Affinage

ACKR4

Atypical chemokine receptor 4 · UniProt Q9NPB9

Length
350 aa
Mass
39.9 kDa
Annotated
2026-06-09
54 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ACKR4 (CCX-CKR/CCR11) is an atypical, scavenging chemokine receptor that shapes extracellular chemokine gradients to direct leukocyte trafficking through lymphoid and barrier tissues (PMID:20562329, PMID:26976955). It binds the CCR7 ligands CCL19 and CCL21 plus CCL25 with high affinity, and systematic profiling defines CCL20 as an agonist and CCL22 as a potent partial agonist (PMID:32480426, PMID:11981810); rather than mediating chemotaxis or canonical signaling, it internalizes and degrades large quantities of bound chemokine, and unlike CCR7 it does not become refractory, sequestering ligand more efficiently with repeated exposure (PMID:16791897). ACKR4 does not couple to canonical Gi or trigger calcium flux but is a β-arrestin-biased receptor: it constitutively pre-associates with β-arrestins and cycles between plasma membrane and endosomes in its apo state, and chemokine binding recruits β-arrestin2 to drive endocytosis and lysosomal scavenging (PMID:23341447, PMID:42143096, PMID:11981810). Receptor regulation is ordered through its C-terminal tail, where GRK5/6 phosphorylate the apo receptor and ligand stimulation recruits GRK2/3 to phosphorylate a C-terminal serine/threonine cluster that controls β-arrestin recruitment and chemokine uptake; the apo receptor forms a ternary complex with GRK2/3 and G protein without activating it (PMID:42143096). β-arrestins are dispensable for scavenging itself, indicating a parallel β-arrestin-independent endocytic route gated by a C-terminal class II PDZ-binding motif (PMID:32391018, PMID:39623381). By scavenging CCL19/CCL21/CCL25 on stromal cells — keratinocytes, lymphatic and collecting-vessel endothelium induced by lymph flow, splenic sinus endothelium, and cortical thymic epithelial cells — ACKR4 establishes functional gradients that govern CCR7-dependent dendritic cell egress, T cell de-adhesion and lymph-node homing, thymocyte distribution, and splenic marginal-zone organization (PMID:26976955, PMID:33875601, PMID:34260918, PMID:35108538, PMID:23152546). It can additionally trans-inhibit CXCR3-driven chemotaxis through heteromerization (PMID:23121557).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2000 Medium

    Established the receptor's initial molecular identity as a high-affinity chemokine receptor, originally assigned an MCP-family ligand profile and chemotactic function.

    Evidence Transfection into L1.2 cells with radiolabeled MCP-4 competition binding and chemotaxis assays

    PMID:10734104

    Open questions at the time
    • This ligand profile was later superseded by recognition of ACKR4 as a CCR7-ligand scavenger
    • Did not address signaling bias or absence of canonical coupling
  2. 2002 Medium

    Defined the now-canonical high-affinity ligands (CCL19, CCL21, CCL25) and showed the receptor fails to mediate calcium flux, the first hint it was atypical.

    Evidence Murine receptor expression in HEK293 cells with radioligand binding and calcium flux assays

    PMID:11981810

    Open questions at the time
    • Did not establish the scavenging mechanism
    • No explanation for the signaling silence
  3. 2006 High

    Demonstrated the receptor's defining function as a non-saturating chemokine scavenger, distinguishing its endocytic route from clathrin/β-arrestin-dependent uptake.

    Evidence Chemokine internalization/degradation assays in transfected HEK293 cells with caveolin-1 overexpression and CCR7 comparison

    PMID:16791897

    Open questions at the time
    • Endocytic mechanism left ambiguous (caveolin block vs. β-arrestin independence)
    • In vivo relevance not addressed
  4. 2010 High

    Confirmed in vivo scavenging of CCL19/CCL21 and linked gradient regulation to T-helper polarization, establishing physiological consequence.

