Affinage

CCL5

C-C motif chemokine 5 · UniProt P13501

Round 2 corrected
Length
91 aa
Mass
10.0 kDa
Annotated
2026-04-28
130 papers in source corpus 47 papers cited in narrative 46 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCL5 (RANTES) is a secreted CC-family chemokine that serves as a principal chemoattractant for monocytes, memory T lymphocytes, and eosinophils, and plays broader roles in angiogenesis, neuronal synaptic function, and tumor microenvironment remodeling (PMID:1699135, PMID:1380064, PMID:22752444, PMID:33931731). CCL5 signals primarily through the Gi-coupled receptor CCR5, activating Jak2/Jak3, p38 MAPK, PI3K/Akt, and NF-κB cascades; its agonist activity is critically dependent on N-terminal integrity, as Met-RANTES acts as a full antagonist (PMID:8663314, PMID:11278738, PMID:8576227). Higher-order oligomerization into double-helical rod polymers and glycosaminoglycan binding via a surface-exposed KKWVR motif cooperate to enable filamentous presentation on activated endothelium, which is required for shear-resistant leukocyte arrest and apoptosis induction through CCR5 (PMID:27091995, PMID:25791723, PMID:16807236). Transcription is controlled by NF-κB, KLF13/RFLAT-1 (governing delayed T-cell expression), Fli-1, SP1 (constitutive in NK cells via JNK), NFATc3, and HIF-1α, while post-transcriptionally, TTP promotes m6A-dependent mRNA decay and YB-1 phosphorylation/calcineurin-mediated dephosphorylation modulates promoter occupancy (PMID:12388374, PMID:11138780, PMID:25098295, PMID:19124744, PMID:31903118, PMID:34877932, PMID:24947514).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1988 High

    Identification of CCL5/RANTES as a novel T-cell-specific gene encoding a small secreted cysteine-rich protein established the founding member of a chemokine subfamily and opened investigation into its immune function.

    Evidence cDNA library screening, Northern blot, sequence analysis of a T-cell-specific transcript

    PMID:2456327

    Open questions at the time
    • No functional activity demonstrated
    • Receptor unknown
    • Protein not yet purified
  2. 1990 High

    Demonstrating that recombinant CCL5 selectively attracts monocytes and memory (UCHL1+) T cells but not naive T cells established its chemotactic specificity and defined it as a bona fide chemokine.

    Evidence Chemotaxis assay with purified and recombinant RANTES, flow cytometric phenotyping of responding cells

    PMID:1699135

    Open questions at the time
    • Receptor identity unknown
    • Signaling mechanism uncharacterized
    • In vivo relevance not yet tested
  3. 1992 High

    Purification of two natural CCL5 forms from platelets (including an O-glycosylated variant) with nanomolar eosinophil chemoattractant potency revealed platelets as a major physiological source and extended the target cell repertoire beyond T cells and monocytes.

    Evidence HPLC purification, electrospray mass spectrometry, eosinophil chemotaxis assay from thrombin-stimulated platelet releasates

    PMID:1380064

    Open questions at the time
    • Receptor identity still unknown
    • Significance of O-glycosylation for activity not determined
  4. 1995 High

    The discovery that CCL5 (with MIP-1α and MIP-1β) constitutes the major HIV-suppressive factor from CD8+ T cells fundamentally linked chemokine biology to HIV pathogenesis and foreshadowed the identification of CCR5 as the HIV co-receptor.

    Evidence Protein purification from CD8+ T-cell supernatants, N-terminal sequencing, neutralizing antibody blockade of HIV-1/HIV-2/SIV suppression

    PMID:8525373

    Open questions at the time
    • Mechanism of HIV suppression unknown at this point
    • Receptor identity not yet confirmed
  5. 1996 High

    Molecular cloning of CCR5 as the Gi-coupled high-affinity receptor for CCL5, combined with the demonstration that Met-RANTES is a full antagonist and that CCL5 blocks HIV entry through CCR5 in a V3-dependent manner, unified the chemotactic and HIV-suppressive activities under a single receptor system and revealed the critical importance of N-terminal integrity for agonism.

