Affinage

CCL1

C-C motif chemokine 1 · UniProt P22362

Length
96 aa
Mass
11.0 kDa
Annotated
2026-06-09
100 papers in source corpus 38 papers cited in narrative 38 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 10/10 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCL1 (I-309/TCA3) is a secreted monomeric CC chemokine that orchestrates leukocyte recruitment, survival, and tissue remodeling primarily through its cognate Gi-coupled receptor CCR8 (PMID:1557400, PMID:9207005, PMID:9211859, PMID:9469461). It was first defined as a monocyte-selective chemoattractant that mobilizes intracellular calcium in monocytes but not lymphocytes or neutrophils (PMID:1557400), with its murine orthologue TCA3 additionally recruiting and activating neutrophils and macrophages through a pertussis toxin-sensitive G-protein pathway (PMID:7963534, PMID:7730638). CCR8 was identified by transfection as the specific high-affinity receptor that confers calcium flux and chemotaxis in response to CCL1 (PMID:9207005, PMID:9211859, PMID:9469461). Beyond chemotaxis, CCL1-CCR8 signaling protects cells from apoptosis via the RAS/MAPK (ERK1/2) cascade, demonstrated by blockade with the MEK inhibitor PD98059 and dominant-negative M-RAS (PMID:8805659, PMID:12645948), and supports an autocrine anti-apoptotic loop in HTLV-1-transformed adult T-cell leukemia cells (PMID:11493464). CCL1 acts on endothelial cells through CCR8 to drive chemotaxis, invasion, and angiogenesis (PMID:11110671, PMID:11133740), and is the principal endothelial monocyte chemoattractant induced by apolipoprotein(a) at atherosclerotic plaques (PMID:10942748). Structurally, CCL1 is distinguished by a unique third intramolecular disulfide bond (C26-C68) that terminates its C-terminal helix and is required for secretion (PMID:8077676, PMID:10821677). In vivo, CCL1 is mechanistically required for regulatory T-cell recruitment, governing statin-mediated anti-inflammatory responses, atherosclerosis, and tumor microenvironment immunosuppression (PMID:18714025, PMID:31121182). CCL1-CCR8 also controls tumor cell entry into lymph nodes during metastasis (PMID:23878309) and mediates spinal neuropathic and postoperative pain via NMDA and GluA1-AMPA receptor phosphorylation (PMID:23788036, PMID:31121204). In fibrosis, CCL1 signals through a second receptor, AMFR, driving fibroblast activation by promoting ubiquitination of the ERK inhibitor Spry1 and via CCR8-mediated migration, with both pathways converging on profibrotic Ras signaling and M2 macrophage polarization (PMID:34407391, PMID:37220693). CCL1 transcription is controlled by AhR and calcium in response to polycyclic aromatic hydrocarbons (PMID:16679317), by NF-κB downstream of TNFα and Lp(a) (PMID:19302817), by c-Myc (PMID:38652401), and is suppressed by ALKBH5-mediated m6A demethylation of its mRNA (PMID:40254698) and by STAT5/CIS downstream of JAK2 (PMID:18981157).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 1992 High

    Established CCL1's basic biological identity: it answered whether I-309 was a functional chemoattractant and revealed an unexpected cell-type selectivity for monocytes.

    Evidence In vitro chemotaxis and calcium flux assays with purified recombinant protein on human monocytes, lymphocytes, and neutrophils

    PMID:1557400

    Open questions at the time
    • Receptor mediating the response was unidentified
    • Signaling pathway downstream of calcium flux undefined
  2. 1994 High

    Resolved why CCL1 is structurally atypical among chemokines, showing it stays monomeric and that a unique disulfide bond is required for its secretion.

    Evidence Size exclusion HPLC, ultracentrifugation, cross-linking, and site-directed mutagenesis of C26/C68

    PMID:8077676

    Open questions at the time
    • Functional consequence of monomeric state for receptor binding not tested
    • 3D structural basis not yet resolved
  3. 1994 High

    Demonstrated the orthologue TCA3 acts through a distinct Gi-coupled receptor and activates effector functions, extending CCL1 activity beyond chemotaxis to leukocyte activation.

    Evidence In vivo peritoneal injection, in vitro chemotaxis, calcium flux with pertussis toxin, cross-desensitization, respiratory burst and degranulation assays

    PMID:7730638 PMID:7963534

    Open questions at the time
    • Receptor identity still molecularly undefined
    • Species differences in target cell selectivity unexplained
  4. 1996 High

    Revealed a non-chemotactic function: CCL1 protects cells from apoptosis through a Gi-coupled receptor, broadening its role to cell survival.

    Evidence Apoptosis protection assay on BW5147 thymic lymphoma cells with pertussis toxin and comparative chemokine panel

    PMID:8805659

    Open questions at the time
    • Downstream survival signaling pathway not identified
    • Receptor mediating anti-apoptosis not yet cloned
  5. 1997 High

    Identified CCR8 as the specific cognate receptor for CCL1, settling the long-standing question of which receptor transduces its signals.

    Evidence Receptor transfection into pre-B cells, calcium flux, chemotaxis, radioligand binding (Kd ~1.2 nM), pertussis toxin inhibition; replicated across concurrent labs

    PMID:9207005 PMID:9211859 PMID:9469461

    Open questions at the time
    • Discrepant reports on endogenous CCR8 expression in monocytes vs T cells
    • Structural basis of ligand-receptor interaction unknown
  6. 1998 High

    Showed CCR8 serves as an HIV-1 coreceptor and that CCL1 blocks viral entry, linking the chemokine axis to viral pathogenesis.

    Evidence HIV-1 infection and cell-cell fusion assays with CCL1 inhibition across multiple viral strains

    PMID:9417093

    Open questions at the time
    • In vivo relevance to HIV transmission not established
    • Mechanism of CCL1 fusion inhibition not detailed
  7. 2000 High

    Defined CCL1's 3D solution structure and established the structural consequence of its unique third disulfide bond.

    Evidence 1H NMR with 978 restraints and comparison to related chemokines

    PMID:10821677

    Open questions at the time
    • Receptor-bound conformation not determined
    • N-terminal disordered region functional role unresolved
  8. 2000 High

    Extended CCL1 function to vascular biology, showing it is angiogenic and is the endothelial monocyte chemoattractant induced by apo(a) in atherosclerosis.

    Evidence Matrigel, rabbit cornea and chick CAM angiogenesis assays; monocyte chemotaxis with antibody/antisense blockade and plaque immunohistochemistry

    PMID:10942748 PMID:11110671

    Open questions at the time
    • Signaling pathway driving endothelial differentiation not mapped
    • Causal contribution to atherosclerotic progression in vivo not yet tested genetically
  9. 2001 High

    Confirmed CCR8 as the functional endothelial receptor for CCL1 and identified an autocrine anti-apoptotic loop in leukemia cells.

