ArticleStructure (London, England : 1993)2014
The TLQP-21 peptide activates the G-protein-coupled receptor C3aR1 via a folding-upon-binding mechanism.
Article in Structure (London, England : 1993), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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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
34 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Could VGF and/or its derived peptide act as biomarkers for the diagnosis of neurodegenerative diseases: A systematic review.Frontiers in endocrinology · 2022Pooled it
- Molecular basis of diverse ligand recognition and species-specific pharmacology at the complement anaphylatoxin receptor C3aR.Nature communications · 2026Article
- Nuclear magnetic resonance of membrane proteins-Advances and opportunities.Current opinion in structural biology · 2026Review
- A Novel Class of Complement 3a Receptor Agonists and Antagonists Derived from the TLQP-21 Peptide.Journal of medicinal chemistry · 2025Article
- Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large-Caliber Fibers in Mice.Journal of neurochemistry · 2025Article
- VGF and the VGF-derived peptide AQEE30 stimulate osteoblastic bone formation through the C3a receptor.Experimental & molecular medicine · 2025Article
- Complement C3aR signaling: Immune and metabolic modulation and its impact on Alzheimer's disease.European journal of immunology · 2024Review
- Complement C3aR depletion reverses HIF-1α-induced metabolic impairment and enhances microglial response to Aβ pathology.The Journal of clinical investigation · 2023Article
- TLQP-21 is a low potency partial C3aR activator on human primary macrophages.Frontiers in immunology · 2023Article
- Structure of AQEE-30 of VGF Neuropeptide in Membrane-Mimicking Environments.International journal of molecular sciences · 2022Article
- Thalamocortical axons regulate neurogenesis and laminar fates in the early sensory cortex.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The molecular identity of the TLQP-21 peptide receptor.Cellular and molecular life sciences : CMLS · 2021Review
- VGF as a biomarker and therapeutic target in neurodegenerative and psychiatric diseases.Brain communications · 2021Review
- Changes in VGF and C3aR1 gene expression in human adipose tissue in obesity.Molecular biology reports · 2021Article
- Complement Component C3: A Novel Biomarker Participating in the Pathogenesis of Non-alcoholic Fatty Liver Disease.Frontiers in medicine · 2021Review
- SOX9 promotes stress-responsive transcription of VGF nerve growth factor inducible gene in renal tubular epithelial cells.The Journal of biological chemistry · 2020Article
- Multiscale causal networks identify VGF as a key regulator of Alzheimer's disease.Nature communications · 2020Article
- VGF-derived peptide TLQP-21 modulates microglial function through C3aR1 signaling pathways and reduces neuropathology in 5xFAD mice.Molecular neurodegeneration · 2020Article
- A THP-1 Cell Line-Based Exploration of Immune Responses Toward Heat-Treated BLG.Frontiers in nutrition · 2020Article
- Peptide/Receptor Co-evolution Explains the Lipolytic Function of the Neuropeptide TLQP-21.Cell reports · 2019Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
TLQP-21, a VGF-encoded peptide is emerging as a novel target for obesity-associated disorders. TLQP-21 is found in the sympathetic nerve terminals in the adipose tissue and targets the G-protein-coupled receptor complement-3a receptor1 (C3aR1). The mechanisms of TLQP-21-induced receptor activation remain unexplored. Here, we report that TLQP-21 is intrinsically disordered and undergoes a disorder-to-order transition, adopting an α-helical conformation upon targeting cells expressing the C3aR1. We determined that the hot spots for TLQP-21 are located at the C terminus, with mutations in the last four amino acids progressively reducing the bioactivity and, a single site mutation (R21A) or C-terminal amidation abolishing its function completely. Additionally, the human TLQP-21 sequence carrying a S20A substitution activates the human C3aR1 receptor with lower potency compared to the rodent sequence. These studies reveal the mechanism of action of TLQP-21 and provide molecular templates for designing agonists and antagonists to modulate C3aR1 functions.
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