, which phosphorylates Samd4 in vitro.

Indexed as

MutationSignal Transduction14-3-3 ProteinsAdipocytesAmino Acid MotifsAnimalsBody CompositionFemaleGlucoseGlucose Tolerance TestMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMultiprotein ComplexesMutagenesis14-3-3 ProteinsGlucoseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesRepressor ProteinsRNA-Binding ProteinsSmaug1 protein, mouseTOR Serine-Threonine KinasesAkt/PKBN-ethyl-N-nitrosourea

Identifiers

PMID24799716
PMCPMC4034201
OpenAlexW2027409371

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.