ReviewMolecular and cellular biochemistry2002
Sulfo-N-succinimidyl esters of long chain fatty acids specifically inhibit fatty acid translocase (FAT/CD36)-mediated cellular fatty acid uptake.
Review in Molecular and cellular biochemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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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.
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Who cites it
68 citing papers in PubMed, 147 citations in OpenAlex.
- Unveiling the Small Molecules Binding Site of CD36 Cell Surface Receptor Through Docking and Molecular Dynamics Simulations.Current medicinal chemistry · 2026Article
- SPECT Imaging ofPharmaceutics · 2024Article
- Endothelial cell CD36 regulates membrane ceramide formation, exosome fatty acid transfer and circulating fatty acid levels.Nature communications · 2023Article
- Mannose metabolism inhibition sensitizes acute myeloid leukaemia cells to therapy by driving ferroptotic cell death.Nature communications · 2023Article
- Repurposing a tricyclic antidepressant in tumor and metabolism disease treatment through fatty acid uptake inhibition.The Journal of experimental medicine · 2023Article
- CD1d-dependent rewiring of lipid metabolism in macrophages regulates innate immune responses.Nature communications · 2022Article
- A novel fatty acid metabolism-related signature identifies features of the tumor microenvironment and predicts clinical outcome in acute myeloid leukemia.Lipids in health and disease · 2022Article
- Integrated Multilayer Omics Reveals the Genomic, Proteomic, and Metabolic Influences of Histidyl Dipeptides on the Heart.Journal of the American Heart Association · 2022Article
- Article
- The role of CD36 in cardiovascular disease.Cardiovascular research · 2022Review
- The computational analyses, molecular dynamics of fatty-acid transport mechanism to the CD36 receptor.Scientific reports · 2021Article
- Endothelial Cell Receptors in Tissue Lipid Uptake and Metabolism.Circulation research · 2021Review
- The Nuclear Orphan Receptor NR2F6 Promotes Hepatic Steatosis through Upregulation of Fatty Acid Transporter CD36.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Time for a détente in the war on the mechanism of cellular fatty acid uptake.Journal of lipid research · 2020Article
- Apolipoprotein C2 - CD36 Promotes Leukemia Growth and Presents a Targetable Axis in Acute Myeloid Leukemia.Blood cancer discovery · 2020Article
- REDD1 loss reprograms lipid metabolism to drive progression ofGenes & development · 2020Article
- SSO and other putative inhibitors of FA transport across membranes by CD36 disrupt intracellular metabolism, but do not affect FA translocation.Journal of lipid research · 2020Article
- Scavenger receptor class B, type 1 facilitates cellular fatty acid uptake.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Article
- Identification of Anti-Frontiers in microbiology · 2020Article
- Fatty Acid Metabolism, Bone Marrow Adipocytes, and AML.Frontiers in oncology · 2020Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sulfo-N-succinimidyl esters of LCFAs are a powerful tool to investigate the functional significance of plasmalemmal proteins in the LCFA uptake process. This notion is based on the following observations. First, sulfo-N-succinimidyl oleate (SSO) was found to inhibit the bulk of LCFA uptake into various cell types, i.e. rat adipocytes, type II pneumocytes and cardiac myocytes. Second, using cardiac giant membrane vesicles, in which LCFA uptake can be investigated in the absence of mitochondrial beta-oxidation, SSO retained the ability to largely inhibit LCFA uptake, indicating that inhibition of LCFA transsarcolemmal transport is its primary action. Third, SSO has no inhibitory effect on glucose and octanoate uptake into giant membrane vesicles derived from heart and skeletal muscle, indicating that its action is specific for LCFA uptake. Finally, SSO specifically binds to the 88 kDa plasmalemmal fatty acid transporter FAT, a rat homologue of human CD36, resulting in an arrest of the transport function of this protein. In addition to its inhibitory action at the plasma membrane level, evidence is presented for the lack of a direct inhibitory effect on subsequent LCFA metabolism. First, the relative contribution of oxidation and esterification to LCFA uptake is not altered in the presence of SSO. Second, isoproterenol-mediated channeling of LCFAs into oxidative pathways is not affected by sulfo-N-succinimidyl palmitate (SSP). As an example of its application, we used SSP to study the role of FAT/CD36 in contraction- and insulin-stimulated LCFA uptake by cardiac myocytes, showing that this transporter is a primary site of regulation of cellular LCFA utilization.
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12479588W1599923603What OpenQuestion holds
Registered trials
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.