    Evidence Endothelial chemotaxis with PTX and anti-CCR8 antibody blockade; ATL supernatant neutralization with anti-I-309 antibodies and apoptosis assays

    PMID:11133740 PMID:11493464

    Open questions at the time
    • Intracellular pathway linking CCR8 to survival still undefined at this stage
    • Transcriptional driver of CCL1 overexpression in ATL (Tax) not mechanistically dissected at promoter level
  10. 2003 High

    Mapped the anti-apoptotic signaling cascade to the RAS/MAPK pathway, resolving how CCR8 engagement promotes survival.

    Evidence ERK1/2 phosphorylation, dominant-negative M-RAS, MEK inhibitor PD98059, and CCR8 transfection reconstitution

    PMID:12645948 PMID:14645913

    Open questions at the time
    • Connection between Gi and RAS activation not fully bridged
    • Whether the same pathway operates in non-lymphoma cells untested
  11. 2006 High

    Dissected the structure-function determinants of CCL1-CCR8 engagement and receptor trafficking, defining the N-terminus as critical for binding and β-arrestins for internalization.

    Evidence Ser-CCL1 partial agonist analysis, site-directed CCR8 mutagenesis (Glu-286, Asp-97), β-arrestin manipulation, plus induction-requirement studies (FcγRII + IL-1β/LPS) and AhR/calcium promoter mechanism

    PMID:16679317 PMID:16735693 PMID:17023422

    Open questions at the time
    • Crystal structure of the receptor-ligand complex still lacking
    • Integration of co-stimulatory CCL1 induction with downstream macrophage programming incomplete
  12. 2008 High

    Defined the transcriptional and post-transcriptional control of CCL1 production and established its in vivo requirement for regulatory T-cell recruitment.

    Evidence OSM stimulation of fibroblasts with MAPK inhibitors, c-Jun/c-Fos/STAT5 knockdowns, mRNA stability assays; CCL1-deficient mice in a delayed-type hypersensitivity model with Treg quantification

    PMID:18714025 PMID:18981157

    Open questions at the time
    • Receptor on recruited Tregs not formally identified in this context
    • Relative contribution of transcription vs mRNA stability in physiological settings unclear
  13. 2009 High

    Distinguished an AhR-independent NF-κB route to CCL1 induction, showing Lp(a) acts via de novo TNFα synthesis.

    Evidence Macrophage culture with AhR antagonist, cycloheximide, anti-TNFα neutralization, NF-κB inhibitor, and EMSA on the CCL1 promoter NF-κB element

    PMID:19302817

    Open questions at the time
    • Crosstalk between AhR and NF-κB inputs not resolved
    • In vivo relevance to plaque formation not directly tested
  14. 2012 Medium

    Identified post-translational and upstream-signaling modulators of CCL1: carboxypeptidase M C-terminal clipping tunes CCR8 signaling, and RhoA activation drives CCL1 secretion linking to STAT3.

    Evidence In vitro enzymatic cleavage with mass spectrometry, calcium/binding/apoptosis assays; bacterial CNF treatment with pathway inhibitors and recombinant CCL1 rescue

    PMID:22311973 PMID:22479563

    Open questions at the time
    • Physiological context of CPM clipping in vivo unknown
    • RhoA-CCL1-STAT3 link rests on pharmacological dissection in a single study
  15. 2013 High

    Established CCL1-CCR8 as a driver of lymph node metastasis and a mediator of spinal neuropathic pain, expanding the axis into cancer dissemination and the nervous system.

    Evidence Tumor cell migration with CCR8 blockade/shRNA and in vivo metastasis with intravital microscopy; nerve ligation model with intrathecal CCL1, patch-clamp, NMDA receptor phosphorylation, MK-801, and CCR8 knockdown

    PMID:23788036 PMID:23878309

    Open questions at the time
    • Mechanism of lymphatic-sinus-restricted CCL1 expression unexplained
    • Cell types mediating pain signaling not fully separated
  16. 2014 High

    Determined the crystal structure of synthetic CCL1 and assessed the functional impact of N-glycosylation, completing the structural picture.

    Evidence Total chemical synthesis by native chemical ligation, quasi-racemic crystallization, X-ray crystallography, and chemotaxis assays of glycosylated vs non-glycosylated forms

    PMID:24644239 PMID:24692304

    Open questions at the time
    • Quantitative effect of glycosylation on activity not fully detailed in the corpus
    • Receptor-bound structure still absent
  17. 2019 High

    Revealed broad in vivo physiological roles for CCL1-CCR8: an ILC2 feed-forward loop, regulation of atherosclerosis via Treg recruitment, and additional pain modalities including peripheral analgesia.

    Evidence CCR8-deficient mice in helminth and atherosclerosis models, CCL1/Apoe double knockouts, CCR8 blocking antibodies, and pharmacological pain models with endocannabinoid measurement

    PMID:31121182 PMID:31121204 PMID:31203533 PMID:31537642

    Open questions at the time
    • Context-dependent pro- vs anti-inflammatory outcomes of Treg recruitment not unified
    • Peripheral analgesia mechanism rests on pharmacology in one study
  18. 2021 High

    Discovered a second CCL1 receptor, AMFR, and a distinct profibrotic mechanism, transforming the single-receptor model into a two-receptor system.

    Evidence Conditional Ccl1, Ccr8, and Amfr knockouts, mass spectrometry of CCL1 complexes, Spry1 ubiquitination assays, and anti-CCL1 antibody treatment in a pulmonary fibrosis model

    PMID:34407391

    Open questions at the time
    • Structural basis of CCL1-AMFR interaction unknown
    • Whether AMFR signaling occurs outside fibrosis contexts untested at this point
  19. 2023 High

    Extended the AMFR pathway to macrophage M2 polarization and mapped its downstream CREB/C/EBPβ signaling, corroborating the dual-receptor model.

    Evidence AMFR and CCR8 conditional knockouts in macrophages, migration and M2 polarization assays, CREB/C/EBPβ analysis, and bleomycin fibrosis model

    PMID:37220693

    Open questions at the time
    • How AMFR discriminates between migration and polarization outputs unclear
    • Direct biochemical demonstration of AMFR-CREB coupling incomplete
  20. 2024 Medium

    Identified c-Myc and epigenetic/m6A regulators (HDAC2, ALKBH5) as additional layers controlling CCL1 abundance and downstream immunosuppression.

    Evidence Dual-luciferase reporter and ChIP for c-Myc/HDAC2 in glioma; Alkbh5 KO/KI mice, m6A dot blots, and recombinant CCL1 rescue in acute lung injury

    PMID:38652401 PMID:40254698

    Open questions at the time
    • Interplay among transcriptional, epigenetic, and m6A regulation not integrated
    • ALKBH5-CCL1 axis tested in a limited disease context
  21. 2025 Medium

    Confirmed CCL1-CCR8 as a macrophage-to-stellate-cell signal driving liver fibrosis via JAK/STAT, broadening the profibrotic role across organs.

