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CCR1 (chemokine (C-C motif) receptor 1)

Written2010-04Qiang Gao, Jia Fan
Liver Cancer Institute, Zhong Shan Hospital, Shanghai Medical School, Fudan University, Shanghai, P R China

(Note : for Links provided by Atlas : click)


chemokine (C-C motif) receptor 1
Alias_symbol (synonym)CKR-1
Other aliasCKR1
HGNC (Hugo) CCR1
LocusID (NCBI) 1230
Atlas_Id 44379
Location 3p21.31  [Link to chromosome band 3p21]
Location_base_pair Starts at 46201709 and ends at 46208341 bp from pter ( according to hg19-Feb_2009)  [Mapping CCR1.png]
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)


Note CCR1, a member of the beta chemokine receptor family, is a seven transmembrane protein similar to G protein-coupled receptors. CCR1 is the first human CC chemokine receptor to be identified at the cDNA level. It has a functional viral homolog, US28, which is a human cytomegalovirus.The ligands of this receptor include macrophage inflammatory protein 1 alpha (MIP-1 alpha), regulated on activation normal T expressed and secreted protein (RANTES), monocyte chemoattractant protein 3 (MCP-3), and myeloid progenitor inhibitory factor-1 (MPIF-1). This gene and other chemokine receptor genes, including CCR2, CCRL2, CCR3, CCR5 and CCXCR1, form a gene cluster on chromosome 3p.
Description Sequence length: 6633 bp; coding sequence: CDS 72-1139. 2 exons; number of SNPs: 97.
Transcription 2690 bp mRNA, no alternative splicing.
Pseudogene No pseudogenes have been reported for CCR1.


Note Chemokine receptors are cytokine receptors found on the surface of certain cells, which interact with a type of cytokine called a chemokine. They each have a 7 transmembrane structure and couple to G-protein for signal transduction within a cell, making them members of a large protein family of G protein-coupled receptors. Following interaction with their specific chemokine ligands, chemokine receptors trigger a flux in intracellular calcium (Ca2+) ions (calcium signaling). This causes cell responses, including the onset of a process known as chemotaxis that traffics the cell to a desired location within the organism. Chemokine receptors share many common structural features; they are composed of about 350 amino acids that are divided into a short and acidic N-terminal end, seven helical transmembrane domains with three intracellular and three extracellular hydrophilic loops, and an intracellular C-terminus containing serine and threonine residues that act as phosphorylation sites during receptor regulation. The first two extracellular loops of chemokine receptors are linked together by disulfide bonding between two conserved cysteine residues. The N-terminal end of a chemokine receptor binds to chemokine(s) and is important for ligand specificity. G-proteins couple to the C-terminal end, which is important for receptor signaling following ligand binding.
  Predicted structure and amino acid sequence of CCR1. The typical serpentine structure is depicted with three extracellular (top) and three intracellular (bottom) loops and seven transmembrane domains. The shaded horizontal band represents the cell membrane. Amino acids are listed with a single letter code.
Description 355 amino acids; 41173 Da.
Expression Monocyte/macrophages; T cells; platelets; tonsil B lymphocytes; blood derived mast cells, dendritic cells, basophils and eosinophils; bone marrow stromal cells; microvascular endothelial cells; vascular smooth muscle cells.
Localisation Cell membrane; multi-pass membrane protein.
Function Receptor for a C-C type chemokine. Binds to CCL3 (MIP-1-alpha), CCL5 (RANTES), CCL7 (MCP-3), CCL9 (MIP-1-gamma), CCL14 (HCC-1), CCL15 (MIP-1-delta), CCL16 (HCC-4) and CCL23 (MIP-3), and, less efficiently, to MIP-1-beta or MCP-1 and subsequently transduces a signal by increasing the intracellular calcium ions level. The major function of CCR1 is to regulate leukocyte trafficking in hematopoiesis and in innate and adaptive immunity. Other functions include angiogenic activity, ischemia/reperfusion injury, immune-cell differentiation, phagocyte activation, and affecting stem cell proliferation.
Homology CCR1 protein contains considerable amino acid sequence homology to other C-C chemokines: CCR2B (56%), CCR3 (54%), CCR4 (49%), CCR5 (55%).