    Evidence CCX-CKR-/- mice, chemokine ELISA, MOG/CFA immunization, anti-CCL21 neutralization rescue

    PMID:20562329

    Open questions at the time
    • Cellular source of scavenging not resolved
    • Did not separate CCL19 vs CCL21 contributions
  5. 2013 High

    Resolved the signaling mode by showing β-arrestin recruitment without canonical Gi activation, defining ACKR4 as β-arrestin-biased and DRY-motif dependent.

    Evidence β-arrestin recruitment (EFC, BRET), CRE-reporter assays with pertussis toxin, intracellular-loop chimeras

    PMID:23341447

    Open questions at the time
    • GRK requirements not defined
    • Did not establish whether β-arrestins are needed for scavenging
  6. 2013 Medium

    Identified a non-scavenging function — heteromerization with CXCR3 to trans-inhibit its chemotaxis — broadening the receptor's regulatory repertoire.

    Evidence Co-expression in HEK293 and T cells, chemotaxis assays, co-IP, binding cooperativity assays

    PMID:23121557

    Open questions at the time
    • Heteromer structure and stoichiometry undefined
    • Single lab; physiological CXCR3 cross-regulation not shown in vivo
  7. 2016 High

    Pinned scavenging to specific stromal cells and used genetic epistasis to define CCL19 as the critical inflammatory substrate for APC egress.

    Evidence Ackr4-/- and Ccl19-/- double-knockout rescue, in situ scavenging assays, cell-type expression analysis in skin

    PMID:26976955

    Open questions at the time
    • Did not address collecting-vessel or lymph-node roles
    • Steady-state vs inflammation distinction incomplete
  8. 2020 High

    Dissected the recruitment hierarchy (GRK3>GRK2 preceding β-arrestin) and the C-terminus requirement, while showing β-arrestins are dispensable for scavenging — implying a parallel uptake route.

    Evidence GRK/β-arrestin recruitment assays, C-terminal deletion mutants, GRK inhibitors, β-arrestin1/2 KO cells, fluorescent chemokine uptake

    PMID:32391018

    Open questions at the time
    • Identity of the β-arrestin-independent endocytic machinery unknown
    • Phosphosite map not yet defined
  9. 2020 High

    Established a tumor-immunology role: non-hematopoietic ACKR4 limits CD8+ T cell and CD103+ DC accumulation by regulating intratumoral CCL21.

    Evidence ACKR4-/- mice, tumor growth and flow cytometry, CCL21 quantification, bone-marrow chimeras

    PMID:32289156

    Open questions at the time
    • Specific stromal cell type within tumors not defined
    • Therapeutic targeting not tested
  10. 2020 Medium

    Systematically defined the agonist repertoire, adding CCL20 and CCL22 as agonists and excluding CXCL13.

    Evidence High-sensitivity β-arrestin recruitment screen of all 43 human chemokines

    PMID:32480426

    Open questions at the time
    • Single-method screen; CCL22 and CXCL13 results not orthogonally confirmed
    • In vivo significance of CCL20/CCL22 scavenging unknown
  11. 2021 High

    Refined the CCL21 substrate to both immobilized full-length and cleaved soluble forms, explaining how ACKR4 keeps barrier-tissue gradients functional for DC homing.

    Evidence ACKR4-/- mice, biochemical discrimination of CCL21 forms, DC homing assays, intravital imaging

    PMID:33875601

    Open questions at the time
    • Protease generating soluble CCL21 not defined here
    • Mechanism distinguishing immobilized vs soluble uptake unclear
  12. 2021 High

    Extended the trafficking role to the spleen, where endothelial ACKR4 in the peri-marginal sinus supports T cell homing and marginal-zone organization.

    Evidence ACKR4-GFP reporter mice, immunofluorescence, 3D imaging, T cell homing assays

    PMID:34260918

    Open questions at the time
    • Chemokine substrate driving the splenic phenotype not pinned down
    • Link to systemic scavenging unresolved
  13. 2021 Medium

    Revealed a non-trafficking, pathological function: ACKR4 promotes cardiac fibroblast IL-6 production and EndMT via p38/NF-κB, worsening post-MI dysfunction.