    Evidence Receptor cloning, radioligand binding, calcium flux with pertussis toxin, E. coli-expressed Met-RANTES in calcium/chemotaxis assays, chimeric V3 domain HIV constructs

    PMID:8576227 PMID:8663314 PMID:8699119 PMID:8898753

    Open questions at the time
    • Downstream signaling cascades beyond Gi not characterized
    • Structural basis of N-terminal activation unknown
    • Role of oligomerization not addressed
  6. 2001 High

    Dissection of CCR5 downstream signaling revealed pertussis toxin-insensitive Jak2/Jak3 activation, CCR5 tyrosine phosphorylation, p56lck association with Jak3, and p38 MAPK pathway engagement, distinguishing CCL5/CCR5 signaling from classical Gi-only chemokine cascades; simultaneously, platelet-derived CCL5 was shown to deposit on inflamed endothelium and trigger monocyte arrest under flow.

    Evidence Co-IP and phospho-Western blot in T cells with pertussis toxin and p38 inhibitor controls; parallel-wall flow chamber with Met-RANTES blockade and ex vivo carotid perfusion in apoE−/− mice

    PMID:11278738 PMID:11282909

    Open questions at the time
    • No structural information on CCL5-CCR5 complex
    • Oligomerization requirements for endothelial deposition not tested
    • Link between Jak signaling and chemotaxis vs. activation not resolved
  7. 2002 High

    Promoter dissection identified NF-κB as the primary transcriptional activator of CCL5 in epithelial cells upon TNF-α stimulation, with IFN-γ acting post-transcriptionally to stabilize mRNA, establishing stimulus-specific regulatory layers.

    Evidence Promoter deletion/mutagenesis, luciferase reporter, EMSA, and nuclear fractionation in alveolar epithelial cells

    PMID:12388374

    Open questions at the time
    • Chromatin-level regulation not addressed
    • mRNA stabilization mechanism undefined
    • Tissue-specific differences in promoter usage unclear
  8. 2006 High

    Reconstitution experiments with ligand and receptor mutants demonstrated that CCL5-induced T-cell apoptosis requires three cooperating features: GAG binding, higher-order oligomerization (tetramers as the minimal active species), and CCR5 tyrosine-339 phosphorylation, proceeding through the intrinsic apoptotic pathway (cytochrome c/caspase-9/caspase-3).

    Evidence GAG-binding mutant 44AANA47, oligomerization mutant E66S, CCR5-Y339F mutant, caspase activation and cytochrome c release assays

    PMID:16807236

    Open questions at the time
    • Structural basis for why tetramers are the minimal active species unknown
    • Signaling intermediates between CCR5-pY339 and mitochondrial apoptosis pathway not identified
  9. 2007 High

    Characterization of the KLF13/NF-κB enhancesome at the CCL5 promoter, with KLF13 itself under translational control, provided a molecular explanation for the characteristic 3–5 day delayed CCL5 expression kinetics in activated T cells, distinct from constitutive NK-cell expression driven by JNK→SP1.

    Evidence Promoter analysis, transcription factor interaction studies, and chromatin modification assays for T cells; MAPK inhibitors, ChIP, EMSA, and SP1-site mutagenesis for NK cells

    PMID:17322928 PMID:19124744

    Open questions at the time
    • Translational regulatory mechanism for KLF13 not molecularly defined
    • Whether enhancesome composition differs across T-cell subsets is unknown
  10. 2011 High

    Structural determination of CCL5 oligomers as double-helical rod-shaped polymers, with a fully exposed KKWVR GAG-binding motif distinct from the monomer/dimer BBXB site, provided a unified biophysical framework explaining why oligomerization and GAG binding are jointly required for endothelial surface presentation and leukocyte recruitment.

    Evidence NMR, SAXS, hydroxyl radical footprinting, and later X-ray crystallography of CCL5 polymers

    PMID:21827949 PMID:25791723 PMID:27091995

    Open questions at the time
    • No high-resolution structure of the CCL5–CCR5 signaling complex
    • Dynamics of oligomer assembly/disassembly on endothelial surfaces not resolved
  11. 2014 High

    Identification of Fli-1 as a potent CCL5 transcriptional activator via distal Ets promoter sites, and of the Akt-phosphorylated YB-1/calcineurin axis as a post-translational switch controlling CCL5 promoter occupancy during monocyte differentiation, expanded the regulatory network beyond NF-κB and KLF13.

