Evidence map›Paper›PMID 25874865›Full record

ArticlePloS one2015

MLK3 phophorylates AMPK independently of LKB1.

Lingyu Luo, Shanshan Jiang, Deqiang Huang, Nonghua Lu, Zhijun Luo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. 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
1.5field-weighted citation impact, top 18% 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, 27 citations in OpenAlex.

  1. Translational control of AMPK activity in melanoma.Cell communication and signaling : CCS · 2026
    Article
  2. Lithium and exercise ameliorate insulin-deficient hyperglycemia by independently attenuating pancreatic α-cell mass and hepatic gluconeogenesis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  3. Nutrients · 2023
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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

5 authors at 3 institutions in 2 countries.

Lingyu LuoResearch Institute of Digestive Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.
Shanshan JiangGraduate Program, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, China.
Deqiang HuangResearch Institute of Digestive Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.
Nonghua LuResearch Institute of Digestive Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.
Zhijun LuoInstitute of Basic Medical Sciences, Nanchang University, Nanchang, Jiangxi, 330006, China; Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, 02118, United States of America.
Nanchang University · CNBoston University · USFirst Affiliated Hospital of Jiangxi Medical College · CN

Funding

AMPK regulates angiogenesis by inhibition of the ALK1 signaling pathwayR21EY024388 · NEI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LUO, ZHIJUN · 2014 to 2015
$446k
NEI NIH HHS R21 EY024388
6 · The paper itself

Abstract

Emerging evidence has shown that cellular energy metabolism is regulated by the AMPK and MLK3-JNK signaling pathways, but the functional link between them remains to be determined. The present study aimed to explore the crosstalk between MLK3 and AMPK. We found that both JNK and AMPK were phosphorylated at their activation sites by TNF-α, Anisomycin, H2O2 and sorbitol. Interestingly, sorbitol stimulated phosphorylation of AMPK at T172 in LKB1-deficient cells. Following the screening of more than 100 kinases, we identified that MLK3 induced phosphorylation of AMPK at T172. Our in vitro analysis further revealed that MLK3-mediated phosphorylation of AMPK at T172 was independent of AMP, but addition of AMP caused a mobility shift of AMPK, an indication of autophosphorylation, suggesting that AMP binding and phosphorylation of T172 leads to maximal activation of AMPK. GST-pull down assays showed a direct interaction between AMPKα1 subunit and MLK3. Altogether, our results indicate that MLK3 serves as a common upstream kinase of AMPK and JNK and functions as a direct upstream kinase for AMPK independent of LKB1.

Indexed as

AMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnisomycinCell LineCell Line, TumorDNA, ComplementaryGlutathione TransferaseHEK293 CellsHumansHydrogen PeroxideMAP Kinase Kinase 4MAP Kinase Kinase KinasesMitogen-Activated Protein Kinase Kinase Kinase 11Osmotic PressureOxidative StressPhosphorylationAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnisomycinDNA, ComplementaryGlutathione TransferaseHydrogen PeroxideMAP Kinase Kinase 4MAP Kinase Kinase KinasesMitogen-Activated Protein Kinase Kinase Kinase 11Protein IsoformsProtein Serine-Threonine KinasesSorbitolSTK11 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID25874865
PMCPMC4395454
OpenAlexW2060102571

What OpenQuestion holds

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LicenceCC BY
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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.