Evidence map›Paper›PMID 31300553›Full record

ArticleThe Journal of biological chemistry2019

eIF4G1 and carboxypeptidase E axis dysregulation in

Seokwon Jo, Amber Lockridge, Emilyn U Alejandro

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  9. Review
  10. Posttranslational modifications in diabetes: Mechanisms and functions.Reviews in endocrine & metabolic disorders · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. A nexus of lipid andFrontiers in endocrinology · 2022
    Review
  15. Frontiers in endocrinology · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Seokwon JoDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455.
Amber LockridgeDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455.
Emilyn U AlejandroDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455. Electronic address: ealejand@umn.edu.
University of Minnesota Medical Center · US

Funding

Minnesota Obesity Prevention Training (MnOPT)T32DK083250 · NIDDK · UNIVERSITY OF MINNESOTA · PI KOTZ, CATHERINE M, LASKA, MELISSA N. · 2010 to 2024
$5.1M
The role of O-linked N-Acetylglucosamine Homeostasis in Pancreatic Beta-cell Development and FunctionR01DK115720 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2022
$1.9M
O-linked-N-acetylglucosamine Post-translational Modification in Pancreatic Beta-cells Regulating ER Stress and Mitochondrial FunctionR21DK112144 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2017 to 2019
$576k
Mechanisms of Developmental Programing of beta-cell Susceptibility to GlucolipotoxicityK01DK103823 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2014 to 2017
$572k
Role of placental nutrient-sensor protein mTOR on fetal programming of beta-cell dysfunction and susceptibility to type 2 diabetesR03DK114465 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2019
$360k
Molecular mechanisms of O-GlcNAcylation in prediabetic beta-cell hypersecretion during diet-induced obesityF31DK113694 · NIDDK · UNIVERSITY OF MINNESOTA · PI LOCKRIDGE, AMBER D · 2018 to 2019
$82k
NIDDK NIH HHS F31 DK113694NIDDK NIH HHS K01 DK103823NIDDK NIH HHS R01 DK115720NIDDK NIH HHS R03 DK114465NIDDK NIH HHS R21 DK112144NIDDK NIH HHS T32 DK083250
6 · The paper itself

Abstract

An early hallmark of type 2 diabetes is a failure of proinsulin-to-insulin processing in pancreatic β-cells, resulting in hyperproinsulinemia. Proinsulin processing is quite sensitive to nutrient flux, and β-cell-specific deletion of the nutrient-sensing protein modifier OGlcNAc transferase (βOGTKO) causes β-cell failure and diabetes, including early development of hyperproinsulinemia. The mechanisms underlying this latter defect are unknown. Here, using several approaches, including site-directed mutagenesis, Click

Indexed as

AnimalsCarboxypeptidase HDiabetes MellitusDisease Models, AnimalEukaryotic Initiation Factor-4GInsulin-Secreting CellsMiceMice, KnockoutN-AcetylglucosaminyltransferasesCarboxypeptidase HEif4g1 protein, mouseEukaryotic Initiation Factor-4GN-AcetylglucosaminyltransferasesO-GlcNAc transferaseChopdiabeteseIF4G1ER-stresshyperproinsulinemiainsulin synthesisisletO-GlcNAcylationO-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT)post-translational modification (PTM)

Identifiers

PMID31300553
PMCPMC6721936
OpenAlexW2957263848

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.