    Evidence Macrophage-HSC co-culture, JAK/STAT activation assays, and a liver fibrosis mouse model

    PMID:40122149

    Open questions at the time
    • Mechanistic rigor of the JAK/STAT link limited
    • Contribution of AMFR vs CCR8 in hepatic stellate cells not separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CCL1 discriminates between its two receptors CCR8 and AMFR to deploy distinct downstream programs (chemotaxis/survival vs Spry1 ubiquitination/fibrosis) remains structurally and mechanistically undefined.
  • No co-crystal structure of CCL1 with either receptor
  • Biochemical basis of CCL1-AMFR binding and selectivity unresolved
  • Determinants directing receptor choice in a given cell type unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 4 GO:0060089 molecular transducer activity 3
Localization
GO:0005576 extracellular region 3
Pathway
R-HSA-168256 Immune System 4 R-HSA-1500931 Cell-Cell communication 3 R-HSA-162582 Signal Transduction 3
Partners
AMFRCCR8

Evidence

Reading pass · 38 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 Purified recombinant I-309 (CCL1) specifically stimulated chemotaxis of human monocytes but not neutrophils or lymphocytes, and transiently increased cytoplasmic free calcium in peripheral blood monocytes but not in lymphocytes or neutrophils, establishing CCL1 as a monocyte-selective chemoattractant. In vitro chemotaxis assay and calcium flux measurement using purified recombinant protein from CHO cell transfectant Proceedings of the National Academy of Sciences of the United States of America High 1557400
1994 I-309 (CCL1) remains exclusively monomeric at all concentrations tested, unlike IL-8 and MCP-1 which form dimers. CCL1 contains two unique cysteine residues (C26 and C68) not found in other chemokine family members that form a unique intramolecular disulfide bond, and site-directed mutagenesis showed that integrity of this bond is crucial for protein secretion. Size exclusion HPLC, sedimentation equilibrium ultracentrifugation, chemical cross-linking, cyanogen bromide/trypsin digestion, site-directed mutagenesis Journal of immunology (Baltimore, Md. : 1950) High 8077676
1994 Murine TCA3 (CCL1 orthologue) induced chemoattraction of neutrophils and macrophages in vivo and in vitro, stimulated a transient increase in cytoplasmic free calcium in monocytic cells through a pertussis toxin-sensitive (Gi-coupled) pathway, and acted independently of other beta-chemokines (MIP-1α, RANTES) and IL-8, suggesting a distinct receptor. In vivo peritoneal injection, in vitro chemotaxis assay, calcium flux assay with pertussis toxin inhibition, cross-desensitization studies, receptor transfection assay Journal of immunology (Baltimore, Md. : 1950) High 7963534
1994 Murine TCA3 (CCL1 orthologue) activated neutrophils and macrophages to produce superoxide, hydrogen peroxide, and reactive nitrogen intermediates, induced degranulation (lysozyme and elastase release), and caused integrin-mediated increases in adhesiveness to fibrinogen through a pertussis toxin-sensitive G-protein-linked receptor pathway. Respiratory burst assays, degranulation assays with cytochalasin B, integrin-mediated adhesion assay, pertussis toxin inhibition Journal of immunology (Baltimore, Md. : 1950) High 7730638
1996 I-309/CCL1 (and its murine homologue TCA3) protects murine thymic lymphoma cell lines against dexamethasone-induced apoptosis with half-maximal activity at ~1 ng/ml. This anti-apoptotic activity was inhibited by pertussis toxin, indicating requirement for a Gi-coupled chemokine receptor. Structurally related chemokines (IL-8, MIP-1α, RANTES, MCP-1, MCP-2) lacked this activity; MCP-3 showed a minor effect. Apoptosis protection assay on BW5147 thymic lymphoma cells, pertussis toxin inhibition, comparative chemokine testing, protein purification to homogeneity Journal of immunology (Baltimore, Md. : 1950) High 8805659
1997 CCR8 (previously named CY6/TER1/CKR-L1) was identified as the specific receptor for CCL1/I-309. Transfection of the CY6 open reading frame into mouse pre-B cells conferred calcium flux and chemotaxis in response to I-309 (EC50 = 2 nM) but not 20 other chemokines tested. Signaling was sensitive to pertussis toxin, indicating coupling to a Gi-type G protein. CCR8 is constitutively expressed in monocytes and thymus. Receptor transfection (pre-B cell line), calcium flux assay, chemotaxis assay, pertussis toxin inhibition, flow cytometry for receptor expression The Journal of experimental medicine High 9207005 9211859 9469461
1997 CCR8 (TER1/ChemR1/CKR-L1) expressed in murine pre-B cells 300-19 responded selectively to CCL1/I-309 with intracellular Ca2+ mobilization and chemotaxis; high-affinity binding was demonstrated (Kd = 1.2 nM). CCR8 was not detectably expressed in freshly isolated blood neutrophils, monocytes, cultured macrophages, or PHA-stimulated T lymphocytes; only faint signal in IL-2-treated T lymphocytes. Stable receptor transfection, calcium flux assay, chemotaxis assay, 125I-I-309 radioligand binding (Kd), Northern blot for tissue expression The Journal of biological chemistry High 9211859
1998 CCR8 functions as a coreceptor for diverse T-cell tropic, dual-tropic, and macrophage-tropic HIV-1 strains. CCL1/I-309 was a potent inhibitor of HIV-1 envelope-mediated cell-cell fusion and virus infection, acting through CCR8 blockade. HIV-1 infection assay, cell-cell fusion assay, calcium flux assay, flow cytometry, immunohistochemistry The Journal of biological chemistry High 9417093
1998 Murine CCR8 was cloned (71% identity to human CCR8) and shown to bind both I-309 (CCL1) and its murine homologue TCA-3 with high affinity (Kd ~2 nM for TCA-3). Both ligands induced calcium mobilization in CCR8-transfected 293-EBNA cells. Pertussis toxin (but not cholera toxin) inhibited both calcium flux and migration, confirming Gi-coupling. Competitive binding showed TCA-3 binding was only partially competed (40%) by I-309. Receptor cloning, transient transfection, calcium flux assay, chemotaxis assay, 125I-TCA-3 radioligand binding, pertussis/cholera toxin inhibition Journal of immunology (Baltimore, Md. : 1950) High 9469461
2000 The 3D solution structure of I-309/CCL1 was determined by 1H NMR spectroscopy. CCL1 is monomeric and adopts a 3(10)-helix followed by a triple-stranded antiparallel β-sheet and C-terminal α-helix. The N-terminal region is disordered. The additional third disulfide bond (involving the unique C26 and C68) directly causes early termination of the C-terminal α-helix and a structural change unique among chemokines. 1H NMR spectroscopy and dynamic simulated annealing with 978 experimental restraints, structural comparison with related chemokines Biochemistry High 10821677
2000 CCL1/I-309 binds to endothelial cells via CCR8 (detected by RT-PCR and RNase protection), stimulates chemotaxis and invasion of HUVECs, enhances HUVEC differentiation into capillary-like structures in Matrigel, and acts as an angiogenic molecule in vivo in rabbit cornea and chick chorioallantoic membrane assays. RT-PCR/RNase protection for CCR8 expression, in vitro chemotaxis and invasion assay, Matrigel angiogenesis assay, rabbit cornea assay, chick CAM assay Blood High 11110671
2000 CCL1/I-309 is the principal monocyte chemoattractant produced by human vascular endothelial cells in response to apolipoprotein(a) [apo(a)]. Anti-I-309 and anti-CCR8 antibodies, as well as I-309 antisense oligonucleotides, inhibited apo(a)-induced monocyte chemotactic activity. I-309 protein was identified in human atherosclerotic plaques co-localizing with apo(a). Monocyte chemotaxis assay, neutralizing antibody blockade, antisense oligonucleotide inhibition, ELISA, immunohistochemistry Circulation High 10942748
