Evidence map›Paper›PMID 26230950›Full record

ArticleCell proliferation2015

FGF13 regulates proliferation and differentiation of skeletal muscle by down-regulating Spry1.

Hongzhao Lu, Xine Shi, Guofang Wu, Jiayu Zhu, Chengchuang Song, Qiangling Zhang, Gongshe Yang

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

29 citing papers in PubMed, 74 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

7 authors at 2 institutions in 1 country.

Hongzhao LuLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Xine ShiLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Guofang WuLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Jiayu ZhuLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Chengchuang SongLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Qiangling ZhangLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Gongshe YangLaboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Northwest A&F University · CNShaanxi University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesGenerally, the secretory forms of FGF are known to regulate cell proliferation, differentiation and morphogenesis by binding to the extracellular domain of cell surface receptors. Intracellular FGFs (FGF11-14) are expressed principally in the nervous system. FGF13 is a microtubule-stabilizing protein that regulates neuronal polarization and migration. Previous studies have reported high expression of FGF13 in cultures of single muscle fibres. However, functions of FGF13 in muscle development have not been explored. MATERIALS AND

methodsReal-time RT-PCR was performed to detect expression of FGF13 during C2C12 muscle cell proliferation and differentiation. To further understand the role of FGF13, its effects on proliferation and differentiation were examined by western blot analyses of cells transfected with FGF13 siRNA or FGF13 expression plasmids, or treated with chemical MEK inhibitors. Effects of FGF13 on related signalling pathways in C2C12 cell proliferation and differentiation were determined.

resultsFGF13 inhibited C2C12 cell proliferation by up-regulating p27 mRNA level and by down-regulating Cyclin E protein expression, during cell proliferation. Additionally, FGF13 down-regulated Spry1 protein expression, activating the ERK1/2 pathway by phosphorylation and leading to C2C12 cell differentiation inhibition. Consequently, FGF13 seemed to function as a repressor of myoblast differentiation via the ERK1/2 pathway. Although FGF13 inhibited Spry1 regardless of cell proliferation or differentiation, its pathway activation occurred only during the stage of myoblast differentiation.

conclusionsFGF13 inhibited C2C12 cell proliferation and differentiation by down-regulating Spry1. These findings indicate that FGF13 played a negative regulatory role in skeletal muscle development.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell DifferentiationCell LineCell ProliferationCyclin-Dependent Kinase Inhibitor p27Cyclin EDown-RegulationFibroblast Growth FactorsMembrane ProteinsMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MyoblastsPhosphoproteinsPhosphorylationAdaptor Proteins, Signal TransducingCyclin-Dependent Kinase Inhibitor p27Cyclin Efibroblast growth factor 13Fibroblast Growth FactorsMembrane ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphoproteinsProtein Kinase InhibitorsRNA, Small InterferingSpry1 protein, mouse

Identifiers

PMID26230950
PMCPMC6495275
OpenAlexW1933188251

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.