ArticleArteriosclerosis, thrombosis, and vascular biology2013
Molecular basis of antiangiogenic thrombospondin-1 type 1 repeat domain interactions with CD36.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- Role of lipid-associated fibroblasts and their signature genes FABP4, CD36 and ABCA8 in gastric cancer progression.Oncology letters · 2026Article
- Immunomodulatory role and therapeutic potential of thrombospondin-1 during infectious diseases and autoimmunity.BMC biology · 2026Review
- Endothelial dysfunction and cardiovascular outcomes in pre-menopausal women with high vs low breast fat accumulation: The role of TSP-1.American journal of preventive cardiology · 2025Article
- Investigating the conformational landscape of human histidine-rich glycoprotein using amide HDX-MS.The Biochemical journal · 2025Article
- Review
- Monocyte-cancer cell fusion is mediated by phosphatidylserine-CD36 receptor interaction and induced by ionizing radiation.PloS one · 2025Article
- Article
- Thymidine Phosphorylase Promotes Abdominal Aortic Aneurysm via VSMC Modulation and Matrix Remodeling in Mice and Humans.Cardiovascular therapeutics · 2024Article
- Plasmodium vivax merozoite-specific thrombospondin-related anonymous protein (PvMTRAP) interacts with human CD36, suggesting a novel ligand-receptor interaction for reticulocyte invasion.Parasites & vectors · 2023Article
- CD36 Drives Metastasis and Relapse in Acute Myeloid Leukemia.Cancer research · 2023Article
- Isthmin-A Multifaceted Protein Family.Cells · 2022Review
- CD36, a signaling receptor and fatty acid transporter that regulates immune cell metabolism and fate.The Journal of experimental medicine · 2022Review
- Role of CD36 in cancer progression, stemness, and targeting.Frontiers in cell and developmental biology · 2022Review
- CD36 Signaling in Diabetic Cardiomyopathy.Aging and disease · 2021Review
- CD36 deficiency reduces chronic BBB dysfunction and scar formation and improves activity, hedonic and memory deficits in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- CD36 Senses Dietary Lipids and Regulates Lipids Homeostasis in the Intestine.Frontiers in physiology · 2021Review
- Lipoprotein receptor signalling in atherosclerosis.Cardiovascular research · 2020Review
- Nanoparticle exposure driven circulating bioactive peptidome causes systemic inflammation and vascular dysfunction.Particle and fibre toxicology · 2019Article
- CD36 signaling in vascular redox stress.Free radical biology & medicine · 2019Review
- CD36 Enhances Vascular Smooth Muscle Cell Proliferation and Development of Neointimal Hyperplasia.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveAntiangiogenic activity of thrombospondin-1 and related proteins is mediated by interactions between thrombospondin type 1 repeat (TSR) domains and the CD36, LIMP-2, Emp sequence homology (CLESH) domain of the endothelial cell receptor CD36. We sought to characterize key molecular determinants of the interaction between thrombospondin-1 TSR domains and the CD36 CLESH domain. APPROACH AND
resultsRecombinant thrombospondin-1 TSR2 and TSR(2,3) constructs inhibited microvascular endothelial cell migration, microvascular endothelial cell tube formation, and vessel sprouting in aortic ring assays. Interaction with CD36 CLESH decoy peptides negated these effects. Mutational analyses identified a cluster of residues that confer positive charge to the TSR2 surface and mediate interaction with CD36 CLESH. Antiangiogenic activity was significantly reduced by charge-neutralizing mutations of the Arg-Trp ladder in TSR2, but not TSR3. Additionally, I438 and K464 of TSR2 were shown to be required for CD36 CLESH binding to TSR2. A complementary acidic cluster within CD36 CLESH is also required for antiangiogenic activity.
conclusionsThrombospondin-1 interacts with CD36 CLESH through electrostatic interactions mediated by a positively charged TSR2 surface and multiple negatively charged CD36 CLESH residues. Two key residues serve as specificity determinants that identify other TSR domains that interact with CD36 CLESH.
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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.