2001 CCR8 expressed on human vascular endothelial cells mediates chemotaxis induced by CCL1/I-309 and vMIP-I. Pertussis toxin inhibited endothelial chemotaxis, and anti-CCR8 polyclonal and monoclonal antibodies blocked the activity, establishing CCR8 as an endothelial receptor for CCL1. RNA blot, direct sequence analysis for CCR8 expression, in vitro chemotaxis assay, pertussis toxin inhibition, anti-CCR8 antibody blockade (polyclonal and monoclonal), immunohistochemistry Blood High 11133740
2001 CCL1/I-309 is overexpressed in adult T-cell leukemia (ATL) cells driven by HTLV-1 Tax transactivation. ATL cell supernatants contain CCR8-dependent anti-apoptotic activity specifically inhibitable by anti-I-309 antibodies. Pertussis toxin inhibition of CCR8 signaling increased apoptosis, establishing an autocrine anti-apoptotic loop involving CCL1→CCR8→Gi signaling in ATL cells. Gene expression profiling, antibody neutralization of ATL supernatants, pertussis toxin inhibition, apoptosis assays Blood High 11493464
2003 CCR8-dependent activation of the RAS/MAPK pathway mediates the anti-apoptotic activity of CCL1/I-309. CCL1 and vMIP-I (another CCR8 ligand) both activated ERK1/2 phosphorylation in BW5147 lymphoma cells and in CCR8-transfected CHO cells. The MEK inhibitor PD98059 and dominant-negative M-RAS specifically blocked CCL1 anti-apoptotic activity, placing CCL1→CCR8→RAS/MAPK as the functional signaling pathway. ERK1/2 phosphorylation assay, CCR8 transfection in CHO cells, dominant-negative M-RAS, MEK inhibitor PD98059, apoptosis assay, pertussis toxin inhibition European journal of immunology High 12645948
2003 Yaba-like disease virus protein 7L is a functional cell-surface receptor for human CCL1, binding with Kd = 0.6 nM, coupling to heterotrimeric G-proteins, and activating ERK1/2. Protein 145R (also with 44% identity to hCCR8) does not bind CCL1. YLDV infection assay, vaccinia virus expression of 7L and 145R, radioligand binding assay, ERK1/2 activation assay, G-protein coupling assay The Journal of general virology High 14645913
2006 N-terminal extension of the mature CCL1 sequence by a serine residue (Ser-CCL1) generates a partial agonist of CCR8 with reduced affinity, demonstrating that the N-terminus of CCL1 is critical for binding to an intrahelical site on CCR8. Glutamic acid residue Glu-286 (TM helix 7) is crucial for CCR8 trafficking to the cell surface (not for ligand binding per se), while Asp-97 (TM helix 2) is dispensable. CCR8 internalization requires β-arrestins 1 and 2 but is independent of Gαi signaling. CCR8 transfectants and native T-cell line, calcium flux assay, chemotaxis assay, receptor internalization assay, site-directed mutagenesis of CCR8 (Glu-286, Asp-97), β-arrestin 1/2 expression manipulation The Journal of biological chemistry High 17023422
2006 CCL1 production in human monocytes requires concurrent engagement of FcγRII and exposure to IL-1β or LPS (MyD88-dependent signals), defining an obligate co-stimulatory requirement unique among CC chemokines. This pattern of induction is associated with M2b (Type 2) macrophage activation. IL-10, IL-4, and IFN-γ inhibited CCL1 induction by FcγR ligation. Primary human monocyte culture, ELISA for CCL1 protein, cytokine stimulation panel, FcγR engagement assays, inhibitor treatments Journal of leukocyte biology High 16735693
2006 Benzo[a]pyrene (BP) and TCDD induce CCL1 mRNA and protein in primary human macrophages through aryl hydrocarbon receptor (AhR). AhR binds to a xenobiotic-responsive element (XRE) in the CCL1 promoter as shown by ChIP and EMSA. Additionally, BP induces an early intracellular calcium increase, and chelation of calcium or blockade of store-operated channels fully blocks CCL1 upregulation, revealing both AhR-dependent and calcium-dependent mechanisms. Primary human macrophage culture, siRNA knockdown of AhR, CCL1 promoter-reporter assay, ChIP, EMSA, calcium imaging, calcium chelator (BAPTA-AM) and channel inhibitor (2-APB) treatments, in vivo mouse lung model The Journal of biological chemistry High 16679317
2008 Oncostatin M (OSM) stimulates CCL1 expression in primary human dermal fibroblasts through ERK1/2 and p38 MAPK. c-Jun and c-Fos (ERK1/2 targets) are required for CCL1 expression; depletion of c-Jun or c-Fos strongly decreases CCL1. p38 MAPK prolongs CCL1 mRNA half-life through inhibition of tristetraprolin. STAT5, activated via JAK2/CIS, negatively regulates CCL1 expression; CIS (not STAT5 itself) is required for this suppression. Primary human dermal fibroblast cultures, OSM stimulation, ERK1/2 and p38 inhibitors, siRNA knockdown of c-Jun/c-Fos/STAT transcription factors, mRNA stability assay, JAK2 V617F constitutive activation, ELISA and monocyte/T-cell migration assay Journal of immunology (Baltimore, Md. : 1950) High 18981157
2008 Lovastatin induces recruitment of regulatory T cells (Tregs) to sites of inflammation in a CCL1-dependent manner. The anti-inflammatory effect of lovastatin was abrogated in CCL1-deficient mice, demonstrating that CCL1 is mechanistically required for statin-induced Treg recruitment in vivo. Murine delayed-type hypersensitivity model (Candida albicans), CCL1-deficient (knockout) mice, flow cytometry for Treg quantification in inflamed tissue and lymph nodes Journal of immunology (Baltimore, Md. : 1950) High 18714025
2012 Carboxypeptidase M (CPM) cleaves the C-terminal basic amino acids of CCL1/I-309 in vitro. C-terminal clipping augments CCR8-mediated intracellular calcium release and increases anti-apoptotic activity in BW5147 cells, while reducing CCR8 binding affinity. A carboxypeptidase inhibitor blocked these effects, identifying CPM as a novel post-translational modifier of CCL1 that modulates CCR8 signaling. In vitro enzymatic cleavage assay, mass spectrometry for substrate identification, calcium flux assay, CCR8 radioligand binding, apoptosis assay (BW5147), carboxypeptidase inhibitor (MGTA) PloS one High 22479563
2012 RhoA activation by bacterial cytotoxic necrotizing factors (CNFs) triggers secretion of CCL1/I-309, which then acts in an auto/paracrine manner to activate JAK-STAT3 signaling. The pathway requires ROCK and JNK activation and AP1-induced de novo protein synthesis upstream of CCL1 production. CCL1 was identified as the essential secreted factor linking RhoA activation to STAT3 phosphorylation. Bacterial toxin (CNF) treatment of cells, STAT3 phosphorylation assay, pathway inhibitors (ROCK, JNK, AP1), CCL1 identification by functional screening, rescue experiments with recombinant CCL1 The Journal of biological chemistry Medium 22311973
2013 CCL1 expressed by lymph node lymphatic sinuses (but not peripheral lymphatics) controls tumor cell entry into lymph nodes via active CCR8-dependent migration. Blocking CCR8 with a soluble antagonist or CCR8 shRNA knockdown significantly decreased lymph node metastasis in mouse models. Inhibition arrested tumor cells at collecting lymphatic vessels at the junction with the subcapsular sinus. In vitro tumor cell migration assay with CCR8/CCL1 blockade, CCR8 shRNA knockdown in tumor cells, in vivo mouse metastasis model, intravital microscopy, immunohistochemistry of human/mouse tissues The Journal of experimental medicine High 23878309
2013 CCL1/CCR8 signaling in the spinal cord contributes to neuropathic pain. CCL1 is upregulated in ipsilateral dorsal root ganglion after partial sciatic nerve ligation; CCR8 is upregulated in neurons, microglia, and astrocytes in the superficial dorsal horn. Intrathecal CCL1 transiently enhanced excitatory synaptic transmission (patch-clamp) and induced phosphorylation of NMDA receptor subunits NR1 and NR2B. NMDA receptor antagonist MK-801 prevented CCL1-induced allodynia. Neutralizing anti-CCL1 antibody and CCR8 knockdown attenuated nerve ligation-induced tactile allodynia. Mouse partial sciatic nerve ligation model, qRT-PCR and immunofluorescence for expression, intrathecal CCL1 injection, patch-clamp recordings from spinal cord slices, NMDA receptor phosphorylation assay, MK-801 pharmacology, neutralizing antibody, CCR8 shRNA knockdown Cell death & disease High 23788036