    Evidence ACKR4 KO and AAV9 overexpression mice, IL-6 neutralization rescue, p38/NF-κB inhibition, CF proliferation and EndMT assays

    PMID:33610913

    Open questions at the time
    • How a scavenging receptor drives IL-6/p38 signaling mechanistically is unexplained
    • Reconciliation with β-arrestin-biased silent signaling not addressed
  14. 2022 High

    Showed ACKR4 expression is mechanosensitively induced by lymph flow in collecting-vessel endothelium and enables T cell de-adhesion for transport to draining nodes.

    Evidence Intravital microscopy, flow-induced expression assays, ACKR4-/- TPA inflammation model, T cell migration assays

    PMID:35108538

    Open questions at the time
    • Mechanotransduction pathway inducing ACKR4 unknown
    • Molecular link between scavenging and de-adhesion incomplete
  15. 2024 High

    Identified a C-terminal class II PDZ-binding motif that controls β-arrestin pre-association and switches endocytosis between β-arrestin-dependent and -independent routes.

    Evidence Fluorescent CCL19 internalization, NanoBiT bystander assays, C-terminal tagging and PDZ mutagenesis, β-arrestin DKO cells, live-cell confocal

    PMID:39623381

    Open questions at the time
    • PDZ partner protein not identified
    • How the motif arbitrates between the two endocytic routes is unresolved
  16. 2026 High

    Provided a comprehensive phosphoregulatory model: GRK5/6 phosphorylate apo ACKR4, CCL19 recruits GRK2/3 to phosphorylate a C-terminal Ser/Thr cluster, and apo receptor forms a non-activating ternary complex with GRK2/3 and G protein.

    Evidence Phosphosite mutagenesis, MS phosphoproteomics, NanoBiT/BRET GRK and β-arrestin assays, fluorescent CCL19 uptake, ternary-complex co-IP

    PMID:42143096

    Open questions at the time
    • Structural basis of the non-activating ternary complex not solved
    • Why the receptor sequesters G protein without activating it unexplained

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ACKR4 reconciles its β-arrestin-independent scavenging route with active signaling outputs (e.g., IL-6/p38 in fibroblasts) and the identity of its PDZ-binding partner remain open.
  • No identified PDZ-domain partner protein
  • No structural model of the apo ternary complex or the β-arrestin-independent endocytic machinery
  • Mechanism linking a scavenging receptor to active p38/NF-κB signaling is undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 4 GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 1
Localization
GO:0005768 endosome 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-168256 Immune System 4 R-HSA-1500931 Cell-Cell communication 3 R-HSA-162582 Signal Transduction 2
Partners
ARRB2CXCR3GRK2GRK3GRK5GRK6

