Evidence map›Paper›PMID 42909095›Full record

ArticleiScience2026

Overexpression of endoplasmic reticulum acetyl-CoA transporter AT-1 alters neuronal metabolism, growth, and synaptic activity.

Eric R McGregor, Cassandra J McGill, Nicholas L Arp, Josef P Clark, Dominique A Baldwin, Yusi Cui, Alexander Nassar, Di Kuang, Gonzalo Fernandez-Fuente, Yun Hwa Choi and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Eric R McGregorDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Cassandra J McGillDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Nicholas L ArpMorgridge Institute for Research, Madison, WI, USA.
Josef P ClarkDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Dominique A BaldwinDepartment of Biochemistry, University of Wisconsin-Madison, Madison, WI, USA.
Yusi CuiDepartment of Chemistry, University of Wisconsin-Madison, Madison, WI, USA.
Alexander NassarDepartment of Chemistry, University of Wisconsin-Madison, Madison, WI, USA.
Di KuangDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Gonzalo Fernandez-FuenteWaisman Center, University of Wisconsin-Madison, Madison, WI, USA.
Yun Hwa ChoiWaisman Center, University of Wisconsin-Madison, Madison, WI, USA.
Keenan S PearsonDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Jason K NagorskiDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Lingjun LiDepartment of Chemistry, University of Wisconsin-Madison, Madison, WI, USA.
Judith A SimcoxDepartment of Biochemistry, University of Wisconsin-Madison, Madison, WI, USA.
Jing FanMorgridge Institute for Research, Madison, WI, USA.
Luigi PuglielliDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Rozalyn M AndersonDivision of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetyl-CoA is a molecule central to cellular metabolic homeostasis. As part of the secretory pathway, acetyl-CoA is imported into the endoplasmic reticulum (ER) by a membrane-bound transporter AT-1 (SLC33A1). AT-1 mutations have been linked to peripheral neuropathy, developmental delay with premature death, and intellectual disability with progeria. Here, we show that AT-1 overexpression impacts diverse phenotypes related to neuronal function and plasticity. Differences in ribosomal, synaptic processing, and metabolic pathways were identified at transcriptomic and proteomic levels. Metabolic adaptations included changes in mitochondrial membrane potential, architecture, and respiration, and tracing experiments revealed changes in the fate of glucose favoring glycogen storage over the pentose phosphate pathway. Altered redox was linked to NAD-dependent proteins SIRT1 and CtBP2. Depletion of lipid stores was associated with greater plasticity in fuel substrate utilization. Metabolic adaptation was coincident with decreased synaptic activity, indicating that neuronal communication is coordinated, in part, through acetyl-CoA metabolism.

Indexed as

acetyl-CoAglucose utilizationlipidsmetabolismmitochondrianeuron

Identifiers

PMID42909095
PMCPMC13683758

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.