2014 X-ray crystal structure of Ser-CCL1 (the 74-residue non-glycosylated CCL1 variant) was solved at 2.1–2.6 Å resolution using quasi-racemic crystallization strategy with total chemically synthesized protein. The glycan moiety was largely disordered; only the N-linked GlcNAc sugar was resolved. Superimposition of glycosylated and non-glycosylated Ser-CCL1 structures showed no significant alteration of protein fold by N-glycosylation. Total chemical synthesis by native chemical ligation, quasi-racemic crystallization, X-ray crystallography (2.1–2.7 Å resolution) Angewandte Chemie (International ed. in English) High 24692304
2014 Glycosylated CCL1 and non-glycosylated CCL1/Ser-CCL1 were synthesized by total chemical synthesis and tested for chemotactic activity. The effect of N-glycosylation on CCL1 chemotactic activity was systematically characterized using homogeneous preparations of defined covalent structure. Total chemical synthesis by native chemical ligation, chemotaxis assay with glycosylated and non-glycosylated forms Angewandte Chemie (International ed. in English) Medium 24644239
2019 Activated mouse and human ILC2s produce CCL1 and are a major source of CCL1 in vivo during type 2 responses. CCL1 signaling to ILC2s via CCR8 regulates their proliferation and supports their capacity to protect against helminthic infections, establishing an autocrine/paracrine CCL1-CCR8 feed-forward loop in ILC2 biology. In vitro CCL1 production assay, in vivo helminth infection model, CCR8-deficient mice, flow cytometry for ILC2 proliferation The Journal of experimental medicine High 31537642
2019 CCL1-CCR8 axis promotes atherosclerosis by inhibiting Treg recruitment. CCL1/Apoe double-knockout mice exhibited enhanced atherosclerosis with reduced Treg content in aorta/spleen and reduced plasma IL-10. CCR8 blocking antibodies in LDLR-null mice also reduced Treg recruitment and aggravated atherosclerosis. In vitro flow chamber assays confirmed CCL1 role in leukocyte recruitment. Double-knockout mouse model (CCL1/Apoe null), CCR8 blocking antibody treatment in fat-fed LDLR-null mice, in vitro flow chamber assay, intravital microscopy, flow cytometry for Treg quantification Journal of molecular and cellular cardiology High 31121182
2021 CCL1 promotes pulmonary fibrosis through two distinct receptor pathways: (1) CCR8-mediated fibroblast migration and (2) AMFR-mediated fibroblast activation via ubiquitination of the ERK inhibitor Spry1, thereby activating Ras-mediated profibrotic protein synthesis. Alveolar macrophages and CD4+ T cells were identified as the major cellular sources of CCL1 in PF. Targeted deletion of Ccl1 in these cells blunted fibrosis pathology. Antibody blockade of CCL1 ameliorated PF. Conditional Ccl1 knockout in macrophages and CD4+ T cells, Ccr8 knockout in fibroblasts, Amfr knockout in fibroblasts, mass spectrometry of CCL1 complexes, ubiquitination assay for Spry1, Ras/ERK signaling assay, anti-CCL1 antibody treatment in mouse PF model Immunity High 34407391
2023 CCL1 promotes macrophage migration via CCR8 and drives macrophage M2 polarization via AMFR. AMFR-CCL1 interaction enhances CREB/C/EBPβ signaling to promote the M2 program. Deficiency in either AMFR or CCR8 in macrophages protected mice from bleomycin-induced pulmonary fibrosis. AMFR and CCR8 conditional knockout in macrophages, in vitro macrophage migration assay, M2 polarization assay, CREB/C/EBPβ signaling analysis, bleomycin mouse PF model International immunopharmacology High 37220693
2009 Lp(a)-triggered induction of CCL1 expression in human macrophages is mediated by AhR-independent de novo synthesis of TNFα followed by NF-κB activation. TNFα alone increased CCL1 expression; NF-κB inhibitor Bay 11-7082 blocked Lp(a)-triggered CCL1 induction; EMSA showed Lp(a) induced NF-κB binding to a CCL1 promoter NF-κB element in a TNFα-dependent manner. Primary human macrophage culture, AhR antagonist, cycloheximide (translational inhibitor), anti-TNFα neutralizing antibodies, NF-κB inhibitor, EMSA with CCL1 promoter NF-κB element Life sciences High 19302817
2017 Sox2-overexpression in breast cancer cells activates NF-κB-CCL1 signaling to recruit Tregs, mediated by reduced binding of H3K27Me3 on promoter regions of p65 and Ccl1. Tregs recruited via CCL1 upregulate stemness properties of breast cancer cells in a paracrine manner. Sox2 overexpression in tumor cells, NF-κB pathway analysis, ChIP for H3K27Me3 on Ccl1 and p65 promoters, Treg co-culture with breast cancer cells, sphere formation and ALDH assays Stem cells (Dayton, Ohio) Medium 29044882
2019 Spinal CCL1/CCR8 signaling mediates postoperative pain after tibial fracture surgery through phosphorylation of GluA1-containing AMPA receptors in the spinal dorsal horn. Intrathecal CCL1 facilitated phosphorylated GluA1-AMPA receptor expression and acute pain behaviors in naïve mice; co-application of the GluA1-AMPA antagonist NASPM reversed these effects. CCL1/CCR8 inhibition impaired mechanical and cold allodynia and reduced phospho-GluA1. Mouse tibial fracture model, intrathecal CCL1 injection, GluA1-AMPA receptor phosphorylation assay (Western blot), CCR8 inhibitor, NASPM (AMPA antagonist), behavioral pain testing Neuroscience research Medium 31121204
2019 Systemic subcutaneous CCL1 produces thermal analgesia through peripheral CCR8 receptors on leukocytes, acting via release of the endocannabinoid 2-arachidonoylglycerol (2-AG) and subsequent CB2 receptor activation. CB2 antagonist SR144528 blocked analgesia; cyclophosphamide-induced leukocyte depletion abolished the effect; ELISA confirmed increased 2-AG after CCL1 administration. Hot plate test in mice, CCR8 antagonist R243, CB1 antagonist AM251, CB2 antagonist SR144528, naloxone (opioid antagonist), cyclophosphamide-induced leukocyte depletion, 2-AG ELISA Cellular and molecular neurobiology Medium 31203533
2024 The HDAC inhibitor SAHA suppresses CCL1 transcription by inhibiting HDAC2, which prevents c-Myc from binding to the CCL1 promoter. c-Myc was shown by dual-luciferase reporter assay and ChIP to directly bind the CCL1 promoter and drive its transcription, establishing c-Myc as a transcriptional activator of CCL1 in glioma stem cells. Dual-luciferase reporter assay with CCL1 promoter, chromatin immunoprecipitation (ChIP) for c-Myc binding, HDAC2 inhibition (SAHA), ELISA, flow cytometry in mouse GBM intracranial model Journal of neuro-oncology Medium 38652401
2025 ALKBH5 (an m6A RNA demethylase) binds to and destabilizes Ccl1 mRNA by removing m6A modifications, thereby reducing CCL1 protein levels and limiting Treg recruitment. ALKBH5 knockout increased Ccl1 m6A levels and protected mice from LPS-induced acute lung injury. Recombinant CCL1 restored Treg recruitment in Alkbh5-deficient conditions. Alkbh5 knockout and knock-in mouse models, m6A dot blot assay, RNA-seq, flow cytometry for Treg quantification, ALKBH5 antagonist DDO-2728, recombinant Ccl1 rescue experiments Cell proliferation Medium 40254698
2025 Macrophage-derived CCL1 activates hepatic stellate cells (HSCs) via CCR8 and promotes liver fibrosis by activating the JAK/STAT signaling pathway. CCR8 was identified as the CCL1 receptor on HSCs. Co-culture of macrophages and HSCs, CCL1/CCR8 expression analysis, JAK/STAT pathway activation assay, liver fibrosis mouse model Biochemical pharmacology Medium 40122149