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 CCX-CKR (ACKR4) mediates rapid CCL19 internalization and progressive sequestration/degradation of large quantities of CCL19. Unlike CCR7, CCX-CKR does not become refractory for CCL19 uptake over time, and its sequestration activity is enhanced with repeated chemokine exposure. CCX-CKR internalization is not critically dependent on β-arrestins or clathrin-coated pits, but caveolin-1 overexpression blocks CCL19 uptake by CCX-CKR. Transfected HEK293 cells, chemokine internalization/degradation assays, caveolin-1 overexpression, comparison with CCR7-expressing cells European journal of immunology High 16791897
2010 CCX-CKR (ACKR4) scavenges CCR7-ligand homeostatic chemokines CCL19 and CCL21 in vivo. CCX-CKR-/- mice show a 5-fold increase in CCL21 protein in blood and 2-3-fold increases in CCL19 and CCL21 in peripheral lymph nodes, confirming scavenger function in vivo. Loss of CCX-CKR skews CD4+ T-cell responses toward Th17 rather than Th1, associated with increased IL-23 in spleen and increased CCL21 in CNS; early disease onset is reversed by anti-CCL21 neutralizing antibody. CCX-CKR-/- mouse generation, ELISA for chemokine levels, immunization with MOG peptide/CFA, cytokine profiling, anti-CCL21 antibody neutralization Blood High 20562329
2013 CCX-CKR (ACKR4) recruits β-arrestin2 upon CCL19, CCL21, and CCL25 binding (demonstrated by enzyme-fragment complementation and BRET). Wild-type CCX-CKR and chimeras with substituted intracellular loops induce CRE activity in response to chemokines only in the presence of pertussis toxin (Gi inhibitor), and this signaling requires an intact DRY motif, suggesting inactive Gi proteins impair CCX-CKR signaling to pertussis toxin-insensitive G proteins. CCX-CKR does not activate canonical Gi signaling. β-arrestin recruitment assays (enzyme-fragment complementation, BRET), CRE-reporter gene assay, pertussis toxin treatment, intracellular loop chimera construction The Journal of biological chemistry High 23341447
2013 Co-expression of human CCX-CKR (ACKR4) completely inhibits CXCR3-induced chemotaxis. CCX-CKR forms heteromeric complexes with CXCR3, and negative binding cooperativity is induced by ligands for both receptors, suggesting heteromerization underlies the inhibition of CXCR3-dependent chemotaxis. Co-expression in HEK293 and human T cells, chemotaxis assays, co-immunoprecipitation to detect complexes, binding cooperativity assays British journal of pharmacology Medium 23121557
2016 ACKR4 on stromal cells (keratinocytes and a subset of dermal lymphatic endothelial cells) scavenges CCL19 in mouse skin to facilitate CCR7-dependent APC egress. During inflammation, ACKR4-mediated scavenging of CCL19 (not CCL21) is critical: aberrant APC trafficking in Ackr4-deficient mice is completely rescued by genetic deletion of Ccl19. Ackr4-/- mice, Ccl19-/- double knockout rescue experiment, in situ ACKR4-dependent chemokine scavenging assays, cell-type-specific expression analysis Journal of immunology High 26976955
2020 ACKR4 recruits GRK3 (and to a lesser extent GRK2) to chemokine-stimulated receptor, and GRK3 recruitment precedes β-arrestin recruitment. GRK2/3 inhibition partially interferes with steady-state interaction and chemokine-driven β-arrestin recruitment. β-arrestins interact with ACKR4 in the steady state and contribute to spontaneous trafficking in the absence of chemokines. Deleting the ACKR4 C-terminus disrupts both β-arrestin interaction and fluorescent chemokine uptake. β-arrestins are dispensable for chemokine scavenging, as β-arrestin-deficient cells retain CCL19 uptake ability. GRK recruitment assays, β-arrestin recruitment assays, ACKR4 C-terminal deletion mutants, GRK inhibitor treatment, fluorescently labeled chemokine internalization assays, β-arrestin1/2 knockout cell lines Frontiers in immunology High 32391018
