Publication for CCR5 and CCR2

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
hsa CCR5 C-C motif chemokine receptor 5 1234 [link]
hsa CCR2 C-C motif chemokine receptor 2 729230

Pubmed ID Priority Text
28454543 0.98 CCR-2 and CCR-5) and M2 macrophage markers (TREM-2, CD163, CD206, IL-4 and IL-10) in the biopsy tissues are shown in Fig. 1.
0.98 CCR-2 and CCR-5 in omentum, subcutaneous and liver biopsy samples of obese diabetics compared to obese non-diabetics and non-obese subjects (N = 5 non-obese; 16 obese non-diabetics; 17 obese diabetics)
0.98 CCR2 and CCR5 in the omentum (Fig. 3A), subcutaneous (Fig. 3B) and liver (Fig. 3C) biopsies of obese subjects compared to non-obese subjects.
0.98 CCR-2 and CCR-5) and M2 macrophage markers (TREM-2, CD163, CD206, IL-4 and IL-10) of each group biopsy samples was measured in the stained slides using Image-J software.
0.98 CCR-2 and CCR-5) and down-regulation of M2 markers (CD2016,CD163 and IL-4) in liver biopsy tissues compared to obese non-diabetics (Table 3).
0.98 CCR-2 and CCR-5) or M2 macrophage markers (TREM-2, CD163, CD206, IL-4 and IL-10) were analyzed among obese non-diabetics (OND) and obese diabetics (OD) using Chi square (chi2) and Pearson's correlation analysis.
0.97 CCR-2 and CCR-5) and down-regulation of M2 markers (CD206, CD163 and IL-4) in liver biopsy compared to obese non-diabetics.
0.97 CCR2 and CCR5), and their respective ligands, C-C chemokine ligand types 2 (CCL2/MCP-1) and 5 (CCL5/RANTES) play an important role in polarizing monocytes to M1 macrophages.
0.97 CCR-2 and CCR-5 only in omentum (not in liver and subcutaneous) biopsies of obese non-diabetics compared to non-obese subjects.
0.97 CCR5 and CD163 and Alexa 594-red for anti-human TREM-1, CD206, IL4, CCR2 and CCR7, counterstained with DAPI.
0.97 CCR2 and CCR5 (Aj, Ak) and co-localization of CD163 and CCR7 (Am, An).
0.97 CCR-2 and CCR-5) in liver biopsies of obese diabetics compared to obese non-diabetics.
0.96 CCR2 and CCR5 in the isolated CD14+ positive cells from the biopsy samples of obese non-diabetics and obese diabetics.
0.96 CCR2 and CCR5 (Bj, Bk) and co-localization of CD163 and CCR7 (Bm, Bn).
0.95 CCR-2, and CCR5 that was positively associated with TREM-1 over-expression in liver biopsy tissues.
0.94 CCR-2 and CCR-5 and down regulation of TREM-2, CD163, CD206, IL-4 and IL-10 were analyzed between obese non-diabetics and obese diabetics using Chi square (chi2) and Pearson's correlation analysis for categorical variables.
0.91 CCR-2 and CCR-5) and M2 macrophage markers (TREM-2, CD163, CD206, IL-4 and IL-10).
0.91 CCR-2 (Aj, Ak, Al) and co-localization of CD68 and CCR-5 (Am, An, Ao).
0.90 CCR-2 and CCR-5 and decreases in TREM-2, CD206, CD163, IL-4 and IL-10 in omentum fat samples of both obese diabetic and non-diabetic subjects, but not in subcutaneous fat.
0.88 CCR-2 (Bj, Bk, Bl) and co-localization of CD68 and CCR-5 (Bm, Bn, Bo).
0.84 CCR2/CCL2 and CCR5 axis.
0.66 CCR-2 (Cj, Ck, Cl) and co-localization of CD68 and CCR-5 (Cm, Cn, Co).
0.52 CCR-2 and CCR-5 (Alexa 594-red) antibodies to co-localize CD68 with TNF-alpha, IL-6, MCP-1, CCR-2 and CCR-5 respectively, counterstained with DAPI.
24691126 0.98 CCR2-AP, and CCR5-AP.