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 IL-12 produced by dendritic cells augments CD8+ T cell activation through the production of the chemokines CCL1 and CCL17. Journal of immunology (Baltimore, Md. : 1950) 206 19050277
1997 Identification of CCR8: a human monocyte and thymus receptor for the CC chemokine I-309. The Journal of experimental medicine 179 9207005
2005 CCL1-CCR8 interactions: an axis mediating the recruitment of T cells and Langerhans-type dendritic cells to sites of atopic skin inflammation. Journal of immunology (Baltimore, Md. : 1950) 174 15814739
2013 Tumor cell entry into the lymph node is controlled by CCL1 chemokine expressed by lymph node lymphatic sinuses. The Journal of experimental medicine 159 23878309
1992 The human cytokine I-309 is a monocyte chemoattractant. Proceedings of the National Academy of Sciences of the United States of America 156 1557400
1997 Identification of CCR8, the receptor for the human CC chemokine I-309. The Journal of biological chemistry 147 9211859
1998 The CC chemokine I-309 inhibits CCR8-dependent infection by diverse HIV-1 strains. The Journal of biological chemistry 143 9417093
2006 Differential regulation of chemokine production by Fcgamma receptor engagement in human monocytes: association of CCL1 with a distinct form of M2 monocyte activation (M2b, Type 2). Journal of leukocyte biology 132 16735693
2000 Human NK cells express CC chemokine receptors 4 and 8 and respond to thymus and activation-regulated chemokine, macrophage-derived chemokine, and I-309. Journal of immunology (Baltimore, Md. : 1950) 115 10754297
1994 The chemokines IL-8, monocyte chemoattractant protein-1, and I-309 are monomers at physiologically relevant concentrations. Journal of immunology (Baltimore, Md. : 1950) 105 8077676
2021 The chemokine CCL1 triggers an AMFR-SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis. Immunity 102 34407391
2001 Autocrine antiapoptotic stimulation of cultured adult T-cell leukemia cells by overexpression of the chemokine I-309. Blood 100 11493464
2002 Adenosine monophosphoramidase activity of Hint and Hnt1 supports function of Kin28, Ccl1, and Tfb3. The Journal of biological chemistry 96 11805111
2017 Sox2 Communicates with Tregs Through CCL1 to Promote the Stemness Property of Breast Cancer Cells. Stem cells (Dayton, Ohio) 93 29044882
2006 Aryl hydrocarbon receptor- and calcium-dependent induction of the chemokine CCL1 by the environmental contaminant benzo[a]pyrene. The Journal of biological chemistry 92 16679317
2010 Blockade of CCL1 inhibits T regulatory cell suppressive function enhancing tumor immunity without affecting T effector responses. Journal of immunology (Baltimore, Md. : 1950) 91 20483762
2000 CC chemokine I-309 is the principal monocyte chemoattractant induced by apolipoprotein(a) in human vascular endothelial cells. Circulation 83 10942748
2008 Statins induce regulatory T cell recruitment via a CCL1 dependent pathway. Journal of immunology (Baltimore, Md. : 1950) 79 18714025
2022 Tumor-derived exosomes drive pre-metastatic niche formation in lung via modulating CCL1+ fibroblast and CCR8+ Treg cell interactions. Cancer immunology, immunotherapy : CII 78 35428909
2002 Skin-homing CLA+ T cells and regulatory CD25+ T cells represent major subsets of human peripheral blood memory T cells migrating in response to CCL1/I-309. European journal of immunology 77 12442333
2012 Normal ageing is associated with an increase in Th2 cells, MCP-1 (CCL1) and RANTES (CCL5), with differences in sCD40L and PDGF-AA between sexes. Clinical and experimental immunology 73 23039889
2001 The chemokine receptor CCR8 mediates human endothelial cell chemotaxis induced by I-309 and Kaposi sarcoma herpesvirus-encoded vMIP-I and by lipoprotein(a)-stimulated endothelial cell conditioned medium. Blood 72 11133740
2000 I-309 binds to and activates endothelial cell functions and acts as an angiogenic molecule in vivo. Blood 72 11110671
1994 Inhibition of in vivo tumor growth by the beta chemokine, TCA3. Journal of immunology (Baltimore, Md. : 1950) 72 7963535
1996 I-309/T cell activation gene-3 chemokine protects murine T cell lymphomas against dexamethasone-induced apoptosis. Journal of immunology (Baltimore, Md. : 1950) 69 8805659
1998 Identification of CCR8 as the specific receptor for the human beta-chemokine I-309: cloning and molecular characterization of murine CCR8 as the receptor for TCA-3. Journal of immunology (Baltimore, Md. : 1950) 65 9469461
2007 Recruitment and activation of macrophages by pathogenic CD4 T cells in type 1 diabetes: evidence for involvement of CCR8 and CCL1. Journal of immunology (Baltimore, Md. : 1950) 64 17947648
2002 Kin28 is found within TFIIH and a Kin28-Ccl1-Tfb3 trimer complex with differential sensitivities to T-loop phosphorylation. Molecular and cellular biology 64 11839796
1999 Sequence polymorphisms in the chemokines Scya1 (TCA-3), Scya2 (monocyte chemoattractant protein (MCP)-1), and Scya12 (MCP-5) are candidates for eae7, a locus controlling susceptibility to monophasic remitting/nonrelapsing experimental allergic encephalomyelitis. Journal of immunology (Baltimore, Md. : 1950) 61 10438970
2019 A CCL1/CCR8-dependent feed-forward mechanism drives ILC2 functions in type 2-mediated inflammation. The Journal of experimental medicine 60 31537642
1990 Sequence and chromosomal location of the I-309 gene. Relationship to genes encoding a family of inflammatory cytokines. Journal of immunology (Baltimore, Md. : 1950) 60 2212659
2018 CCL1 is a major regulatory T cell attracting factor in human breast cancer. BMC cancer 59 30572845
