Evidence map›Paper›PMID 29391597›Full record

ArticleScientific reports2018

IGFBPL1 Regulates Axon Growth through IGF-1-mediated Signaling Cascades.

Chenying Guo, Kin-Sang Cho, Yingqian Li, Kissauo Tchedre, Christian Antolik, Jie Ma, Justin Chew, Tor Paaske Utheim, Xizhong A Huang, Honghua Yu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

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  20. A Role for Second Messengers in Axodendritic Neuronal Polarity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Review
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

13 authors at 5 institutions in 4 countries.

Chenying GuoSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Kin-Sang ChoSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Yingqian LiSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Kissauo TchedreSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Christian AntolikSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Jie MaSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Justin ChewSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Tor Paaske UtheimSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Xizhong A HuangSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Honghua YuSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Muhammad Taimur A MalikSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Nada AnzakSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA.
Dong Feng ChenSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA, 02114, USA. dongfeng_chen@meei.harvard.edu.
Harvard University · USMassachusetts Eye and Ear Infirmary · USSmith-Kettlewell Eye Research Institute · USUniversity of Chicago · USVA Boston Healthcare System · US

Funding

VISION RESEARCHP30EY003790 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI Tobias Elze · 1985 to 2026
$25.5M
Training Program in the Molecular Bases of Eye DiseasesT32EY007145 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI Patricia Ann D'Amore, MEREDITH GREGORY-KSANDER · 1997 to 2026
$4.5M
The Molecular Basis Underlying Optic Nerve Growth in Development and RegenerationR01EY025259 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI CHEN, DONG FENG · 2016 to 2020
$3.2M
MOLECULAR MECHANISMS UNDERLYING OPTIC NERVE REGENERATIONR01EY012983 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI CHEN, DONG FENG · 2000 to 2005
$2.0M
Functional Restoration of the Optic Nerve After Disease or DamageR01EY017641 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI CHEN, DONG FENG · 2008 to 2010
$1.5M
The Big Eye-dea: 3D/4D single cell resolution imaging of the mouse eye using lightsheet microscopyR21EY027067 · NEI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI BENTLEY, KATIE · 2016 to 2017
$514k
A Visual Assessment System for Retinal Function/Drug DiscoveryR41EY025913 · NEI · AFASCI, INC. · PI CHEN, DONG FENG, LUO, GANG · 2015 to 2015
$233k
Biological Inquiry into the Mechanisms and Neuroprotective Strategy for TBII01RX000110 · VA · VA BOSTON HEALTH CARE SYSTEM · PI CHEN, DONG FENG · 2009 to 2014
–
NEI NIH HHS P30 EY003790NEI NIH HHS R01 EY012983NEI NIH HHS R01 EY017641NEI NIH HHS R01 EY025259NEI NIH HHS R21 EY027067NEI NIH HHS T32 EY007145RRD VA I01 RX000110
6 · The paper itself

Abstract

Activation of axonal growth program is a critical step in successful optic nerve regeneration following injury. Yet the molecular mechanisms that orchestrate this developmental transition are not fully understood. Here we identified a novel regulator, insulin-like growth factor binding protein-like 1 (IGFBPL1), for the growth of retinal ganglion cell (RGC) axons. Expression of IGFBPL1 correlates with RGC axon growth in development, and acute knockdown of IGFBPL1 with shRNA or IGFBPL1 knockout in vivo impaired RGC axon growth. In contrast, administration of IGFBPL1 promoted axon growth. Moreover, IGFBPL1 bound to insulin-like growth factor 1 (IGF-1) and subsequently induced calcium signaling and mammalian target of rapamycin (mTOR) phosphorylation to stimulate axon elongation. Blockage of IGF-1 signaling abolished IGFBPL1-mediated axon growth, and vice versa, IGF-1 required the presence of IGFBPL1 to promote RGC axon growth. These data reveal a novel element in the control of RGC axon growth and suggest an unknown signaling loop in the regulation of the pleiotropic functions of IGF-1. They suggest new therapeutic target for promoting optic nerve and axon regeneration and repair of the central nervous system.

Indexed as

Calcium SignalingNeuronal OutgrowthAnimalsCells, CulturedInsulin-Like Growth Factor Binding ProteinsInsulin-Like Growth Factor IMiceMice, Inbred C57BLPC12 CellsProtein BindingRatsRetinal Ganglion CellsTOR Serine-Threonine KinasesTumor Suppressor ProteinsIGFBPL1 protein, humanInsulin-Like Growth Factor Binding ProteinsInsulin-Like Growth Factor ITOR Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID29391597
PMCPMC5794803
OpenAlexW2800547418

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.