CX3CL1   Click here for help

GtoPdb Ligand ID: 856

Synonyms: fractalkine | neurotactin
Immunopharmacology Ligand
Compound class: Endogenous peptide in human, mouse or rat
Comment: This is the only member of the CX3C chemokine family [1].
Species: Human
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Ligand Activity Visualisation Charts

These are box plot that provide a unique visualisation, summarising all the activity data for a ligand taken from ChEMBL and GtoPdb across multiple targets and species. Click on a plot to see the median, interquartile range, low and high data points. A value of zero indicates that no data are available. A separate chart is created for each target, and where possible the algorithm tries to merge ChEMBL and GtoPdb targets by matching them on name and UniProt accession, for each available species. However, please note that inconsistency in naming of targets may lead to data for the same target being reported across multiple charts.

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View interactive charts of activity data across species
Natural/Endogenous Targets
Target
CX3CR1
Enzymes Catalysing Reactions with this Compound as a Substrate or Product
Enzyme EC number Reaction Reference
glutaminyl-peptide cyclotransferase like
Selectivity at GPCRs
Key to terms and symbols Click column headers to sort
Target Sp. Type Action Value Parameter Concentration range (M) Reference
CX3CR1 Ligand is endogenous in the given species Hs Agonist Full agonist 8.9 pIC50 - 5
⤷ pIC50 8.9 [5]
Targets where the ligand is described in the comment field
Target Comment
glutaminyl-peptide cyclotransferase This glutaminyl cyclase is a soluble enzyme (soluble QC, or sQC) that catalyses post-translational pyroglutamation (cyclization of N-terminal glutamine) of substrate proteins such as CCL2 (CCL2, P13500) and CX3CL1 (CX3CL1, P78423) and a number of neuroendocrine peptides (e.g. TRH (TRH, P20396) and GnRH I (GNRH1, P01148)) [8]. Pyroglutamation is known to enhance protein stability and bioactive conformation, and dysregulated pyroglutamation has been associated with human diseases, including neurodegeneratrive diseases and cancer [3-4,12-13]. Selective inhibitors are proposed to reduce post-translational pyroglutamate modification of amyloid-β that is associated with amyloid-β neurotoxicity [2].