    Evidence ChIP, promoter-reporter/deletion analysis, DNA-binding domain mutagenesis for Fli-1; Co-IP of YB-1–calcineurin, phospho-Ser102-specific analysis, cyclosporine A in vivo for YB-1

    PMID:24947514 PMID:25098295

    Open questions at the time
    • Relative contributions of Fli-1 vs. other Ets factors in different immune cell types unknown
    • Whether YB-1 phosphorylation integrates with the KLF13 enhancesome is untested
  12. 2021 High

    Multiple studies revealed expanded functional roles for CCL5: support of hippocampal synaptic plasticity via mitochondrial metabolism and purine synthesis (demonstrated by KO and rescue); TTP-mediated m6A-dependent mRNA decay as a post-transcriptional off-switch; and tumor microenvironment remodeling through CCR5-dependent DNA damage repair in glioblastoma and macrophage M2 polarization in multiple cancers.

    Evidence CCL5-KO mice with lentiviral rescue, metabolomics, FDG-PET, and LTP electrophysiology; TTP overexpression with m6A methylation and mRNA stability assays; pericyte depletion/maraviroc in GBM xenografts; CCL5/CCR5 blockade in chordoma organoids and xenografts

    PMID:33931731 PMID:34239070 PMID:34877932 PMID:37185233

    Open questions at the time
    • Receptor and signaling pathway mediating CCL5's metabolic effects in neurons not identified
    • Whether TTP-m6A mechanism operates in all CCL5-expressing cell types is unknown
    • Relative contribution of CCL5 vs. other CCR5 ligands in tumor immune evasion unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution structure of the CCL5–CCR5 signaling complex, the mechanism linking CCR5 Y339 phosphorylation to divergent outcomes (chemotaxis vs. apoptosis), and the identity of the receptor mediating CCL5's neuronal metabolic effects remain unresolved.
  • No experimental CCL5–CCR5 co-structure
  • Signaling branch point between chemotaxis, survival, and apoptosis undefined
  • Neuronal CCL5 receptor and metabolic signaling pathway uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 6 GO:0098631 cell adhesion mediator activity 3
Localization
GO:0005576 extracellular region 7
Pathway
R-HSA-168256 Immune System 9 R-HSA-162582 Signal Transduction 7 R-HSA-109582 Hemostasis 4 R-HSA-5357801 Programmed Cell Death 1
Partners
CCR1CCR5FLI1KLF13NFATC3PF4SP1YB1

