Evidence map›Paper›PMID 30078228›Full record

ArticleJournal of cellular physiology2019

Mutual regulation between IGF-1R and IGFBP-3 in human corneal epithelial cells.

Rossella Titone, Meifang Zhu, Danielle M Robertson

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  9. IGFBP-3 functions as a molecular switch that mediates mitochondrial and metabolic homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
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  12. Review
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  17. Insulin receptor preserves mitochondrial function by binding VDAC1 in insulin insensitive mucosal epithelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    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.

Rossella TitoneThe Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas.ORCID 0000-0002-1528-331X
Meifang ZhuThe Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas.
Danielle M RobertsonThe Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas.
The University of Texas Southwestern Medical Center · US

Funding

Effects of Systemic Disease on Corneal Epithelial PathophysiologyR01EY024546 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI DANIELLE M. ROBERTSON · 2015 to 2026
$4.3M
Core Grant for Vision ResearchP30EY020799 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI NIEDERKORN, JERRY · 2010 to 2016
$4.1M
Interactive effects of OSA and T2DM on corneal and ocular surface diseaseR21EY024433 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI ROBERTSON, DANIELLE M. · 2014 to 2015
$433k
NEI NIH HHS P30 EY020799NEI NIH HHS R01 EY024546NEI NIH HHS R21 EY024433
6 · The paper itself

Abstract

The insulin-like growth factor type 1 receptor (IGF-1R) is part of the receptor tyrosine kinase superfamily. The activation of IGF-1R regulates several key signaling pathways responsible for maintaining cellular homeostasis, including survival, growth, and proliferation. In addition to mediating signal transduction at the plasma membrane, in serum-based models, IGF-1R undergoes SUMOylation by SUMO 1 and translocates to the nucleus in response to IGF-1. In corneal epithelial cells grown in serum-free culture, however, IGF-1R has been shown to accumulate in the nucleus independent of IGF-1. In this study, we report that the insulin-like growth factor binding protein-3 (IGFBP-3) mediates nuclear translocation of IGF-1R in response to growth factor withdrawal. This occurs via SUMOylation by SUMO 2/3. Further, IGF-1R and IGFBP-3 undergo reciprocal regulation independent of PI3k/Akt signaling. Thus, under healthy growth conditions, IGFBP-3 functions as a gatekeeper to arrest the cell cycle in G0/G1, but does not alter mitochondrial respiration in cultured cells. When stressed, IGFBP-3 functions as a caretaker to maintain levels of IGF-1R in the nucleus. These results demonstrate mutual regulation between IGF-1R and IGFBP-3 to maintain cell survival under stress. This is the first study to show a direct relationship between IGF-1R and IGFBP-3 in the maintenance of corneal epithelial homeostasis.

Indexed as

Active Transport, Cell NucleusCell Cycle CheckpointsCell LineEpithelial CellsEpithelium, CornealHomeostasisHumansInsulin-Like Growth Factor Binding Protein 3Primary Cell CultureReceptor, IGF Type 1Receptors, SomatomedinSignal TransductionSmall Ubiquitin-Related Modifier ProteinsStress, PhysiologicalSumoylationUbiquitinsIGF1R protein, humanIGFBP3 protein, humanInsulin-Like Growth Factor Binding Protein 3Receptor, IGF Type 1Receptors, SomatomedinSmall Ubiquitin-Related Modifier ProteinsSUMO2 protein, humanSUMO3 protein, humanUbiquitinscorneaepitheliuminsulininsulin-like growth factor binding protein-3 (IGFBP-3)insulin-like growth factor type 1 receptor (IGF-1R)SUMO

Identifiers

PMID30078228
PMCPMC6415676
OpenAlexW2887437071

What OpenQuestion holds

Textmetadata
LicenceTDM
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.