0.97 CCR2-AP, and CCR5-AP were expressed together, we observed CXCR4-CXCR4 homodimers and CXCR4-CCR2 and CXCR4-CCR5 heterodimers.
0.93 CCR2, and CCR5.
0.93 CCR2 and CCR5, dual channel flow cytometry measurements were performed for cells expressing pairs of CXCR4-BirA and a GPCR-AP.
0.93 CCR2, as well as literature pointing to heterodimerization of CXCR4 with CCR5.
0.92 CCR2-AP, and CCR5-AP (Figure 4A).
0.91 CCR5 then CXCR4-CCR2 dimerization but no significant difference between pairs (p = 0.087).
0.91 CCR2-CXCR4 heterodimer, p = 0.001; no difference between dimer proportions containing CXCR4-AP, CCR2-AP, CCR5-AP, p = 0.087).
0.89 CCR2, and CCR5.
0.88 CCR2-AP, or CCR5-AP all exhibited significant fluorescent labeling.
0.87 CCR2-AP, or CCR5-AP together with CXCR4-BirA, all showed substantial degree of biotinylation (Figure 3A).
0.86 CCR2 and CCR5.
0.79 CCR2-AP, and CCR5-AP.
0.73 CCR2 and CCR5, it is not entirely clear whether this predisposes equal propensity for CXCR4 to heterodimerize with either receptor.
0.70 CCR2 and CXCR4/CCR5 heterodimers were observed after 5 minutes biotinylation.
0.61 CCR5 as positive controls, we found that retinal pigment epithelial (RPE) cells contain undetectable levels of CXCR4, CCR2, and CCR5 and are deemed suitable for the current study (Figure S1).
26738816 0.98 CCR5 and CCR2 measured.
0.97 CCR5 and CCR2 genes, as well as the HBB and HBD should be italicized in this context genes.
0.95 CCR5 and HBB genes and strong discrimination against homologous sequences within CCR2 and HBD.
0.93 CCR5 target (left target) while discriminating against the CCR2 sequence (Supplementary Fig. 5).
0.93 CCR5 and CCR2 sequences, while remaining in close proximity to the desired cut site, by slightly shifting and expanding our target.
0.92 CCR5 target), with a secondary selection for, against or neutral for URA3 (CCR2 target).
0.91 CCR5 target and provide discrimination against the CCR2 target (Fig. 2a).
0.86 CCR5 sequence but against the CCR2 sequence.
0.84 CCR5 versus CCR2 and haemoglobin beta (HBB) versus haemoglobin delta (HBD).
0.83 CCR5-targeting nucleases confirms negligible CCR2 activity and demonstrates minimal off-target activity genome wide.
0.82 CCR5 and CCR2 (Fig. 3a,b).
0.82 CCR2 activity of the MR-B1H-produced ZFNs appears to be primarily related to the specificity of the right monomer and its ability to bind the adenine that differentiates CCR2 from CCR5 (see SELEX results, Fig. 3b).
0.77 CCR5 and CCR2 targets (Fig. 3c).
0.72 CCR5 and CCR2 measured (left and middle tables).
0.71 CCR5 in this study, with a threefold preference versus cleavage of CCR2.
0.71 CCR5 and CCR2 loci were measured for each ZFN pair (Fig. 4c).
17417600 0.98 CCR5 gene and in patients with the CCR2 wild-type genotype pc=0.02 and pc=0.04, respectively.
0.98 CCR2 V64I, CCR5-59029G/A, and CCR5 del.
0.97 CCR2 and CCR5 in immune-mediated PSU by analyzing the association of genetic polymorphisms of these four genes with the clinical outcome in patients with PSU.
0.97 CCR5 -59029G allele, while -59029G homozygosity was not observed in subjects with the CCR2 64I allele.
0.95 CCR2 and CCR5 genes are located on chromosome 3p21, and the SNPs studied here also show a strong degree of linkage.
0.90 CCR2 (receptors for MCP-1/CCL2) and CCR5 genes on posterior segment extracts have also been found in animal models of posterior uveitis.