2020 ACKR4 inhibits intratumor CD8+ T cell accumulation and activation by regulating intratumor CCL21 abundance. ACKR4 inhibits CD103+ dendritic cell retention in tumors via CCL21 regulation. Non-hematopoietic ACKR4 expression is critical for this effect. ACKR4-/- mice, tumor growth assays, flow cytometry of intratumoral immune cells, CCL21 quantification, bone marrow chimera experiments to define non-hematopoietic source The Journal of experimental medicine High 32289156
2020 Systematic β-arrestin recruitment screening of all 43 human chemokines confirmed CCL19, CCL21, CCL25, and CCL20 as ACKR4 agonists, identified CCL22 as a potent partial agonist of ACKR4, and disproved agonist activity of CXCL13 toward ACKR4. Highly sensitive β-arrestin recruitment assay (systematic screening of 43 chemokines against ACKR4) Journal of leukocyte biology Medium 32480426
2021 ACKR4 scavenges two forms of CCL21 in barrier tissues: full-length immobilized CCL21 and cleaved soluble CCL21. Without ACKR4, extracellular CCL21 gradients in barrier sites are saturated and nonfunctional, DCs cannot home directly to lymphatic vessels, and excess soluble CCL21 from peripheral tissues accumulates in downstream lymph nodes. ACKR4-/- mice, detection and quantification of full-length vs. cleaved CCL21, DC homing assays, intravital microscopy/imaging of CCL21 gradients Proceedings of the National Academy of Sciences of the United States of America High 33875601
2021 ACKR4 promotes IL-6 generation and proliferation of cardiac fibroblasts (CFs). ACKR4 facilitates endothelial-to-mesenchymal transition (EndMT) in endothelial cells through IL-6 paracrine signaling. The p38 MAPK/NF-κB signaling pathway is involved in ACKR4-facilitated IL-6 generation. ACKR4 overexpression in vivo via AAV9 aggravated cardiac functional impairment post-MI, which was abolished by IL-6 neutralizing antibody. ACKR4 knockout mice, AAV9-mediated ACKR4 overexpression in vivo, IL-6 neutralizing antibody rescue, p38 MAPK/NF-κB pathway inhibition assays, CF proliferation assays, EndMT assays Biochemical and biophysical research communications Medium 33610913
2021 ACKR4 is expressed in endothelial cells of a vascular compartment (peri-marginal sinus) in the splenic red pulp. In the absence of ACKR4, T cell homing into the spleen and subsequent migration into T cell areas is impaired, and organization of the marginal zone is severely affected. ACKR4-GFP reporter mice, immunofluorescence, three-dimensional imaging, T cell homing assays in ACKR4-deficient mice Cell reports High 34260918
2022 ACKR4 expression in lymphatic collecting vessel endothelial cells is induced by lymph flow (mechanosensitive induction). ACKR4 in collecting vessel endothelium scavenges CCL19 and CCL21, enabling T cell de-adhesion from the vessel wall and passive transport by lymph flow toward draining lymph nodes. In the absence of ACKR4, T cells accumulate in dermal collecting vessel segments and fail to efficiently reach draining lymph nodes. Intravital microscopy, flow-induced ACKR4 expression assays in lymphatic endothelial cells, ACKR4-/- mice in TPA inflammation model, T cell migration assays Cell reports High 35108538