Implicated in

Entity Hematolymphoid neoplasia
Prognosis CCR1 expression correlates with overall survival in the non-germinal center subtype of diffuse large B-cell lymphoma. In follicular lymphoma, high levels of CCR1 are associated with a shorter survival interval, and CCR1 is a marker of an immune switch between macrophages and a T cell-dominant response.
Oncogenesis CCR1 is expressed in intraepithelial B cells of human tonsil and granulocytic/monocytic cells in the bone marrow. Immunohistochemical analysis of 944 cases of hematolymphoid neoplasia identified CCR1 expression in a subset of B- and T-cell lymphomas, plasma cell myeloma, acute myeloid leukemia, and classical Hodgkin lymphoma. In 13 patients with chronic lymphocytic leukemia (CLL), 9 with hairy cell leukemia (HCL), 5 with mantle cell lymphoma (MCL), 5 with marginal zone B-cell lymphoma (MZL), 6 with small lymphocytic lymphoma (SLL), and 5 with follicular cell lymphoma (FCL), flow cytometry analysis demonstrated that CCR1 was expressed in 70% of patients with CLL and 40% of those with HCL but was lacking in patients with MCL, MZL, SLL, and circulating normal B cells.
Circulating CD3+ T cells derived from healthy individuals and acute myelogenous leukemia patients with therapy-induced cytopenia after conventional chemotherapy or allogeneic stem cell transplantation showed no qualitative differences in CCR1 expression, that is, low expression for all the three groups.
Entity Multiple myeloma
Prognosis In 80 multiple myeloma (MM) patients with bone marrow samples, patients with active disease showed a significantly lower expression of CCR1, CCR2, as well as CXCR4 than patients with non-active disease. This chemokine receptor expression profile correlated with serum beta2-microglobulin, C-reactive protein and hemoglobin. Multivariate analysis identified the chemokine receptor expression profile as an independent prognostic factor.
Oncogenesis Human MM cells express at least three different chemokine receptors that are functionally involved in MM cell migration, i.e. CCR1, CCR2 and CXCR4, some also CCR6 and CXCR3. cDNA arrays identified CCR1 and CCR2 are overexpressed in myeloma cells compared to autologous B-lymphoblastoid cell lines. The expression of CCR1 and the migration to their ligands, RANTES and MIP-1alpha, respectively, were demonstrated in MM cell lines and primary MM cells.
Osteoclasts (OCL) secrete high levels of CCL3 and MM cells the express CCR1, the interaction between which plays a key role in the pathogenesis of MM-related osteolytic bone disease. Through CCL3-CCR1 axis OCL cells promote OCL formation and, in turn, OCL enhance MM cell proliferation.
In murine models of MM, MIP-1alpha, an OCL stimulatory factor produced by primary MM cells, increases bone destruction and tumor burden, by interacting with chemokine receptors CCR1 and CCR5 that widely expressed in human OCL precursors, myeloma cell lines, and purified marrow plasma cells from MM patients. Neutralizing antibodies to CCR1 or CCR5 inhibited MIP-1alpha-induced OCL formation. Furthermore, MCP-3, which binds CCR1 but not CCR5, and the CCR1-specific antagonist, BX471, markedly inhibited OCL formation stimulated with MIP-1alpha. Anti-CCR1, anti-CCR5, or BX471 also inhibited the upregulation of beta1 integrin myeloma cells induced by MIP-1alpha, as well as the adherence of myeloma cells to stromal cells and IL-6 production by stromal cells in response to myeloma cells.
The oncogene c-maf is translocated in approximately 5%-10% of MM. By gene expression profiling, three c-maf target genes, cyclin D2, integrin beta7 and CCR1, were identified.