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1988 CCL5 (RANTES) was identified as a novel T cell-specific secreted molecule belonging to a new gene family of small proteins characterized by conserved cysteine residues; the gene product is predicted to be ~8 kDa after signal peptide cleavage with 4 cysteines and no N-linked glycosylation sites. cDNA library screening, sequence analysis, Northern blot Journal of immunology High 2456327
1990 CCL5/RANTES protein selectively attracts human blood monocytes and CD4+/UCHL1+ memory T lymphocytes but not naive T cells, demonstrating chemokine activity for specific leukocyte subsets. Chemotaxis assay with purified/recombinant RANTES, flow cytometry cell phenotyping Nature High 1699135
1992 CCL5/RANTES released by thrombin-stimulated platelets is a potent eosinophil chemoattractant; purification revealed two natural forms: a full-length form (EoCP-2, ~7,863 Da, with methionine oxidation) and an O-glycosylated form (EoCP-1, ~8,355 Da), both with ED50 ~2 nM for eosinophil chemotaxis. HPLC purification, NH2-terminal sequencing, electrospray mass spectrometry, eosinophil chemotaxis assay Journal of Experimental Medicine High 1380064
1993 The RANTES/CCL5 gene spans ~7.1 kb, is composed of 3 exons (133, 112, and 1075 bases) and 2 introns, with conserved intron/exon boundaries relative to other CC chemokines. The ~1 kb promoter contains consensus elements for T cell/hematopoietic, myeloid, and ubiquitous transcription factors; promoter activity is cell-type specific (high in mature T cells and erythroleukemic cells, absent in early T cell lines). Genomic cloning, promoter-luciferase reporter assays, deletion analysis Journal of Immunology High 7689610
1995 CCL5/RANTES (together with MIP-1α and MIP-1β) was identified as a major HIV-suppressive factor produced by CD8+ T cells; recombinant CCL5 dose-dependently inhibited HIV-1, HIV-2, and SIV, and combination neutralizing antibodies against all three chemokines abrogated CD8+ T cell HIV-suppressive activity. Protein purification from CD8+ T cell supernatants, N-terminal sequencing, neutralizing antibody blockade, HIV replication assay Science High 8525373
1996 Retention of the initiating methionine (Met-RANTES) completely abolishes CCL5 agonist activity in calcium mobilization and chemotaxis assays while producing a potent selective antagonist of both RANTES and MIP-1α through competition for their shared receptor CC-CKR-1, demonstrating that the integrity of the amino terminus is critical for receptor activation. Recombinant protein expression in E. coli, calcium flux assay, chemotaxis assay, radioligand competition binding on THP-1 cells and transfected HEK cells Journal of Biological Chemistry High 8576227
1996 CCL5/RANTES blocks HIV-1 entry into cells through a pertussis toxin-insensitive mechanism; the V3 domain of gp120 is a critical determinant of susceptibility to CCL5-mediated HIV suppression, linking CCR5 co-receptor usage to chemokine-mediated blocking. HIV infection assay, pertussis toxin treatment, chimeric V3 domain constructs Nature Medicine High 8898753
1996 CCR5 was molecularly cloned as the high-affinity G protein-coupled receptor for CCL5/RANTES, MIP-1β, and MIP-1α on monocytes; receptor activation leads to inositol phosphate generation and calcium flux, both blocked by pertussis toxin, establishing CCR5 as a Gi-coupled receptor for CCL5. cDNA cloning, stable transfection, radioligand binding, calcium flux assay, pertussis toxin treatment Journal of Biological Chemistry High 8663314 8699119
1998 CCL5/RANTES induces a unique biphasic Ca2+ signal in T cells: the first phase is G-protein-mediated and chemotaxis-associated; the second phase (at >100 nM) is tyrosine kinase-linked, correlates with CD3 expression level, and is partially dependent on TCR co-stimulation, indicating a T cell activation pathway distinct from chemotaxis. Ca2+ flux assay, cell sorting by CD3 expression, anti-CD3 pre-stimulation experiments Journal of Immunology Medium 9552000
1998 CCL5-RANTES fusion antibody retains both CCR5-binding activity and chemoattractant function; the fusion protein induces actin polymerization in THP-1 cells, supports T cell transendothelial migration, and blocks HIV-1 CCR5-mediated entry, demonstrating that the functional domains of CCL5 can be preserved in fusion constructs. Flow cytometry, actin polymerization assay, transendothelial migration assay, HIV infection inhibition assay Journal of Immunology Medium 9759898
1998 CCL5/RANTES and other chemokines (SDF-1α, fractalkine) regulate Ca2+ signaling and reduce voltage-dependent Ca2+ currents and excitatory postsynaptic current frequency in hippocampal neurons, and protect neurons from gp120-induced apoptosis, establishing direct chemokine receptor signaling in CNS neurons. Fura-2 Ca imaging, whole-cell patch clamp, RT-PCR for receptor expression, apoptosis assay PNAS High 9826729
2000 RANTES/CCL5 expression in T lymphocytes is regulated 'late' (3–5 days post-activation) by RFLAT-1, a Krüppel-like family transcription factor whose expression is itself translationally regulated after T cell activation, providing a mechanism for the delayed kinetics of CCL5 expression. Promoter characterization, transcription factor identification, translational regulation assays Immunological Reviews Medium 11138780