2024 The C-terminal tip of ACKR4 contains a putative class II PDZ-binding domain critical for receptor function. Addition of a C-terminal tag to ACKR4 significantly augments CCL19 internalization, elevates pre-association of β-arrestins with the plasma membrane, reduces chemokine-driven β-arrestin recruitment, and shifts endocytosis from a β-arrestin-dependent to a β-arrestin-independent pathway. Mutation of the putative PDZ-binding domain at the C-terminal tip recapitulates these effects. Flow cytometry of fluorescent CCL19 internalization, NanoBiT bystander assays for β-arrestin recruitment, C-terminal tagging and PDZ-domain mutagenesis, β-arrestin1/2-double deficient cell lines, live-cell confocal microscopy Cell communication and signaling : CCS High 39623381
2026 ACKR4 in its apo state constitutively pre-associates with β-arrestins and cycles between the plasma membrane and endosomal compartments. Distinct serine and threonine residues in the ACKR4 C-terminal tail regulate steady-state trafficking and chemokine uptake; a C-terminal serine/threonine cluster is key for ligand-mediated β-arrestin recruitment and efficient chemokine uptake. GRK5/6 primarily phosphorylate ACKR4 in the absence of chemokines; CCL19 stimulation recruits GRK2/3 to enhance ACKR4 phosphorylation at two serine and one threonine residues. Apo ACKR4 forms a ternary complex with GRK2/3 and G protein without activating it. GRK2 plays a leading role in β-arrestin recruitment and CCL19 internalization. Phosphosite mutagenesis, mass spectrometry phosphoproteomics, NanoBiT/BRET assays for GRK and β-arrestin recruitment, fluorescent CCL19 internalization assays, co-immunoprecipitation of ternary complex Nature communications High 42143096
2000 CCR11 (ACKR4), the human homolog of bovine PPR1, functions as a high-affinity receptor for MCP family chemokines (CCL13/MCP-4, CCL8/MCP-2, CCL2/MCP-1) mediating chemotaxis in L1.2 cells. Radiolabeled MCP-4 binding revealed a single high-affinity binding site (IC50 = 0.14 nM). Eotaxin and MCP-3 bind with higher affinity than MCP-1 but act as agonists only at 100-fold higher concentrations. Transfection into murine L1.2 cells, chemotaxis assays, radiolabeled MCP-4 competition binding assays The Journal of biological chemistry Medium 10734104
2002 Murine CCX-CKR (ACKR4) is a high-affinity receptor for mCCL21, mCCL19, and mCCL25, but unlike most chemokine receptors, is unable to mediate Ca2+ fluxes upon ligand binding when expressed in HEK293 cells. Receptor expression in HEK293 cells, calcium flux assays, radioligand binding European journal of immunology Medium 11981810
2012 CCX-CKR (ACKR4) deletion in mice results in fewer cortical thymic epithelial cells (cTECs) per thymocyte, accumulation of DN2 cells in the medulla, reduced DN3 thymocyte precursors, and decreased CCL25 within the thymic cortex. cTECs express the highest level of CCX-CKR in the thymus. CCX-CKR on cTECs regulates CCL25 availability, which in turn controls thymocyte distribution and frequency. CCX-CKR-/- mice, flow cytometric thymocyte subset analysis, CCL25 immunostaining, cell frequency and distribution analysis Blood High 23152546
2018 In mouse intestine, ACKR4 expression is restricted to a population of submucosal fibroblasts that form physical interactions with lymphatic endothelial cells and engage in molecular interactions via VEGFD/VEGFR3 and CCL21/ACKR4 pathways. Ackr4 deficiency does not affect dendritic cell abundance in the small intestine and mesenteric lymph nodes under steady state or after R848-induced mobilization. Ackr4-GFP reporter mice, immunofluorescence, flow cytometry, transcriptional profiling, DC migration assays in Ackr4-/- mice Journal of immunology Medium 29760193