Entity Hepatocellular carcinoma
Oncogenesis Hepatic myofibroblast LI90 cells express and secrete MCP-1/CCL2. Through its receptors CCR1 and CCR2 as well, LI90 induces human hepatocellular carcinoma (HCC) Huh7 cell migration and invasion, which are strongly inhibited by heparin, beta-D-xyloside and anti-syndecan-1 and -4 antibodies. RANTES/CCL5 strongly stimulates the migration and the invasion of Huh7 cells by stimulating the tyrosine phosphorylation of focal adhesion kinase as well as activating matrix metalloproteinase-9, and to a lesser extent that of Hep3B cells. The RANTES-induced migration and invasion of Huh7 cells are also strongly inhibited by anti-CCR1 antibodies and heparin, as well as by beta-d-xyloside treatment of the cells, suggesting that CCR1 and glycosaminoglycans are involved in these events. We found that the miRNA-mediated knockdown expression of CCR1 significantly inhibited the invasive ability of and reduced the secretion of MMP-2 in hepatocellular carcinoma HCCLM3 cells, but only had a minor effect on the cellular proliferation. CCR1 expression was also detected on primary HCC cells and to a lesser degree, on endothelial cells in HCC tissues but not in normal liver tissues. Similarly, CCL3 expression was detected in HCC cells, endothelial cells, and to a lesser degree, fibroblast-like cells in HCC tissue, whereas only occasional vascular endothelial cells and inflammatory cells in normal liver tissues were weakly positive for CCL3. IL-1 enhances the local production of CCL3, which interact with CCR1 expressed on HCC cells, in an autocrine and/or paracrine manner. In a murine HCC model, injected tumor cells were transfected with HSV-thymidine kinase gene and then treated with ganciclovir (GCV). GCV treatment induced massive tumor cell apoptosis accompanied with intratumoral CCR1+CCR5+ dendritic cell infiltration. Tumor-infiltrating T cells and macrophages expressed CCL3, suggesting CCR1-CCL3 play a crucial role in the regulation of intratumoral dendritic cell accumulation and the subsequent establishment of tumor immunity following induction of tumor apoptosis by suicide genes. CCL3 and CCR1 are also expressed in 2 different models of HCC, i.e., N-nitrosodiethylamine (DEN)-induced HCC and HCC induced by hepatitis B virus. After DEN treatment, tumor foci number and sizes were remarkably reduced in CCR1- and CCL3-deficient mice, comparing with wild-type (WT) mice. Also, tumor angiogenesis markedly diminished, intratumoral Kupffer cells number reduced, MMP9 gene expression attenuated and MMP9+ cell numbers decreased in CCL3- and CCR1-deficient mice, as compared with WT mice. These observations suggest the contribution of the CCR1-CCL3 axis to HCC progression.
Entity Colorectal cancer
Prognosis The expression of CCR1 is higher in colorectal carcinoma than normal tissues, and correlates with lymph node metastasis, deep invasion, poor differentiation and advanced Dukes' stage.
Oncogenesis Inactivation of TGF-beta family signaling within colon cancer increases CCL9 and promotes recruitment of the matrix metalloproteinase-expressing stromal cells that carry CCR1. Lack of CCR1 prevents the accumulation of MMP-expressing cells at the invasive front and suppresses tumor invasion. In a murine model of invasive colorectal cancer in which TGF-beta family signaling is blocked, CD34+ CCR1+ immature myeloid cell is recruited from the bone marrow to the tumor invasive front where expression of CCL9 is increased. These immature myeloid cells express MMP9, MMP2 and CCR1 and migrate toward the ligand CCL9. Lack of CCR1 prevents accumulation of CD34+ immature myeloid cell at the invasive front and suppresses tumor invasion.