2001 CCL5/RANTES secreted by thrombin-stimulated platelets is deposited on the surface of inflamed or atherosclerotic endothelium (requiring endothelial activation by IL-1β) and triggers shear-resistant monocyte arrest under flow conditions via RANTES receptors, as blocked by Met-RANTES or anti-RANTES antibody. Parallel-wall flow chamber, ELISA, immunofluorescence, ex vivo carotid artery perfusion, immunohistochemistry in apoE-/- mice Circulation High 11282909
2001 CCL5/RANTES activates Jak2 and Jak3 (pertussis toxin-insensitive), induces tyrosine phosphorylation of CCR5 and Src kinase p56lck (which associates with Jak3), and activates the p38 MAPK pathway (evidenced by p38 and MAPKAP kinase-2 phosphorylation) in CCR5-expressing T cells. Immunoprecipitation, Western blot for phosphorylation, pertussis toxin inhibition, pharmacological p38 inhibition Journal of Biological Chemistry High 11278738
2002 CCL5/RANTES transcription in alveolar epithelial cells is controlled primarily through an NF-κB cis-element in the promoter after TNF-α stimulation; IFN-γ does not activate transcription but stabilizes RANTES mRNA. TNF-α induces nuclear translocation of IRF-3, but unlike viral infection, TNF-α-induced IRF-3 does not bind the RANTES ISRE, revealing stimulus-specific regulation. Promoter deletion/mutagenesis, luciferase reporter assay, EMSA, nuclear fractionation American Journal of Physiology - Lung High 12388374
2003 H. pylori induces RANTES/CCL5 transcription in gastric epithelial cells through NF-κB activation via IKK and NIK (not through TLR/MyD88 or MEK1 pathways); this requires an intact cag pathogenicity island, as shown by kinase-deficient IKK/NIK mutant transfection. Reporter gene assay, transfection of kinase-deficient mutants, coculture with H. pylori Infection and Immunity High 12819056
2003 17β-estradiol (E2) inhibits NF-κB-dependent CCL5 transcription in keratinocytes by competing with the p65 subunit for limiting amounts of the coactivator CBP/CREB-binding protein, without affecting IκBα degradation or NF-κB DNA binding; both ERα and ERβ mediate this effect. Promoter-luciferase assay, EMSA, immunofluorescence, co-transfection with coactivators/receptor mutants Journal of Investigative Dermatology High 12603855
2004 CCL5 heterophilic interactions with platelet factor 4 (PF4) require structural motifs important for CCL5 higher-order oligomerization (the tetrameric E26A mutant supports PF4 binding but not amplification of monocyte arrest); PF4-RANTES heterodimer formation amplifies RANTES-triggered shear-resistant monocyte arrest on endothelium and involves monocytic chondroitin sulfate. Surface plasmon resonance, ligand blot, flow chamber monocyte adhesion assay, RANTES oligomerization mutants Blood High 15459010
2005 Platelet microparticles (PMPs) contain substantial RANTES/CCL5 and serve as a transcellular delivery system, depositing RANTES on activated endothelium during transient rolling interactions in a flow-dependent manner; PMP-dependent RANTES deposition requires P-selectin, GPIb, GPIIb/IIIa, and JAM-A differentially, and promotes subsequent monocyte arrest. Flow chamber with video microscopy, blocking antibodies, genetic deficiency of PMP adhesion receptors, immunofluorescence Arteriosclerosis, Thrombosis, and Vascular Biology High 15890969
2006 CCL5-induced apoptosis in CCR5-expressing T cells requires: (1) GAG binding on the cell surface (exogenous heparin/chondroitin sulfate or GAG digestion prevents apoptosis; non-GAG-binding mutant 44AANA47-CCL5 does not induce apoptosis); (2) higher-order oligomerization (dimer-forming E66S mutant fails to induce apoptosis; tetramers are the minimal active aggregate); (3) CCR5 tyrosine 339 (CCR5Y339F cells are resistant). The mechanism involves cytochrome c release, caspase-9 and caspase-3 activation. T cell apoptosis assay, GAG digestion, exogenous GAG competition, CCL5 oligomerization mutants, CCR5 tyrosine mutant, caspase activation assays, cytochrome c release Journal of Biological Chemistry High 16807236
2006 In vivo lung-specific CCL5 overexpression in transgenic mice preferentially induces neutrophil infiltration (rather than eosinophils), and upregulates expression of MIP-2, IP-10, and MCP-1 in the lung, demonstrating a role for CCL5 in neutrophil trafficking. Inducible transgenic mouse model, bronchoalveolar lavage, differential cell counts, RT-PCR American Journal of Physiology - Lung Medium 11000125
2006 CCL5-evoked Ca2+ elevation in human microglia via CCR5 requires Jak activity, inhibitory G protein (pertussis toxin-sensitive component), PI3K, Btk, and PLC-mediated IP3-dependent Ca2+ release from intracellular stores; the majority of the Ca2+ increase is derived from NAD metabolite-activated sources: cADPR releases Ca2+ from intracellular stores and ADPR evokes Ca2+ influx via nimodipine-sensitive channels. Fura-2 calcium imaging, pharmacological inhibitors (Jak inhibitor, PI3K inhibitor, BTK inhibitor, PLC inhibitor), pertussis toxin, nimodipine Journal of Neuroscience Research High 16547971
2007 The transcription factor KLF13 (RFLAT-1), together with NF-κB rel proteins p50/p65 and scaffolding proteins, forms a molecular enhancesome at the RANTES promoter in T lymphocytes that recruits chromatin-modifying enzymes (acetylation, methylation, phosphorylation), and KLF13 itself is translationally regulated to control the delayed (3–5 day) RANTES expression after T cell activation. Promoter analysis, transcription factor interaction studies, chromatin modification assays Nature Clinical Practice Nephrology Medium 17322928