Source papers

Stage 0 corpus · 54 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1994 Crystal structure of a PPR1-DNA complex: DNA recognition by proteins containing a Zn2Cys6 binuclear cluster. Genes & development 146 7958913
1984 Yeast regulatory gene PPR1. I. Nucleotide sequence, restriction map and codon usage. Journal of molecular biology 124 6096561
2006 The chemokine receptor CCX-CKR mediates effective scavenging of CCL19 in vitro. European journal of immunology 123 16791897
1996 DNA sequence preferences of GAL4 and PPR1: how a subset of Zn2 Cys6 binuclear cluster proteins recognizes DNA. Molecular and cellular biology 94 8668194
2002 Characterization of mouse CCX-CKR, a receptor for the lymphocyte-attracting chemokines TECK/mCCL25, SLC/mCCL21 and MIP-3beta/mCCL19: comparison to human CCX-CKR. European journal of immunology 80 11981810
1995 The sequence and binding specificity of UaY, the specific regulator of the purine utilization pathway in Aspergillus nidulans, suggest an evolutionary relationship with the PPR1 protein of Saccharomyces cerevisiae. The EMBO journal 74 7729421
2009 Involvement of a novel chemokine decoy receptor CCX-CKR in breast cancer growth, metastasis and patient survival. Clinical cancer research : an official journal of the American Association for Cancer Research 72 19383822
2010 The atypical chemokine receptor CCX-CKR scavenges homeostatic chemokines in circulation and tissues and suppresses Th17 responses. Blood 66 20562329
2016 ACKR4 on Stromal Cells Scavenges CCL19 To Enable CCR7-Dependent Trafficking of APCs from Inflamed Skin to Lymph Nodes. Journal of immunology (Baltimore, Md. : 1950) 61 26976955
2000 CCR11 is a functional receptor for the monocyte chemoattractant protein family of chemokines. The Journal of biological chemistry 55 10734104
2020 ACKR4 Recruits GRK3 Prior to β-Arrestins but Can Scavenge Chemokines in the Absence of β-Arrestins. Frontiers in immunology 45 32391018
2012 A rhodanine derivative CCR-11 inhibits bacterial proliferation by inhibiting the assembly and GTPase activity of FtsZ. Biochemistry 37 22703373
2013 β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR. The Journal of biological chemistry 35 23341447
2021 Scavenging of soluble and immobilized CCL21 by ACKR4 regulates peripheral dendritic cell emigration. Proceedings of the National Academy of Sciences of the United States of America 34 33875601
1993 The 5' untranslated region of the PPR1 regulatory gene dictates rapid mRNA decay in yeast. Gene 34 8370540
2012 CCX-CKR deficiency alters thymic stroma impairing thymocyte development and promoting autoimmunity. Blood 33 23152546
2020 ACKR4 restrains antitumor immunity by regulating CCL21. The Journal of experimental medicine 32 32289156
2018 Expression of the Atypical Chemokine Receptor ACKR4 Identifies a Novel Population of Intestinal Submucosal Fibroblasts That Preferentially Expresses Endothelial Cell Regulators. Journal of immunology (Baltimore, Md. : 1950) 32 29760193
1984 Yeast regulatory gene PPR1. II. Chromosomal localization, meiotic map, suppressibility, dominance/recessivity and dosage effect. Journal of molecular biology 32 6096562
2022 Mechanosensitive ACKR4 scavenges CCR7 chemokines to facilitate T cell de-adhesion and passive transport by flow in inflamed afferent lymphatics. Cell reports 28 35108538
2017 A Novel Computational Model Predicts Key Regulators of Chemokine Gradient Formation in Lymph Nodes and Site-Specific Roles for CCL19 and ACKR4. Journal of immunology (Baltimore, Md. : 1950) 27 28807994
2018 Fluorescently Tagged CCL19 and CCL21 to Monitor CCR7 and ACKR4 Functions. International journal of molecular sciences 26 30518137
2015 CCRL1/ACKR4 is expressed in key thymic microenvironments but is dispensable for T lymphopoiesis at steady state in adult mice. European journal of immunology 26 25521433
2020 Systematic reassessment of chemokine-receptor pairings confirms CCL20 but not CXCL13 and extends the spectrum of ACKR4 agonists to CCL22. Journal of leukocyte biology 23 32480426
2010 Generation of a panel of monoclonal antibodies against atypical chemokine receptor CCX-CKR by DNA immunization. Journal of pharmacological and toxicological methods 23 21184834
2003 The Upf-dependent decay of wild-type PPR1 mRNA depends on its 5'-UTR and first 92 ORF nucleotides. Nucleic acids research 23 12799443
