Evidence map›Paper›PMID 38344800›Full record

ReviewAmerican journal of physiology. Cell physiology2024

Depalmitoylation and cell physiology: APT1 as a mediator of metabolic signals.

Sarah L Speck, Xiaochao Wei, Clay F Semenkovich

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

10 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. S-palmitoylation in ferroptosis: molecular mechanisms, modulators, and interplay with autophagy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  7. Review
  8. Palmitoylation in cardiovascular diseases: Molecular mechanism and therapeutic potential.International journal of cardiology. Heart & vasculature · 2025
    Review
  9. Article
  10. Article
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

3 authors at 1 institution in 1 country.

Sarah L SpeckDivision of Endocrinology, Metabolism and Lipid Research, Washington University in St. Louis, St. Louis, Missouri, United States.
Xiaochao WeiDivision of Endocrinology, Metabolism and Lipid Research, Washington University in St. Louis, St. Louis, Missouri, United States.
Clay F SemenkovichDivision of Endocrinology, Metabolism and Lipid Research, Washington University in St. Louis, St. Louis, Missouri, United States.ORCID 0000-0003-1163-1871
Washington University in St. Louis · US

Funding

NATIONAL RESEARCH SERVICE AWARD-MEDICAL SCIENTISTT32GM007200 · NIGMS · WASHINGTON UNIVERSITY · PI YOKOYAMA, WAYNE M. · 1985 to 2024
$59.8M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI James Alexander Fitzpatrick · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
MODULATING PHYSIOLOGIC EFFECTS OF PHOSPHOLIPID METABOLISM IN OBESITY AND DIABETESR01DK101392 · NIDDK · WASHINGTON UNIVERSITY · PI SEMENKOVICH, CLAY F. · 2015 to 2019
$2.0M
Lipidation and Vascular DiseaseR01HL157154 · NHLBI · WASHINGTON UNIVERSITY · PI SEMENKOVICH, CLAY F. · 2021 to 2024
$1.6M
PALMITOYLATION DYNAMICS, DIABETES AND VASCULAR INTEGRITYR21AG051900 · NIA · WASHINGTON UNIVERSITY · PI WEI, XIAOCHAO · 2016 to 2017
$381k
Depalmitoylation regulates hepatic glucose metabolismF30DK131830 · NIDDK · WASHINGTON UNIVERSITY · PI SPECK, SARAH LILLY · 2021 to 2023
$136k
NHLBI NIH HHS R01 HL157154NIA NIH HHS R21 AG051900NIDDK NIH HHS F30 DK131830NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P60 DK020579NIDDK NIH HHS R01 DK101392NIGMS NIH HHS T32 GM007200
6 · The paper itself

Abstract

More than half of the global population is obese or overweight, especially in Western countries, and this excess adiposity disrupts normal physiology to cause chronic diseases. Diabetes, an adiposity-associated epidemic disease, affects >500 million people, and cases are projected to exceed 1 billion before 2050. Lipid excess can impact physiology through the posttranslational modification of proteins, including the reversible process of S-palmitoylation. Dynamic palmitoylation cycling requires the S-acylation of proteins by acyltransferases and the depalmitoylation of these proteins mediated in part by acyl-protein thioesterases (APTs) such as APT1. Emerging evidence points to tissue-specific roles for the depalmitoylase APT1 in maintaining homeostasis in the vasculature, pancreatic islets, and liver. These recent findings raise the possibility that APT1 substrates can be therapeutically targeted to treat the complications of metabolic diseases.

Indexed as

LipoylationThiolester HydrolasesCell Physiological PhenomenaHumansThiolester Hydrolasesacyl-protein thioesterasediabetesinsulinobesityS-acylation

Identifiers

PMID38344800
PMCPMC11193526
OpenAlexW4391748648

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.