2007 Inhibition of CCL1-CCR8 interaction prevents aggregation of macrophages and development of peritoneal adhesions. Journal of immunology (Baltimore, Md. : 1950) 56 17404314
2013 CCL-1 in the spinal cord contributes to neuropathic pain induced by nerve injury. Cell death & disease 54 23788036
1994 Biologic activities of the murine beta-chemokine TCA3. Journal of immunology (Baltimore, Md. : 1950) 51 7963534
2003 CCR8-dependent activation of the RAS/MAPK pathway mediates anti-apoptotic activity of I-309/ CCL1 and vMIP-I. European journal of immunology 48 12645948
2013 Possible involvement of CCL1-CCR8 interaction in lymphocytic recruitment in IgG4-related sclerosing cholangitis. Journal of hepatology 47 23811304
2002 Increased responsiveness of murine eosinophils to MIP-1beta (CCL4) and TCA-3 (CCL1) is mediated by their specific receptors, CCR5 and CCR8. Journal of leukocyte biology 46 12050188
2020 Human Adipose-Derived Mesenchymal Stem Cells-Derived Exosomal microRNA-19b Promotes the Healing of Skin Wounds Through Modulation of the CCL1/TGF-β Signaling Axis. Clinical, cosmetic and investigational dermatology 44 33364805
2017 Lack of the COMPASS Component Ccl1 Reduces H3K4 Trimethylation Levels and Affects Transcription of Secondary Metabolite Genes in Two Plant-Pathogenic Fusarium Species. Frontiers in microbiology 43 28119673
2000 Inhibition by IL-12 and IFN-alpha of I-309 and macrophage-derived chemokine production upon TCR triggering of human Th1 cells. European journal of immunology 43 10760790
2015 Fibroblast ERα promotes bladder cancer invasion via increasing the CCL1 and IL-6 signals in the tumor microenvironment. American journal of cancer research 42 26045993
1995 Biologic activities of the beta-chemokine TCA3 on neutrophils and macrophages. Journal of immunology (Baltimore, Md. : 1950) 41 7730638
1988 The expression and regulation of a potential lymphokine gene (TCA3) in CD4 and CD8 T cell clones. Journal of immunology (Baltimore, Md. : 1950) 41 2457620
2019 Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice. Journal of molecular and cellular cardiology 40 31121182
2014 (Quasi-)racemic X-ray structures of glycosylated and non-glycosylated forms of the chemokine Ser-CCL1 prepared by total chemical synthesis. Angewandte Chemie (International ed. in English) 40 24692304
2017 Participation of CCL1 in Snail-Positive Fibroblasts in Colorectal Cancer Contribute to 5-Fluorouracil/Paclitaxel Chemoresistance. Cancer research and treatment 37 28934847
2017 Spinal CCL1/CCR8 signaling interplay as a potential therapeutic target - Evidence from a mouse diabetic neuropathy model. International immunopharmacology 37 28961489
2017 MicroRNA-20a-5p suppresses IL-17 production by targeting OSM and CCL1 in patients with Vogt-Koyanagi-Harada disease. The British journal of ophthalmology 37 28972028
2021 Serum Biomarker Profile Including CCL1, CXCL10, VEGF, and Adenosine Deaminase Activity Distinguishes Active From Remotely Acquired Latent Tuberculosis. Frontiers in immunology 34 34691031
2014 Total chemical synthesis and biological activities of glycosylated and non-glycosylated forms of the chemokines CCL1 and Ser-CCL1. Angewandte Chemie (International ed. in English) 34 24644239
2006 A single nucleotide polymorphism in the CCL1 gene predicts acute exacerbations in chronic obstructive pulmonary disease. American journal of respiratory and critical care medicine 34 16864713
1990 Expression and characterization of TCA3: a murine inflammatory protein. Journal of immunology (Baltimore, Md. : 1950) 34 2212660
1996 Subunits of yeast RNA polymerase II transcription factor TFIIH encoded by the CCL1 gene. The Journal of biological chemistry 33 8557668
2012 Expression of CCL1 and CCL18 in atopic dermatitis and psoriasis. Clinical and experimental dermatology 32 22680616
2006 Structure/function relationships of CCR8 agonists and antagonists. Amino-terminal extension of CCL1 by a single amino acid generates a partial agonist. The Journal of biological chemistry 31 17023422
2008 Oncostatin M-induced and constitutive activation of the JAK2/STAT5/CIS pathway suppresses CCL1, but not CCL7 and CCL8, chemokine expression. Journal of immunology (Baltimore, Md. : 1950) 28 18981157
2000 Human CC chemokine I-309, structural consequences of the additional disulfide bond. Biochemistry 28 10821677
1997 HIV-1-specific cell-mediated immunity is enhanced by co-inoculation of TCA3 expression plasmid with DNA vaccine. Immunology 27 9038705
1997 Rig2, a RING finger protein that interacts with the Kin28/Ccl1 CTD kinase in yeast. Molecular & general genetics : MGG 27 9294030
2015 Genetic polymorphisms of CCL1 rs2072069 G/A and TLR2 rs3804099 T/C in pulmonary or meningeal tuberculosis patients. International journal of clinical and experimental pathology 26 26722451
2003 Human cord blood-derived mast cells synthesize and release I-309 in response to IgE. Life sciences 25 12967681
1996 The rapeseed mitochondrial gene encoding a homologue of the bacterial protein Ccl1 is divided into two independently transcribed reading frames. Molecular & general genetics : MGG 25 8842149
1996 Beta-chemokine TCA3 binds to mesangial cells and induces adhesion, chemotaxis, and proliferation. Journal of immunology (Baltimore, Md. : 1950) 24 8543828
1996 Ccl1, a cyclin associated with protein kinase Kin28, controls the phosphorylation of RNA polymerase II largest subunit and mRNA transcription. Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie 24 8761664
1996 Beta-chemokine TCA3 binds to and activates rat vascular smooth muscle cells. Journal of immunology (Baltimore, Md. : 1950) 23 8757339
