Evidence map›Paper›PMID 24488767›Full record

ArticleHuman molecular genetics2014

Fat mass and obesity-associated (FTO) protein interacts with CaMKII and modulates the activity of CREB signaling pathway.

Li Lin, Chadwick M Hales, Kathryn Garber, Peng Jin

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
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  4. Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
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  9. The Mechanism and Role ofJournal of cardiovascular development and disease · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Observational
  15. Article
  16. Article
  17. Calmodulin as CaInternational journal of molecular sciences · 2021
    Article
  18. Article
  19. Article
  20. The role of mRNA mCell & bioscience · 2019
    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

4 authors at 1 institution in 1 country.

Li LinDepartment of Human Genetics and.
Chadwick M HalesDepartment of Neurology and Center for Neurodegenerative Diseases, Emory University School of Medicine, Atlanta, GA 30322, USA.
Kathryn GarberDepartment of Human Genetics and.
Peng JinDepartment of Human Genetics and peng.jin@emory.edu.
Emory University · US

Funding

Molecular Basis of rCGG-Mediated NeurodegenerationR01NS051630 · NINDS · EMORY UNIVERSITY · PI NELSON, DAVID LOREN · 2006 to 2023
$9.8M
Tet-mediated Epigenetic Modulation in AutismR01MH102690 · NIMH · EMORY UNIVERSITY · PI JIN, PENG, WARREN, STEPHEN T. · 2014 to 2017
$2.6M
NIMH NIH HHS R01 MH102690NINDS NIH HHS NS051630NINDS NIH HHS R01 NS051630
6 · The paper itself

Abstract

Polymorphisms in the fat mass and obesity-associated (FTO) gene have been associated with obesity in humans. FTO is a nuclear protein and its physiological function remains largely unknown, but alterations in its expression in mice influence energy expenditure, food intake and, ultimately, body weight. To understand the molecular functions of FTO, we performed a yeast two-hybrid screen to identify the protein(s) that could directly interact with human FTO protein. Using multiple assays, we demonstrate that FTO interacts with three isoforms of calcium/calmodulin-dependent protein kinase II: α, β and γ, which are protein kinases that phosphorylate a broad range of substrates. This interaction is functional; overexpression of FTO delays the dephosphorylation of cAMP response element-binding protein (CREB) in human neuroblastoma (SK-N-SH) cells, which in turn leads to a dramatic increase in the expression of the CREB targets neuropeptide receptor 1 (NPY1R) and brain-derived neurotrophic factor (BDNF), which already are known to regulate food intake and energy homeostasis. Thus, our results suggest that FTO could modulate obesity by regulating the activity of the CREB signaling pathway.

Indexed as

Signal TransductionAlpha-Ketoglutarate-Dependent Dioxygenase FTOBody WeightBrain-Derived Neurotrophic FactorCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell Line, TumorColforsinCREB-Binding ProteinEatingEnergy MetabolismGene Expression RegulationHEK293 CellsHomeostasisHumansPhosphorylationProteinsAlpha-Ketoglutarate-Dependent Dioxygenase FTOBDNF protein, humanBrain-Derived Neurotrophic FactorCalcium-Calmodulin-Dependent Protein Kinase Type 2ColforsinCREB-Binding ProteinCREBBP protein, humanFTO protein, humanneuropeptide Y-Y1 receptorProteinsReceptors, Neuropeptide Y

Identifiers

PMID24488767
PMCPMC4030783
OpenAlexW2104560044

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.