ArticleProteins2022
Exploring CCRL2 chemerin binding using accelerated molecular dynamics.
Article in Proteins, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Gestational diabetes as an inter-generational cardiometabolic risk factor: spotlight on emerging exerkines.Cardiovascular diabetology · 2026Review
- Clitocine suppresses TNBC progression by boosting CCRL2 to block survival signals and neutrophil-driven inflammation.Journal of biological engineering · 2026Article
- BALF editome profiling reveals A-to-I RNA editing associated with severity and complications ofmSphere · 2025Article
- Prognostic significance of serum Chemerin and neutrophils levels in patients with oral squamous cell carcinoma.Heliyon · 2024Article
- Effect of Regulation of Chemerin/Chemokine-like Receptor 1/Stimulator of Interferon Genes Pathway on Astrocyte Recruitment to Aβ Plaques.International journal of molecular sciences · 2024Article
- Molecular dynamics of chemotactic signalling orchestrates dental pulp stem cell fibrosis during aging.Frontiers in cell and developmental biology · 2024Article
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemokine (C-C motif) receptor-like 2 (CCRL2), is a seven transmembrane receptor closely related to the chemokine receptors CCR1, CCR2, CCR3, and CCR5. Nevertheless, CCRL2 is unable to activate conventional G-protein dependent signaling and to induce cell directional migration. The only commonly accepted CCRL2 ligand is the nonchemokine chemotactic protein chemerin (RARRES2). The chemerin binding to CCLR2 does induce leukocyte chemotaxis, yet, genetic targeting of CCRL2 was shown to modulate the inflammatory response in different experimental models. This mechanism was shown to be crucial for lung dendritic cell migration, neutrophil recruitment, and Natural Killer cell-dependent immune surveillance in lung cancer. To gain more insight in the interactions involved in the CCRL2-chemerin, the binding complexes were generated by protein-protein docking, then submitted to accelerated molecular dynamics. The obtained trajectories were inspected by principal component analyses followed by kernel density estimation to identify the ligand-receptor regions most frequently involved in the binding. To conclude, the reported analyses led to the identification of the putative hot-spot residues involved in CCRL2-chemerin binding.
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What 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.