Entity Non-small cell lung cancer
Oncogenesis CCR1 expression correlated with the aggressive phenotype of the non-small cell lung cancer (NSCLC) cells. CCR1 knockdown significantly suppressed the invasiveness of NSCLC cells and significantly reduced the expression of matrix metalloproteinase-9, but had only a minor effect on cell proliferation.
Entity Oral squamous cell carcinoma
Oncogenesis Expression of CCL3 and CCR1 is significant higher in oral squamous cell carcinoma compared with the normal controls. The percentages of CCL3+ and CCR1+ cells were observed to be similar in parenchyma and stroma in cases without lymph node metastasis when compared with lymph node metastasis positive cases.
Entity Ovarian cancer
Oncogenesis mRNA for CCR1, -2a, -2b, -3, -4, -5, and -8 was detected in cells from human ovarian cancer ascites. Further, flowcytometry showed CD14+ macrophages within ascites consistently expressed CCR1, -2, and -5, and >60% of all T cells expressed CCR1. Although ovarian cancer ascitic and blood monocyte/macrophages express CCR1, they failed to migrate in response to the RANTES. Compared with that of normal blood, cell surface expression level for CCR1 was higher in ascites. In a monocytic cell line in vitro, CCR1 mRNA expression was increased 5-fold by hypoxia. In 25 patients with ovarian cancer, CCR1 was detected in samples from 75% of patients, where CCR1 localised to macrophages and lymphocytes, and there was a correlation between numbers of CD8+ cells and CCR1+ cells.
Entity Prostate cancer
Oncogenesis Androgen receptor negative human prostate cancer cell line DU-145 cells selectively expressed CXCR4 and CCR1 at high levels compared with DU-145/AR cells that express androgen receptor. DU-145 showed vigorous migratory responses to CXCL12 and CCL3. In contrast, neither CXCL12 nor CCL3 affected the migration of DU-145/AR cells.
Entity Breast cancer
Oncogenesis The expression of CCR5 was higher than that of CCR1 in the peripheral blood mononuclear cells (PBMC) of healthy women, while the PBMC of the breast cancer patients showed overexpression of CCR1 and downregulation of CCR5. The differential effects of MIP-1alpha and MIP-1beta on the PBMC of healthy women and breast cancer patients correlated with the expression levels of CCR1 and CCR5 in these monocytes. In murine model of breast cancer, CCL5 (RANTES) was produced by the tumor cells, and its receptors, CCR1 and CCR5, were expressed by the infiltrating leukocytes. In mice treatment with Met-CCL5, an antagonist of CCR1 and CCR5, the volume and weight of tumors were significantly decreased compared with control-treated tumors. The total cell number obtained after collagenase digestion was decreased in Met-CCL5-treated tumors as was the proportion of infiltrating macrophages. Furthermore, chemokine antagonist treatment increased stromal development and necrosis.
Entity Glioma
Oncogenesis Co-cultured human glioma U87 cells induced an activated phenotype in HUVECs. These tumour-activated endothelial cells coordinately expressed matching pairs of receptors/ligands were found to be, including CCR1-RANTES axis.
Entity Osteogenic sarcoma
Oncogenesis The activities of phospholipase C (PLC), protein kinase C delta (PKCdelta) and NF-kappaB were enhanced by Lkn-1 (CCL15) stimulation on CCR1+ human osteogenic sarcoma cells. Inhibitors of G protein, PLC, PKCdelta and NF-kappaB inhibited the chemotactic activity of Lkn-1 on CCR1+ osteogenic sarcoma cells indicating that Lkn-1-induced chemotaxis involving these signaling pathways.