2009 JNK MAPK pathway controls constitutive CCL5 expression in peripheral blood NK cells (unlike delayed expression in T cells) through SP1 binding to a compact promoter region (-75 to -56 bp upstream of TSS), as shown by promoter-reporter assays, EMSA, ChIP, and site-directed mutagenesis of the SP1 binding site. Specific MAPK inhibitors, promoter-reporter assay, EMSA, ChIP, heterologous promoter constructs, site-directed mutagenesis Journal of Immunology High 19124744
2009 CCL5 promotes macrophage survival in human adipose tissue by protecting macrophages from free cholesterol-induced apoptosis via activation of the Akt and Erk pathways, and triggers adhesion and transmigration of blood monocytes through endothelial cells of human adipose tissue. Monocyte transmigration assay, apoptosis assay with free cholesterol, Western blot for Akt/Erk phosphorylation Arteriosclerosis, Thrombosis, and Vascular Biology Medium 19893003
2010 Endothelial CCL5 expression, induced by selectin-mediated tumor cell interactions, promotes monocyte recruitment to metastatic tumor cells; CCL5 receptor antagonist treatment during early metastasis reduced tumor cell survival and attenuated metastasis, establishing a mechanistic role for CCL5 in forming the metastatic microenvironment. Microarray, flow chamber monocyte recruitment assay, CCL5 receptor antagonist treatment, in vivo metastasis model Blood Medium 19779041
2010 CCL5 stimulates externalization of S100A4 protein via microparticle shedding from plasma membranes of tumor and stroma cells; conversely, released S100A4 induces fibronectin upregulation in fibroblasts and RANTES upregulation in tumor cells, establishing a positive feedback loop. In vivo, tumor-derived CCL5 promotes S100A4 release into circulation and increases metastatic burden. Microparticle shedding assay, cytokine induction assay, wound healing/migration assay, wild-type vs. S100A4-/- mouse models PloS One Medium 20442771
2011 CCL5 oligomers form rod-shaped, double-helical polymers; the E66 and E26 mutations that disrupt oligomerization are explained by the structural model. GAG binding by CCL5 oligomers uses a positively charged, fully exposed KKWVR motif (distinct from the partially buried BBXB motif used by monomers/dimers), providing a unified mechanism for how oligomerization and GAG binding cooperate in CCL5 function. NMR residual dipolar couplings, SAXS, hydroxyl radical footprinting, NMR cross-saturation, structural modeling Structure High 21827949
2012 CCL5 promotes osteosarcoma cell migration and upregulates αvβ3 integrin through CCR5 (not CCR1 or CCR3), activating a MEK→ERK→NF-κB signaling cascade; CCR5 mAb, siRNA, and specific inhibitors of MEK, ERK, and NF-κB all abolish CCL5-enhanced migration and integrin upregulation. Migration assay, flow cytometry (integrin expression), siRNA, pharmacological inhibitors, dominant-negative constructs PloS One Medium 22506069
2012 CCL5-mediated angiogenesis in vitro and in vivo is dependent on both G protein-coupled receptors CCR1 and CCR5, and on heparan sulfate proteoglycans (syndecan-1, syndecan-4, CD44); chemokine oligomerization and GAG binding are both essential for pro-angiogenic effects, as oligomerization-deficient (E66A) and GAG-binding-deficient (44AANA47) mutants lose angiogenic activity. Pro-angiogenic signaling involves MMP-9 and VEGF secretion by endothelial cells. In vitro endothelial migration/tube formation, rat subcutaneous angiogenesis model, receptor-blocking antibodies, CCL5 oligomerization/GAG mutants, anti-VEGFR antibodies Angiogenesis High 22752444
2012 CCL5/CCR5 interaction in chondrosarcoma cells activates PI3K→Akt→NF-κB signaling, leading to upregulation of MMP-3, which mediates increased cell migration; PI3K, Akt, and NF-κB inhibitors and MMP-3 siRNA all block CCL5-induced migration. Migration assay, MMP-3 siRNA/inhibitor, pharmacological inhibitors of PI3K/Akt/NF-κB, Western blot Biochemical Pharmacology Medium 19682436
2014 The Fli-1 transcription factor (Ets family member) drives CCL5 transcription by binding to Ets sites in the distal CCL5 promoter; Fli-1 transactivation is stronger than Ets1, and Ets1 acts as a dominant-negative. Systematic deletion of a 225-bp promoter region identifies critical Fli-1 binding sites; mutation of the Fli-1 DNA-binding domain reduces CCL5 promoter transactivation. Fli-1 siRNA knockdown, promoter-reporter assays, ChIP of endogenous Ets binding sites, deletion analysis, DNA-binding domain mutation Journal of Immunology High 25098295
2014 YB-1 phosphorylation at Ser-102 (mediated by Akt) increases its binding affinity and trans-activating capacity at the CCL5 promoter during early monocyte/macrophage differentiation; calcineurin (CN) subsequently dephosphorylates YB-1 at Ser-102, preventing CCL5 promoter binding, as demonstrated by Co-IP of YB-1/CN interaction and in vivo cyclosporine A effects on YB-1 phosphorylation status. Co-immunoprecipitation, Western blot for phospho-YB-1, promoter-reporter assay, calcineurin inhibitor (cyclosporine A) in vivo Journal of Biological Chemistry High 24947514
2014 Computational modeling of the CCL5:CCR5 complex structure reveals that both CCL5 and HIV-1 gp120 V3 loop primarily interact with the same CCR5 residues, providing structural insight into CCL5's mechanism of blocking HIV-1 entry via competitive occupation of the CCR5 binding interface. Computational free energy calculations and molecular dynamics simulations, validated against experimental mutagenesis data Scientific Reports Low 24965094
