ArticleNature communications2021
Inositol triphosphate-triggered calcium release blocks lipid exchange at endoplasmic reticulum-Golgi contact sites.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
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- Cardiac metabolic remodeling drives dicarbonyl stress-induced mitochondrial dysfunction in experimental heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2026Article
- The role of ER-associated degradation and ER-phagy in health and disease.Signal transduction and targeted therapy · 2026Review
- Cellular signaling pathway of Shiga toxin-induced ATP release.Frontiers in cellular and infection microbiology · 2026Article
- Inter-Organellar CaCells · 2025Review
- Multiomic Evidence for a Unified Model of Alzheimer's Disease Etiology Linking Microglial Flux Capacity and Astrocyte-Neuron Metabolic Breakdown.bioRxiv : the preprint server for biology · 2025Article
- Phosphatidic acid phosphatase LPIN1 in phospholipid metabolism and stemness in hematopoiesis and AML.HemaSphere · 2025Article
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- Identification of 17 novel epigenetic biomarkers associated with anxiety disorders using differential methylation analysis followed by machine learning-based validation.Clinical epigenetics · 2025Article
- Defective mitochondrial COX1 translation due to loss of COX14 function triggers ROS-induced inflammation in mouse liver.Nature communications · 2024Article
- ERLIN1/2 scaffolds bridge TMUB1 and RNF170 and restrict cholesterol esterification to regulate the secretory pathway.Life science alliance · 2024Article
- Ferroptosis: principles and significance in health and disease.Journal of hematology & oncology · 2024Review
- INPP5A phosphatase is a synthetic lethal target in GNAQ and GNA11-mutant melanomas.Nature cancer · 2024Article
- Glucosylceramide in bunyavirus particles is essential for virus binding to host cells.Cellular and molecular life sciences : CMLS · 2024Article
- Enhancing drug penetration in solid tumors via nanomedicine: Evaluation models, strategies and perspectives.Bioactive materials · 2024Review
- Unraveling the Connection: Cholesterol, Calcium Signaling, and Neurodegeneration.Neuroscience insights · 2024Article
- NPC1-dependent alterations in KNature communications · 2023Article
- The Ebola virus VP40 matrix layer undergoes endosomal disassembly essential for membrane fusion.The EMBO journal · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Vesicular traffic and membrane contact sites between organelles enable the exchange of proteins, lipids, and metabolites. Recruitment of tethers to contact sites between the endoplasmic reticulum (ER) and the plasma membrane is often triggered by calcium. Here we reveal a function for calcium in the repression of cholesterol export at membrane contact sites between the ER and the Golgi complex. We show that calcium efflux from ER stores induced by inositol-triphosphate [IP
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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.