Evidence map›Paper›PMID 29254681›Full record

ArticleEBioMedicine2018

Mice with an Oncogenic HRAS Mutation are Resistant to High-Fat Diet-Induced Obesity and Exhibit Impaired Hepatic Energy Homeostasis.

Daiju Oba, Shin-Ichi Inoue, Sachiko Miyagawa-Tomita, Yasumi Nakashima, Tetsuya Niihori, Seiji Yamaguchi, Yoichi Matsubara, Yoko Aoki

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Syndromic forms of congenital hyperinsulinism.Frontiers in endocrinology · 2023
    Review
  10. New prospectives on treatment opportunities in RASopathies.American journal of medical genetics. Part C, Seminars in medical genetics · 2022
    Review
  11. Article
  12. Article
  13. The RASopathies: from pathogenetics to therapeutics.Disease models & mechanisms · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Daiju ObaDepartment of Medical Genetics, Tohoku University School of Medicine, Sendai, Japan.
Shin-Ichi InoueDepartment of Medical Genetics, Tohoku University School of Medicine, Sendai, Japan. Electronic address: sinoue@med.tohoku.ac.jp.
Sachiko Miyagawa-TomitaDepartment of Pediatric Cardiology, Tokyo Women's Medical University, Tokyo, Japan; Division of Cardiovascular Development and Differentiation, Medical Research Institute, Tokyo Women's Medical University, Tokyo, Japan; Department of Veterinary Technology, Yamazaki gakuen University, Tokyo, Japan.
Yasumi NakashimaDepartment of Pediatrics, Seirei Hamamatsu General Hospital, Shizuoka, Japan.
Tetsuya NiihoriDepartment of Medical Genetics, Tohoku University School of Medicine, Sendai, Japan.
Seiji YamaguchiDepartment of Pediatrics, Shimane University, Faculty of Medicine, Shimane, Japan.
Yoichi MatsubaraDepartment of Medical Genetics, Tohoku University School of Medicine, Sendai, Japan; National Research Institute for Child Health and Development, Tokyo, Japan.
Yoko AokiDepartment of Medical Genetics, Tohoku University School of Medicine, Sendai, Japan. Electronic address: aokiy@med.tohoku.ac.jp.
Tohoku University · JPSeirei Hamamatsu General Hospital · JPShimane University · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Costello syndrome is a "RASopathy" that is characterized by growth retardation, dysmorphic facial appearance, hypertrophic cardiomyopathy and tumor predisposition. >80% of patients with Costello syndrome harbor a heterozygous germline G12S mutation in HRAS. Altered metabolic regulation has been suspected because patients with Costello syndrome exhibit hypoketotic hypoglycemia and increased resting energy expenditure, and their growth is severely retarded. To examine the mechanisms of energy reprogramming by HRAS activation in vivo, we generated knock-in mice expressing a heterozygous Hras G12S mutation (Hras

Indexed as

Energy MetabolismHomeostasisOncogenesAnimalsCarnitineDiet, High-FatFaceFatty AcidsFemaleGene Expression RegulationGene Knock-In TechniquesGlucoseGlutamineHypertrophyKidneyLiveracylcarnitineCarnitineFatty AcidsGlucoseGlutamineHras protein, mouseProto-Oncogene Proteins p21(ras)ras ProteinsCancer metabolismCostello syndromeDiet-induced obesityERKHras G12SMitochondrial fatty acid oxidation

Identifiers

PMID29254681
PMCPMC5828294
OpenAlexW2774261748

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.