2021 Inhibition of fibroblast IL-6 production by ACKR4 deletion alleviates cardiac remodeling after myocardial infarction. Biochemical and biophysical research communications 21 33610913
2008 Gene cloning, expression, and characterization of the Geobacillus Thermoleovorans CCR11 thermoalkaliphilic lipase. Molecular biotechnology 21 19107605
2016 Rewiring of the Ppr1 Zinc Cluster Transcription Factor from Purine Catabolism to Pyrimidine Biogenesis in the Saccharomycetaceae. Current biology : CB 20 27321996
2014 The atypical chemokine receptor CCX-CKR regulates metastasis of mammary carcinoma via an effect on EMT. Immunology and cell biology 18 25027038
1990 The C6 zinc finger and adjacent amino acids determine DNA-binding specificity and affinity in the yeast activator proteins LAC9 and PPR1. Molecular and cellular biology 18 2118990
2021 ACKR4 in Tumor Cells Regulates Dendritic Cell Migration to Tumor-Draining Lymph Nodes and T-Cell Priming. Cancers 17 34638505
2014 CCX-CKR expression in colorectal cancer and patient survival. The International journal of biological markers 17 24338720
2013 Inhibition of CXCR3-mediated chemotaxis by the human chemokine receptor-like protein CCX-CKR. British journal of pharmacology 17 23121557
2008 Immobilization in the presence of Triton X-100: modifications in activity and thermostability of Geobacillus thermoleovorans CCR11 lipase. Journal of industrial microbiology & biotechnology 15 18704528
2021 Expression of ACKR4 demarcates the "peri-marginal sinus," a specialized vascular compartment of the splenic red pulp. Cell reports 14 34260918
2021 The relation between ACKR4 and CCR7 genes expression and breast cancer metastasis. Life sciences 13 34102193
2006 Expression of CCX CKR in pulmonary sarcoidosis. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 11 17109071
2019 B cell hyperactivation in an Ackr4-deficient mouse strain is not caused by lack of ACKR4 expression. Journal of leukocyte biology 10 31841228
2017 Molecular characterization and expression analysis of four fish-specific CC chemokine receptors CCR4La, CCR4Lc1, CCR4Lc2 and CCR11 in rainbow trout (Oncorhynchus mykiss). Fish & shellfish immunology 10 28732768
2016 Gene Cloning and Characterization of the Geobacillus thermoleovorans CCR11 Carboxylesterase CaesCCR11, a New Member of Family XV. Molecular biotechnology 9 26603441
1995 Zinc co-ordination in the DNA-binding domain of the yeast transcriptional activator PPR1. FEBS letters 9 7843415
2023 Identification of ACKR4 as an immune checkpoint in pulmonary arterial hypertension. Frontiers in immunology 8 37449198
2020 Biphasic Expression of Atypical Chemokine Receptor (ACKR) 2 and ACKR4 in Colorectal Neoplasms in Association with Histopathological Findings. Biomolecules 7 33374792
2017 Improved expression and immobilization of Geobacillus thermoleovorans CCR11 thermostable recombinant lipase. Biotechnology and applied biochemistry 6 26339949
2016 Transient expression of recombinant ACKR4 (CCRL1) gene, an atypical chemokine receptor in human embryonic kidney (HEK 293) cells. Molecular biology reports 5 27168154
2021 Production and Characterization of Cross-Linked Aggregates of Geobacillus thermoleovorans CCR11 Thermoalkaliphilic Recombinant Lipase. Molecules (Basel, Switzerland) 3 34946651
2015 Endogenous expression of the atypical chemokine receptor CCX-CKR (CCRL1) gene in human embryonic kidney (HEK 293) cells. Molecular and cellular biochemistry 2 26699909
2010 Enzymatic reactions and synthesis of n-butyl caproate: esterification, transesterification and aminolysis using a recombinant lipase from Geobacillus thermoleovorans CCR11. Environmental technology 2 20718292
2024 Atypical chemokine receptor 4 (ACKR4/CCX-CKR): A comprehensive exploration across physiological and pathological landscapes in contemporary research. Cell biochemistry and function 1 38597217
2023 Expression of CCR8 and CCX-CKR on Basophils in Chronic Urticaria Is Amplified by IgE-Mediated Activation. Biomedicines 1 37371632
2026 GPCR kinases shape ACKR4 functions via differential C-terminal phosphorylation. Nature communications 0 42143096
2024 Corrigendum: Identification of ACKR4 as an immune checkpoint in pulmonary arterial hypertension. Frontiers in immunology 0 38444849
2024 Identification of critical residues at the C-terminal tip of ACKR4 regulating chemokine internalization and βarrestin involvement. Cell communication and signaling : CCS 0 39623381

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