ArticleThe Journal of biological chemistry2016
Transmembrane Protein 184A Is a Receptor Required for Vascular Smooth Muscle Cell Responses to Heparin.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Structural insights into OSTα/β-mediated transport of bile acids and steroid conjugates.Nature structural & molecular biology · 2026Article
- Patient-specific iPSC-derived ECs identify QKI-7 as a key regulator of endothelial dysfunction and potential therapeutic target in diabetes.Stem cells translational medicine · 2026Article
- TMEM184A promotes progression and drug resistance in colorectal cancer: a bioinformatics and clinical study.Scientific reports · 2026Article
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- Heparin suppresses FoxO1/pFoxO1 signaling axis in vascular smooth muscle cells.Biochemistry and biophysics reports · 2025Article
- Non-Immune-Mediated, p27-Associated, Growth Inhibition of Glioblastoma by Class-II-Transactivator (CIITA).Cells · 2024Article
- Efficacy and predictors of immune checkpoint inhibitors in patients with gallbladder cancer.Cancer science · 2024Article
- Functional unknomics: Systematic screening of conserved genes of unknown function.PLoS biology · 2023Article
- Epigenome-wide association of neonatal methylation and trimester-specific prenatal PMEnvironmental epidemiology (Philadelphia, Pa.) · 2022Article
- Differential Effects of Platelet Factor 4 (CXCL4) and Its Non-Allelic Variant (CXCL4L1) on Cultured Human Vascular Smooth Muscle Cells.International journal of molecular sciences · 2022Article
- Involvement of transmembrane protein 184a during angiogenesis in zebrafish embryos.Frontiers in physiology · 2022Article
- Endothelial nitric oxide synthase activation is required for heparin receptor effects on vascular smooth muscle cells.American journal of physiology. Cell physiology · 2020Article
- Functional analysis of a novel G87V TNFRSF1A mutation in patients with TNF receptor-associated periodic syndrome.Clinical and experimental immunology · 2019Article
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- CELF1 contributes to aberrant alternative splicing patterns in the type 1 diabetic heart.Biochemical and biophysical research communications · 2018Article
- Using a GFP-tagged TMEM184A Construct for Confirmation of Heparin Receptor Identity.Journal of visualized experiments : JoVE · 2017Article
- Novel Heparin Receptor Transmembrane Protein 184a Regulates Angiogenesis in the Adult Zebrafish Caudal Fin.Frontiers in physiology · 2017Article
- Heparin Decreases in Tumor Necrosis Factor α (TNFα)-induced Endothelial Stress Responses Require Transmembrane Protein 184A and Induction of Dual Specificity Phosphatase 1.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Vascular cell responses to exogenous heparin have been documented to include decreased vascular smooth muscle cell proliferation following decreased ERK pathway signaling. However, the molecular mechanism(s) by which heparin interacts with cells to induce those responses has remained unclear. Previously characterized monoclonal antibodies that block heparin binding to vascular cells have been found to mimic heparin effects. In this study, those antibodies were employed to isolate a heparin binding protein. MALDI mass spectrometry data provide evidence that the protein isolated is transmembrane protein 184A (TMEM184A). Commercial antibodies against three separate regions of the TMEM184A human protein were used to identify the TMEM184A protein in vascular smooth muscle cells and endothelial cells. A GFP-TMEM184A construct was employed to determine colocalization with heparin after endocytosis. Knockdown of TMEM184A eliminated the physiological responses to heparin, including effects on ERK pathway activity and BrdU incorporation. Isolated GFP-TMEM184A binds heparin, and overexpression results in additional heparin uptake. Together, these data support the identification of TMEM184A as a heparin receptor in vascular cells.
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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.