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This paper should be referenced as such :
Gao, Q ; Fan, J
CCR1 (chemokine (C-C motif) receptor 1)
Atlas Genet Cytogenet Oncol Haematol. 2011;15(1):1-6.
Free journal version : [ pdf ]   [ DOI ]
On line version :

External links

HGNC (Hugo)CCR1   1602
Entrez_Gene (NCBI)CCR1  1230  C-C motif chemokine receptor 1
AliasesCD191; CKR-1; CKR1; CMKBR1; 
GeneCards (Weizmann)CCR1
Ensembl hg19 (Hinxton)ENSG00000163823 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000163823 [Gene_View]  ENSG00000163823 [Sequence]  chr3:46201709-46208341 [Contig_View]  CCR1 [Vega]
ICGC DataPortalENSG00000163823
TCGA cBioPortalCCR1
AceView (NCBI)CCR1
Genatlas (Paris)CCR1
SOURCE (Princeton)CCR1
Genetics Home Reference (NIH)CCR1
Genomic and cartography
GoldenPath hg38 (UCSC)CCR1  -     chr3:46201709-46208341 -  3p21.31   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)CCR1  -     3p21.31   [Description]    (hg19-Feb_2009)
EnsemblCCR1 - 3p21.31 [CytoView hg19]  CCR1 - 3p21.31 [CytoView hg38]
Mapping of homologs : NCBICCR1 [Mapview hg19]  CCR1 [Mapview hg38]
Gene and transcription
Genbank (Entrez)AI089760 BC051306 BC064991 BT019908 BT019909
RefSeq transcript (Entrez)NM_001295
RefSeq genomic (Entrez)
Consensus coding sequences : CCDS (NCBI)CCR1
Cluster EST : UnigeneHs.301921 [ NCBI ]
CGAP (NCI)Hs.301921
Alternative Splicing GalleryENSG00000163823
Gene ExpressionCCR1 [ NCBI-GEO ]   CCR1 [ EBI - ARRAY_EXPRESS ]   CCR1 [ SEEK ]   CCR1 [ MEM ]
Gene Expression Viewer (FireBrowse)CCR1 [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
GenevestigatorExpression in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)1230
GTEX Portal (Tissue expression)CCR1
Human Protein AtlasENSG00000163823-CCR1 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtP32246   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtP32246  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProP32246
Splice isoforms : SwissVarP32246
Domaine pattern : Prosite (Expaxy)G_PROTEIN_RECEP_F1_1 (PS00237)    G_PROTEIN_RECEP_F1_2 (PS50262)   
Domains : Interpro (EBI)Chemokine_CCR1    Chemokine_CCR1_euk    Chemokine_rcpt    GPCR_Rhodpsn    GPCR_Rhodpsn_7TM   
Domain families : Pfam (Sanger)7tm_1 (PF00001)   
Domain families : Pfam (NCBI)pfam00001   
Domain families : Smart (EMBL)7TM_GPCR_Srsx (SM01381)  
Conserved Domain (NCBI)CCR1
DMDM Disease mutations1230
Blocks (Seattle)CCR1
PDB (SRS)1Y5D   
PDB (PDBSum)1Y5D   
PDB (IMB)1Y5D   
Structural Biology KnowledgeBase1Y5D   
SCOP (Structural Classification of Proteins)1Y5D   
CATH (Classification of proteins structures)1Y5D   
Human Protein Atlas [tissue]ENSG00000163823-CCR1 [tissue]
Peptide AtlasP32246
Protein Interaction databases
IntAct (EBI)P32246
Ontologies - Pathways
Ontology : AmiGOdendritic cell chemotaxis  phosphatidylinositol phospholipase C activity  chemokine receptor activity  protein binding  plasma membrane  plasma membrane  plasma membrane  integral component of plasma membrane  calcium ion transport  cellular calcium ion homeostasis  exocytosis  chemotaxis  inflammatory response  immune response  cell adhesion  cell surface receptor signaling pathway  G-protein coupled receptor signaling pathway  G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger  positive regulation of cytosolic calcium ion concentration  cell-cell signaling  response to wounding  external side of plasma membrane  negative regulation of gene expression  C-C chemokine receptor activity  cytokine-mediated signaling pathway  cytokine-mediated signaling pathway  C-C chemokine binding  positive regulation of cell migration  negative regulation of bone mineralization  chemokine (C-C motif) ligand 7 binding  positive regulation of osteoclast differentiation  positive regulation of calcium ion transport  chemokine-mediated signaling pathway  positive regulation of ERK1 and ERK2 cascade  chemokine (C-C motif) ligand 5 binding  positive regulation of monocyte chemotaxis  