2014 IL-32θ downregulates CCL5 expression by interacting with PKCδ (shown by Co-IP and pulldown assay), facilitating PKCδ-mediated phosphorylation of STAT3 at Ser-727, which prevents STAT3 from binding to and transactivating the CCL5 promoter. Co-immunoprecipitation, pulldown assay, ELISA, promoter binding assay Cellular Signalling Medium 25280942
2015 CCL5 interactions with chondroitin sulfate hexasaccharides involve both the BBXB motif in the 40s loop and residues in the N-loop (similar to receptor N-terminus interactions); the binding orientation is highly dependent on sulfation pattern of N-acetyl galactosamine groups, as shown by paramagnetic relaxation enhancement and NOE NMR constraints. Solution NMR (PRE, NOE), TEMPO-tagged hexasaccharides, structural modeling Structure High 25982530
2016 Crystal structures of CCL5 oligomers reveal polymerization as a double-helical rod. The CCL5 oligomer uses a distinct positively charged KKWVR motif for GAG binding (not the BBXB motif which is partially buried), while CCL3 oligomers use a GAG-binding groove formed by residues from two partially buried BBXB motifs. N-terminal conformational changes in CCL3 alter surface properties and dimer-dimer interfaces to affect GAG binding. X-ray crystallography, biophysical analysis PNAS High 27091995
2015 CCL5 surface presentation on vascular endothelial cells is filamentous and heparan sulfate-dependent; CCL5 mutants restricted in heparin binding, dimerization, or tetramer formation lose filamentous surface organization, appearing granular or undetectable. Filamentous structures persist under flow conditions, suggesting physiological relevance for leukocyte recruitment. Immunofluorescence, electron microscopy, flow conditions, CCL5 oligomerization/GAG-binding mutants Scientific Reports High 25791723
2020 ASIC1a activation in rheumatoid arthritis synovial fibroblasts mediates Ca2+ influx, which increases [Ca2+]i and activates NFATc3; nuclear NFATc3 directly binds the RANTES/CCL5 promoter and drives CCL5 gene transcription, as shown by ChIP-qPCR and dual-luciferase reporter assay. Ca2+ imaging, flow cytometry, ChIP-qPCR, dual-luciferase reporter assay, Western blot, immunofluorescence Theranostics High 31903118
2021 CCL5 secreted by pericytes activates CCR5 on glioblastoma cells, enabling DNA-PKcs-mediated DNA damage repair (DDR) upon temozolomide treatment; genetic pericyte depletion or CCR5 antagonist maraviroc inhibits pericyte-promoted DDR and improves chemotherapeutic efficacy. Pericyte genetic depletion, Co-culture, Western blot for DNA-PKcs activity, GBM xenografts, maraviroc treatment Cell Research High 34239070
2021 CCL5 promotes hippocampal synaptic function and memory by supporting glucose aerobic metabolism, mitochondrial structural integrity, purine synthesis (de novo), and ATP generation; CCL5-knockout mice show impaired hippocampal LTP, reduced synaptic protein expression, and memory deficits reversed by CCL5 re-expression in the hippocampus. CCL5-KO mice, lentiviral CCL5 re-expression, metabolomics, FDG-PET imaging, seahorse metabolic analysis, electron microscopy of mitochondria, electrophysiology (LTP) Molecular Psychiatry High 33931731
2021 TTP (tristetraprolin) promotes m6A methylation of CCL5 mRNA (and CCL2 mRNA), which accelerates their degradation; TTP overexpression upregulates m6A methylation enzymes (WTAP, METTL14, YTHDF2) and reduces CCL5 mRNA stability, establishing a novel m6A-dependent RNA decay mechanism for CCL5 regulation. RNA m6A methylation assay, mRNA stability assay, TTP overexpression, m6A methyltransferase expression analysis, in vivo mouse model JCI Insight Medium 34877932
2021 CCL5 inhibits influenza A virus replication in alveolar epithelial cells through a PKC-dependent upregulation of the restriction factor SAMHD1; SAMHD1 knockdown abolishes both CCL5-mediated IAV inhibition and CCL5-mediated cell death inhibition. RT-PCR for restriction factor panel, SAMHD1 siRNA knockdown, viral titer assay, PKC inhibitor Frontiers in Cellular and Infection Microbiology Medium 34490131
2021 EZH2 promotes CCL5 expression in lung cancer cells; EZH2 knockdown reduces CCL5 and macrophage chemotaxis, while EZH2 overexpression increases CCL5; CCL5 knockdown abolishes EZH2-induced macrophage chemotaxis and cancer cell migration/invasion, placing EZH2 upstream of CCL5 in a pro-metastatic pathway. EZH2 siRNA, CCL5 siRNA, macrophage chemotaxis assay, wound healing, transwell invasion, in vivo xenograft Biotechnology and Applied Biochemistry Medium 31855281
2021 HIF-1α transcriptionally activates CCL5 expression by binding the CCL5 promoter; inactivation of Cullin-RING ligases (CRLs) by MLN4924 stabilizes HIF-1α levels, increasing CCL5 which drives M2 macrophage infiltration promoting chronic pancreatitis; CCL5 blockade and macrophage depletion both alleviate pancreatic fibrosis. CRL inactivation (MLN4924), HIF-1α stabilization assay, CCL5 promoter reporter, macrophage depletion, CCL5 blockade, in vivo chronic pancreatitis model Cell Death & Disease Medium 33723230
2023 Chordoma cells secrete CCL5 to recruit macrophages via CCR5 and promote their M2 polarization; M2 macrophages reciprocally enhance chordoma proliferation, invasion, and migration; CCL5 knockdown or CCR5 antagonist maraviroc inhibits both M2 polarization and malignant progression in organoids and xenograft models. Flow cytometry, multiplex IF, CCL5 knockdown, transwell/chemotaxis assay, patient-derived organoids, xenograft mouse model Journal for Immunotherapy of Cancer Medium 37185233

