Evidence map›Paper›PMID 32868454›Full record

ArticleThe Journal of biological chemistry2020

Alternative signaling pathways from IGF1 or insulin to AKT activation and FOXO1 nuclear efflux in adult skeletal muscle fibers.

Sarah J Russell, Martin F Schneider

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

18 citing papers in PubMed, 16 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Sarah J RussellDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Martin F SchneiderDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA. Electronic address: mschneid@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Interdisciplinary Training Program Muscle BiologyT32AR007592 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI Aikaterini Kontrogianni-Konstantopoulos · 1996 to 2026
$11.7M
Vascular Biology Training ProgramT32HL007698 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI Rosemary A Kozar, Dudley K. Strickland · 1991 to 2026
$8.7M
Roles of voltage sensor, S100A1 and calmodulin in skeletal muscle Ca2+ signalingR37AR055099 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI SCHNEIDER, MARTIN F · 2012 to 2021
$3.5M
Activity Dependent Signaling in Adult Skeletal Muscle Fiber PlasticityR01AR056477 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI SCHNEIDER, MARTIN F · 2008 to 2012
$1.6M
NHLBI NIH HHS T32 HL007698NIAMS NIH HHS R01 AR056477NIAMS NIH HHS R37 AR055099NIAMS NIH HHS T32 AR007592
6 · The paper itself

Abstract

Muscle atrophy is regulated by the balance between protein degradation and synthesis. FOXO1, a transcription factor, helps to determine this balance by activating pro-atrophic gene transcription when present in muscle fiber nuclei. Foxo1 nuclear efflux is promoted by AKT-mediated Foxo1 phosphorylation, eliminating FOXO1's atrophy-promoting effect. AKT activation can be promoted by insulin-like growth factor 1 (IGF1) or insulin via a pathway including IGF1 or insulin, phosphatidylinositol 3-kinase, and AKT. We used confocal fluorescence time-lapse imaging of FOXO1-GFP in adult isolated living muscle fibers maintained in culture to explore the effects of IGF1 and insulin on FOXO1-GFP nuclear efflux with and without pharmacological inhibitors. We observed that although AKT inhibitor blocks the IGF1- or insulin-induced effect on FOXO1 nuclear efflux, phosphatidylinositol 3-kinase inhibitors, which we show to be effective in these fibers, do not. We also found that inhibition of the protein kinase ACK1 or ATM contributes to the suppression of FOXO1 nuclear efflux after IGF1. These results indicate a novel pathway that has been unexplored in the IGF1- or insulin-induced regulation of FOXO1 and present information useful both for therapeutic interventions for muscle atrophy and for further investigative areas into insulin insensitivity and type 2 diabetes.

Indexed as

Signal TransductionAnimalsCell NucleusFemaleForkhead Box Protein O1InsulinInsulin-Like Growth Factor IMiceMuscle Fibers, SkeletalOptical ImagingPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktForkhead Box Protein O1Foxo1 protein, mouseInsulininsulin-like growth factor-1, mouseInsulin-Like Growth Factor IPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktAktAkt PKBFOXOFoxo1IGF-1insulininsulin-like growth factor (IGF)nuclear translocationprotein phosphorylationskeletal muscle

Identifiers

PMID32868454
PMCPMC7650253
OpenAlexW3082394702

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.