Ontology : EGO-EBIdendritic cell chemotaxis  phosphatidylinositol phospholipase C activity  chemokine receptor activity  protein binding  plasma membrane  plasma membrane  plasma membrane  integral component of plasma membrane  calcium ion transport  cellular calcium ion homeostasis  exocytosis  chemotaxis  inflammatory response  immune response  cell adhesion  cell surface receptor signaling pathway  G-protein coupled receptor signaling pathway  G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger  positive regulation of cytosolic calcium ion concentration  cell-cell signaling  response to wounding  external side of plasma membrane  negative regulation of gene expression  C-C chemokine receptor activity  cytokine-mediated signaling pathway  cytokine-mediated signaling pathway  C-C chemokine binding  positive regulation of cell migration  negative regulation of bone mineralization  chemokine (C-C motif) ligand 7 binding  positive regulation of osteoclast differentiation  positive regulation of calcium ion transport  chemokine-mediated signaling pathway  positive regulation of ERK1 and ERK2 cascade  chemokine (C-C motif) ligand 5 binding  positive regulation of monocyte chemotaxis  
Pathways : BIOCARTASelective expression of chemokine receptors during T-cell polarization [Genes]   
Pathways : KEGGCytokine-cytokine receptor interaction   
REACTOMEP32246 [protein]
REACTOME PathwaysR-HSA-6783783 [pathway]   
NDEx NetworkCCR1
Atlas of Cancer Signalling NetworkCCR1
Wikipedia pathwaysCCR1
Orthology - Evolution
GeneTree (enSembl)ENSG00000163823
Phylogenetic Trees/Animal Genes : TreeFamCCR1
Homologs : HomoloGeneCCR1
Homology/Alignments : Family Browser (UCSC)CCR1
Gene fusions - Rearrangements
Fusion : QuiverCCR1
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerCCR1 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)CCR1
Exome Variant ServerCCR1
ExAC (Exome Aggregation Consortium)ENSG00000163823
GNOMAD BrowserENSG00000163823
Genetic variants : HAPMAP1230
Genomic Variants (DGV)CCR1 [DGVbeta]
DECIPHERCCR1 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisCCR1 
ICGC Data PortalCCR1 
TCGA Data PortalCCR1 
Broad Tumor PortalCCR1
OASIS PortalCCR1 [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICCCR1  [overview]  [genome browser]  [tissue]  [distribution]  
Mutations and Diseases : HGMDCCR1
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD - Leiden Open Variation Database
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
BioMutasearch CCR1
DgiDB (Drug Gene Interaction Database)CCR1
DoCM (Curated mutations)CCR1 (select the gene name)
CIViC (Clinical Interpretations of Variants in Cancer)CCR1 (select a term)
NCG5 (London)CCR1
Cancer3DCCR1(select the gene name)
Impact of mutations[PolyPhen2] [SIFT Human Coding SNP] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Genetic Testing Registry CCR1
NextProtP32246 [Medical]
Target ValidationCCR1
Huge Navigator CCR1 [HugePedia]
snp3D : Map Gene to Disease1230
BioCentury BCIQCCR1
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD1230
Chemical/Pharm GKB GenePA26166
Clinical trialCCR1
canSAR (ICR)CCR1 (select the gene name)
PubMed136 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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indexed on : Mon Jul 16 09:43:40 CEST 2018

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