Evidence map›Paper›PMID 24995978›Full record

ArticleCell2014

Glucose regulates mitochondrial motility via Milton modification by O-GlcNAc transferase.

Gulcin Pekkurnaz, Jonathan C Trinidad, Xinnan Wang, Dong Kong, Thomas L Schwarz

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

184 citing papers in PubMed, 272 citations in OpenAlex.

  1. Article
  2. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  3. Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026
    Review
  4. Review
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  8. Review
  9. Article
  10. Article
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  13. Article
  14. Article
  15. Neurobiology of mitochondrial dynamics in sleep.The Journal of physiology · 2025
    Review
  16. Review
  17. Molecular mechanisms of mitochondrial quality control.Translational neurodegeneration · 2025
    Review
  18. Article
  19. Article
  20. Article

124 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Gulcin PekkurnazThe F.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Jonathan C TrinidadDepartment of Chemistry, Biological Mass Spectrometry Facility, Indiana University, Bloomington, IN 47405, USA.
Xinnan WangDepartment of Neurosurgery, Stanford University, Stanford, CA 94304, USA.
Dong KongDivision of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Thomas L SchwarzThe F.M. Kirby Neurobiology Center, Boston Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: thomas.schwarz@childrens.harvard.edu.
Boston Children's Hospital · USBeth Israel Deaconess Medical Center · USIndiana University Bloomington · USStanford University · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Transgenic CoreP30DK046200 · NIDDK · TUFTS MEDICAL CENTER · PI GREENBERG, ANDREW S, PERISSI, VALENTINA · 1992 to 2021
$25.0M
Milton/Trak 1/2 Protein and the Transport of MitochondriaR01GM069808 · NIGMS · CHILDREN'S HOSPITAL BOSTON · PI SCHWARZ, THOMAS L. · 2004 to 2022
$5.2M
Dendritic Spines on AgRP Neurons as Communication Hubs Controlling FeedingK01DK094943 · NIDDK · TUFTS UNIVERSITY BOSTON · PI KONG, DONG · 2013 to 2015
$456k
NICHD NIH HHS P30 HD018655NICHD NIH HHS P30HD18655NIDDK NIH HHS K01 DK094943NIDDK NIH HHS K01DK094943NIDDK NIH HHS P30 DK046200NIDDK NIH HHS P30DK46200NIGMS NIH HHS 5R01GM069808-08NIGMS NIH HHS R01 GM069808
6 · The paper itself

Abstract

Cells allocate substantial resources toward monitoring levels of nutrients that can be used for ATP generation by mitochondria. Among the many specialized cell types, neurons are particularly dependent on mitochondria due to their complex morphology and regional energy needs. Here, we report a molecular mechanism by which nutrient availability in the form of extracellular glucose and the enzyme O-GlcNAc Transferase (OGT), whose activity depends on glucose availability, regulates mitochondrial motility in neurons. Activation of OGT diminishes mitochondrial motility. We establish the mitochondrial motor-adaptor protein Milton as a required substrate for OGT to arrest mitochondrial motility by mapping and mutating the key O-GlcNAcylated serine residues. We find that the GlcNAcylation state of Milton is altered by extracellular glucose and that OGT alters mitochondrial motility in vivo. Our findings suggest that, by dynamically regulating Milton GlcNAcylation, OGT tailors mitochondrial dynamics in neurons based on nutrient availability.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsAxonsCarrier ProteinsDrosophila melanogasterGene Knockdown TechniquesGlucoseHippocampusHumansMaleMiceMice, Inbred C57BLMitochondriaN-AcetylglucosaminyltransferasesRatsSequence AlignmentAdaptor Proteins, Vesicular TransportCarrier ProteinsGlucoseN-AcetylglucosaminyltransferasesO-GlcNAc transferaseTRAK1 protein, humanTrak1 protein, mouse

Identifiers

PMID24995978
PMCPMC4224014
OpenAlexW2061237420

What OpenQuestion holds

Textmetadata
LicenceTDM
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.