2019 Peritumoural CCL1 and CCL22 expressing cells in hepatocellular carcinomas shape the tumour immune infiltrate. Pathology 21 31445808
2012 C-terminal clipping of chemokine CCL1/I-309 enhances CCR8-mediated intracellular calcium release and anti-apoptotic activity. PloS one 20 22479563
2007 Combination of 17beta-estradiol with the environmental pollutant TCDD is involved in pathogenesis of endometriosis via up-regulating the chemokine I-309-CCR8. Fertility and sterility 20 17693327
2016 IL-11 and CCL-1: Novel Protein Diagnostic Biomarkers of Lung Adenocarcinoma in Bronchoalveolar Lavage Fluid (BALF). Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 19 27524264
1994 Transcriptional regulation of the TCA3 gene in mast cells after Fc epsilon RI cross-linking. Journal of immunology (Baltimore, Md. : 1950) 19 8207245
2023 The chemokine CCL1 facilitates pulmonary fibrosis by promoting macrophage migration and M2 polarization. International immunopharmacology 18 37220693
2012 Toxin-induced RhoA activity mediates CCL1-triggered signal transducers and activators of transcription protein signaling. The Journal of biological chemistry 17 22311973
2019 Spinal CCL1/CCR8 regulates phosphorylation of GluA1-containing AMPA receptor in postoperative pain after tibial fracture and orthopedic surgery in mice. Neuroscience research 16 31121204
2000 A transcriptional autoregulatory loop for KIN28-CCL1 and SRB10-SRB11, each encoding RNA polymerase II CTD kinase-cyclin pair, stimulates the meiotic development of S. cerevisiae. Yeast (Chichester, England) 15 10861906
2021 Hsa_circ_0134111 promotes osteoarthritis progression by regulating miR-224-5p/CCL1 interaction. Aging 14 34413269
2020 CCL1 blockade alleviates human mesenchymal stem cell (hMSC)-induced pulmonary fibrosis in a murine sclerodermatous graft-versus-host disease (Scl-GVHD) model. Stem cell research & therapy 14 32586381
2017 Neuropathic pain inhibitor, RAP-103, is a potent inhibitor of microglial CCL1/CCR8. Neurochemistry international 14 29248693
2002 Overexpression of ccl1-2 can bypass the need for the putative apocytochrome chaperone CycH during the biogenesis of c-type cytochromes. Molecular microbiology 14 12421312
1999 Role of the C-C chemokine, TCA3, in the protective anticryptococcal cell-mediated immune response. Journal of immunology (Baltimore, Md. : 1950) 14 10202026
1993 Serologic analysis of a murine chemokine, TCA3. Journal of immunology (Baltimore, Md. : 1950) 14 7678629
2024 Suberanilohydroxamic acid (SAHA), a HDAC inhibitor, suppresses the effect of Treg cells by targeting the c-Myc/CCL1 pathway in glioma stem cells and improves PD-L1 blockade therapy. Journal of neuro-oncology 12 38652401
2009 TNFalpha- and NF-kappaB-dependent induction of the chemokine CCL1 in human macrophages exposed to the atherogenic lipoprotein(a). Life sciences 12 19302817
1996 Activated lymphocytes induce promoter activity of the TCA3 gene in mast cells following cell-to-cell contact. Biochemical and biophysical research communications 11 8629992
2015 The Ccl1-Kin28 kinase complex regulates autophagy under nitrogen starvation. Journal of cell science 10 26567215
2006 In vitro selection of RNA aptamers that block CCL1 chemokine function. Biochemical and biophysical research communications 10 16930539
2011 Identification of CCL1 as a Gene Differentially Expressed in CD4 T Cells Expressing TIM-3. Immune network 9 22039368
2025 Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8. Frontiers in immunology 8 40051629
2021 CCR8 Signaling via CCL1 Regulates Responses of Intestinal IFN-γ Producing Innate Lymphoid CelIs and Protects From Experimental Colitis. Frontiers in immunology 8 33613532
2021 Overexpressing Pleurotus ostreatus rho1b results in transcriptional upregulation of the putative cellulolytic enzyme-encoding genes observed in ccl1 disruptants. Environmental microbiology 8 34622510
2006 Selective neutralization of the chemokine TCA3 reduces the increased injury of partial versus whole liver transplants induced by cold preservation. Transplantation 8 17164723
2003 Yaba-like disease virus protein 7L is a cell-surface receptor for chemokine CCL1. The Journal of general virology 8 14645913
2025 Inhibition of Alkbh5 Attenuates Lipopolysaccharide-Induced Lung Injury by Promoting Ccl1 m6A and Treg Recruitment. Cell proliferation 6 40254698
2004 Autocrine stimulation of rhadinovirus-transformed T cells by the chemokine CCL1/I-309. Oncogene 6 15378023
2003 Ty3/gypsy-like retrotransposons in Candida albicans and Candida dubliniensis: Tca3 and Tcd3. Yeast (Chichester, England) 6 12722183
2023 MMP9-Associated Tumor Stem Cells, CCL1-Silenced Dendritic Cells, and Cytokine-Induced Killer Cells Have a Remarkable Therapeutic Efficacy for Acute Myeloid Leukemia by Activating T Cells. Stem cells international 5 37200633
2023 MiR-184-5p represses neuropathic pain by regulating CCL1/CCR8 signaling interplay in the spinal cord in diabetic mice. Neurological research 5 37842802
2019 The Systemic Administration of the Chemokine CCL1 Evokes Thermal Analgesia in Mice Through the Activation of the Endocannabinoid System. Cellular and molecular neurobiology 5 31203533
2025 CCR8/CCL1 and CXCR3/CXCL10 axis-mediated memory T-cell activation in patients with recalcitrant drug-induced hypersensitivity. The British journal of dermatology 4 39503255
2025 Macrophage-derived CCL1 targets CCR8 receptor in hepatic stellate cells to promote liver fibrosis through JAk/STAT pathway. Biochemical pharmacology 4 40122149

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