Evidence map›Paper›PMID 26788505›Full record

ArticleBioMed research international2015

Activated Integrin-Linked Kinase Negatively Regulates Muscle Cell Enhancement Factor 2C in C2C12 Cells.

Zhenguo Dong, Wei Pan, Haiqing Wu, Dongjun Liu, Ming Cang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Integrin-linked kinase (ILK): the known vs. the unknown and perspectives.Cellular and molecular life sciences : CMLS · 2022
    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

5 authors at 1 institution in 1 country.

Zhenguo DongKey Laboratory of Mammalian Reproductive Biology and Biotechnology, Ministry of Education, Inner Mongolia University, Inner Mongolia, Hohhot 010021, China.
Wei PanKey Laboratory of Mammalian Reproductive Biology and Biotechnology, Ministry of Education, Inner Mongolia University, Inner Mongolia, Hohhot 010021, China.
Haiqing WuKey Laboratory of Mammalian Reproductive Biology and Biotechnology, Ministry of Education, Inner Mongolia University, Inner Mongolia, Hohhot 010021, China.
Dongjun LiuKey Laboratory of Mammalian Reproductive Biology and Biotechnology, Ministry of Education, Inner Mongolia University, Inner Mongolia, Hohhot 010021, China.
Ming CangKey Laboratory of Mammalian Reproductive Biology and Biotechnology, Ministry of Education, Inner Mongolia University, Inner Mongolia, Hohhot 010021, China.
Inner Mongolia University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous study reported that muscle cell enhancement factor 2C (MEF2C) was fully activated after inhibition of the phosphorylation activity of integrin-linked kinase (ILK) in the skeletal muscle cells of goats. It enhanced the binding of promoter or enhancer of transcription factor related to proliferation of muscle cells and then regulated the expression of these genes. In the present investigation, we explored whether ILK activation depended on PI3K to regulate the phosphorylation and transcriptional activity of MEF2C during C2C12 cell proliferation. We inhibited PI3K activity in C2C12 with LY294002 and then found that ILK phosphorylation levels and MEF2C phosphorylation were decreased and that MCK mRNA expression was suppressed significantly. After inhibiting ILK phosphorylation activity with Cpd22 and ILK-shRNA, we found MEF2C phosphorylation activity and MCK mRNA expression were increased extremely significantly. In the presence of Cpd22, PI3K activity inhibition increased MEF2C phosphorylation and MCK mRNA expression indistinctively. We conclude that ILK negatively and independently of PI3K regulated MEF2C phosphorylation activity and MCK mRNA expression in C2C12 cells. The results provide new ideas for the study of classical signaling pathway of PI3K-ILK-related proteins and transcription factors.

Indexed as

AnimalsCell LineCell ProliferationCreatine Kinase, MM FormGene Expression RegulationMEF2 Transcription FactorsMiceMuscle CellsPhosphatidylinositol 3-KinasesPhosphorylationProtein Serine-Threonine KinasesRNA, MessengerScaffold Protein ILKSignal TransductionTranscriptional ActivationCreatine Kinase, MM FormMEF2 Transcription FactorsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesRNA, MessengerScaffold Protein ILK

Identifiers

PMID26788505
PMCPMC4695646
OpenAlexW2202537313

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.