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Identification of RANTES, MIP-1 alpha, and MIP-1 beta as the major HIV-suppressive factors produced by CD8+ T cells. Science (New York, N.Y.) 2550 8525373
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1990 Selective attraction of monocytes and T lymphocytes of the memory phenotype by cytokine RANTES. Nature 1317 1699135
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
1992 Cytokine RANTES released by thrombin-stimulated platelets is a potent attractant for human eosinophils. The Journal of experimental medicine 638 1380064
1998 Chemokines regulate hippocampal neuronal signaling and gp120 neurotoxicity. Proceedings of the National Academy of Sciences of the United States of America 569 9826729
1997 In vivo evolution of HIV-1 co-receptor usage and sensitivity to chemokine-mediated suppression. Nature medicine 530 9359702
2008 The inflammatory chemokines CCL2 and CCL5 in breast cancer. Cancer letters 481 18439751
2001 RANTES deposition by platelets triggers monocyte arrest on inflamed and atherosclerotic endothelium. Circulation 463 11282909
1988 A human T cell-specific molecule is a member of a new gene family. Journal of immunology (Baltimore, Md. : 1950) 461 2456327
1996 The V3 domain of the HIV-1 gp120 envelope glycoprotein is critical for chemokine-mediated blockade of infection. Nature medicine 450 8898753
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