0.89 CCR5 and CCR2 genes can affect the outcome of the disease.
0.83 CCR2 and CCR5 SNPs indicate that a locus for genetic susceptibility for IPSU may be located on chromosome 3 in close proximity to these SNPs.
0.68 CCR2 V64I, CCR5-59029G/A, and CCR5 32 bp deletion) were analyzed by sequence specific primers polymerase chain reaction.
0.59 CCR2 V64I was tightly linked with CCR5 -59029, and del.
24843011 0.98 CCR5 locus and the highly homologous sequences located within the CCR2 locus.
0.98 CCR5 and CCR2 loci after LP- and plasmid-directed ZFN delivery.
0.98 CCR5- and CCR2-directed cleavage were performed on the same genomic DNA samples.
0.97 CCR5 target locus and the nearby and highly similar CCR2 locus.
0.96 CCR5-directed ZFNs in the neighboring CCR2 locus after ZFN delivery into HEK293 cells by protein transduction and plasmid DNA transfection, respectively.
0.90 CCR2-CCR5 fusion fragments.
0.89 CCR2 locus by both protein transduction and plasmid transfection but not in the non-treated cells (Figure 5B), indicating that both LP-delivered and DNA-encoded ZFNs induced simultaneous double-stranded DNA breaks within the CCR2 and CCR5 loci.
0.82 CCR2 locus, we designed a PCR method that would detect NHEJ between fragments created by ZFN activity at both the CCR5 and CCR2 locus leading to deletion of the intervening sequence (Figure 5A).
0.74 CCR2 locus has high homology to CCR5 and has been identified as a major off-target site of CCR5-targeting ZFNs.
27791451 0.98 CCR5/CCR2 antagonist Cenicriviroc as the most advanced currently in phase II clinical studies.
0.97 CCR5 inhibitors for treatment of HIV infection has rested largely on studies of Maraviroc and a second-generation dual CCR5/CCR2 antagonist Cenicriviroc.
0.97 CCR5 (CCL 3, 4, 5, and 8) have commonality with other chemokine receptors including CCR1 (CCL 3, 4, and 5), CCR2 (CCL8), CCR3 (CCL5), CCR4 (CCL3 and 5), and CCR8 (CCL4).
0.92 CCR5, CCR2, and CXCR4.
0.91 CCR5 receptor, as no intrinsic CCR2 activity has been reported with this drug.
0.77 CCR5/CXCR4 and/ or CCR5/CCR2) are the entry inhibitors of tomorrow and have the potential to provide benefits in comparison to MVC such as curbing inflammation associated with chronic HIV infection in treatment-experienced patients with undetectable viral loads and eliminating the need for tropism testing.
0.61 CCR2 and CCR5, respectively.
0.53 CCR2/CCR5 inhibitors have been reported, but many have been pursued as anti-inflammatory agents.
0.50 CCR5-CCR2 activity.
19099182 0.98 CCR2/CCR5 heterodimers required lower chemokine concentrations for activity, and the heterodimer complexes signaled through Gq/11, likely mediating cell adhesion but not chemotaxis.
0.97 CCR5), or decreased co-receptor activity involving viral fusion, all of which were unchanged in comparison to WT CCR2 activity.
0.96 CCR2 and CCR5.
0.81 CCR5 and CXCR4 when stimulated by the CCR2 ligand, CCL2.
0.78 CCR5 could heterodimerize with CCR2V64I, providing a potential explanation for the effects of the variant; however, Percherancier et al. later found that CXCR4 heterodimerization was indistinguishable with WT CCR2 compared to the mutant.
0.71 CCR2 and CCR5 oligomerize, and display an equivalent propensity for homo- and heterodimer formation.
0.55 CCR2 and CCR5 with CCL2 and CCL5 resulted in CCR2/CCR5 heterodimerization.
19513280 0.98 CCR2-64I and CCR5Delta32 Polymorphisms in Korean Patients with Myasthenia Gravis
0.94 CCR2-64I and CCR5Delta32 polymorphisms were determined by the PCR-RFLP method.
0.91 CCR2 and RANTES binds to CCR5 with high affinity, the CCR2 and CCR5 polymorphisms might be important genetic factors for MG initiation and progression.
