ArticleCellular and molecular life sciences : CMLS2017
Phospholipid flippases attenuate LPS-induced TLR4 signaling by mediating endocytic retrieval of Toll-like receptor 4.
Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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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
34 citing papers in PubMed, 50 citations in OpenAlex.
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- Pharmacogenomic Pathways Underlying Variable Vedolizumab Response in Crohn's Disease Patients: A Rare-Variant Analysis.Biomedicines · 2026Article
- Sepsis Biomarkers in Evolution: Comparative Insights and the Promising Roles of MDW and Presepsin.Medicina (Kaunas, Lithuania) · 2026Review
- Overexpression of lncRNA ATP11A-AS1 in Colorectal Cancer and Its Association WithInternational journal of genomics · 2026Article
- ATP8B1 regulates PIP2 localization and cleavage of pyroptotic executioner Gasdermin D.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The roles and functions of TMEM protein family members in cancers, cardiovascular and kidney diseases (Review).Biomedical reports · 2025Review
- Cardiolipin's multifaceted role in immune response: a focus on interacting proteins.Frontiers in immunology · 2025Review
- Context-specific eQTLs reveal causal genes underlying shared genetic architecture of critically ill COVID-19 and idiopathic pulmonary fibrosis.medRxiv : the preprint server for health sciences · 2024Article
- Bromodomain-containing Protein 4 Regulates Innate Inflammation in Airway Epithelial Cells via Modulation of Alternative Splicing.bioRxiv : the preprint server for biology · 2023Article
- Bromodomain-containing Protein 4 regulates innate inflammation via modulation of alternative splicing.Frontiers in immunology · 2023Article
- Structural, topological, and functional characterization of transmembrane proteins TMEM213, 207, 116, 72 and 30B provides a potential link to ccRCC etiology.American journal of cancer research · 2023Article
- Physiological and Pathological Functions of TMEM30A: An Essential Subunit of P4-ATPase Phospholipid Flippases.Journal of lipids · 2023Review
- The phospholipid flippase ATP8B1 is required for lysosomal fusion in macrophages.Cell biochemistry and function · 2022Article
- Modulation of macrophage inflammatory function through selective inhibition of the epigenetic reader protein SP140.BMC biology · 2022Article
- PMEnvironmental research · 2022Article
- Genetic overlap between idiopathic pulmonary fibrosis and COVID-19.The European respiratory journal · 2022Article
- Mechanisms of immune regulation for acupuncture on chronic respiratory diseases.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- Presepsin as Early Marker of Sepsis in Emergency Department: A Narrative Review.Medicina (Kaunas, Lithuania) · 2021Review
- Pulmonary lipid modulation: A possible therapeutic target for SARS-CoV-2 infection.Medical hypotheses · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
P4-ATPases are lipid flippases that catalyze the transport of phospholipids to create membrane phospholipid asymmetry and to initiate the biogenesis of transport vesicles. Here we show, for the first time, that lipid flippases are essential to dampen the inflammatory response and to mediate the endotoxin-induced endocytic retrieval of Toll-like receptor 4 (TLR4) in human macrophages. Depletion of CDC50A, the β-subunit that is crucial for the activity of multiple P4-ATPases, resulted in endotoxin-induced hypersecretion of proinflammatory cytokines, enhanced MAP kinase signaling and constitutive NF-κB activation. In addition, CDC50A-depleted THP-1 macrophages displayed reduced tolerance to endotoxin. Moreover, endotoxin-induced internalization of TLR4 was strongly reduced and coincided with impaired endosomal MyD88-independent signaling. The phenotype of CDC50A-depleted cells was also induced by separate knockdown of two P4-ATPases, namely ATP8B1 and ATP11A. We conclude that lipid flippases are novel elements of the innate immune response that are essential to attenuate the inflammatory response, possibly by mediating endotoxin-induced internalization of TLR4.
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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.