0.91 CCR2 and CCR5 polymorphisms did not differ between the MG patients and controls.
0.86 CCR2-64I and CCR5Delta32 polymorphisms.
0.85 CCR2-64I and CCR5Delta32 polymorphisms influence MG susceptibility.
0.73 CCR2-64I allelic frequency is lower in patients with pulmonary sarcoidosis compared to controls, while the frequency of the CCR5Delta32 is significantly increased in the same population, suggesting specific roles for these polymorphisms in disease protection and susceptibility.
22403612 0.98 CCR2 and CCR5 expression in response to M. tuberculosis has also been described.
0.98 CCR2, CCR4, CCR5, CCR6, CXCR3 and CXCR4 on leukocytes from whole peripheral heparinized blood (WB) and PBMC isolated by density gradient Ficoll (Ficoll-PBMC).
0.97 CCR2, CCR4, CCR5 CCR6, CXCR3 and CXCR4.
0.96 CCR2 and CCR5.
0.72 CCR2-PE, anti-CXCR3-PE and anti-CCR5-PE (isotype control , chemokine receptor ).
0.71 CCR2, CCR4, CCR5, CCR6, CXCR3 and CXCR4 on different leukocyte subsets using whole blood (WB) plus erythrocyte lysis and density gradient isolation (Ficoll).
26424571 0.98 CCR2, neither HDR nor capture of the AAV.CCR5.GFP donor events was detected at the CCR2 locus by PCR analysis (fig. S7B).
0.96 CCR5 or off-target at the highly similar CCR2 locus or other sites.
0.95 CCR2 and KIAA1257 (an uncharacterized gene) were identified as potential megaTAL off-targets on the basis of homology to the CCR5 target site combined with the CCR5-megaTAL one-off specificity profile.
0.87 CCR5 disruption also exhibited off-target activity within CCR2.
0.86 CCR5 shares high sequence identity (74%) to that of CCR2, particularly within the region encoding the seven trans-membrane domains (84%), where the megaTAL and TALEN target sites are located.
0.72 CCR2 by TIDE sequencing showed that NHEJ rates for the megaTAL and TALEN here were 21.8 and 1.8%, respectively, compared with 42% at the CCR5 locus for both (fig. S7A).
16259633 0.98 CCR2, CCR5, CXCR2 and CXCR4 mRNAs, and trace levels of CCR4 and CCR7 mRNA.
0.97 CCR2 mRNA expression but not that of CCR1, CCR5 or CXCR4 was dramatically downregulated (Figure 1C, panel II).
0.95 CCR2, CCR5, CCR7, CXCR2 and CXCR4.
0.80 CCR2 and CCR5.
0.53 CCR2, CCR5, and CXCR4 mRNAs remained elevated after two days in culture, while that of CXCR2 decreased and that of CCR7 temporarily increased.
30179264 0.98 CCR2 and CCR5), and their respective ligands, C-C chemokine ligand types 2 (CCL2; also known as monocyte chemoattractant protein-1 [MCP-1]) and CCL5 (also known as regulated on activation, normal T cell expressed and secreted [RANTES]) are implicated in liver inflammation and macrophage (MO) recruitment to the liver.
0.96 CCR2 and CCR5 expression and immune cell infiltration to the liver is increased in human alcoholic cirrhosis patients.
0.84 Ccr2 and Ccr5 compared to control livers (Fig. 1C).
0.74 CCR2 and CCR5 is a promising approach for the treatment of ALD.
22479344 0.97 CCR2 and CCR5.
0.96 CCR2 and CCR5 receptors.
0.96 CCR2/CCR5) and results were analyzed.
0.96 CCR2 and CCR5), and a 60% identity between the active sites of template and query.
0.96 CCR2 and CCR5 was 2e-33 and 1e-33, respectively.
0.96 CCR2-Glu291; CCR5-Glu283).
0.93 CCR2 and CCR5.
0.90 CCR2 and CCR5) with a lower MolPdf value and the one that displayed a lesser RMSD was selected for further computational analysis.
0.90 CCR2 and CCR5 were further used for docking analyses and are shown in materials S4 and S5 , respectively.
0.90 CCR2 model and TAK779 with CCR5 model over the template structure (CXCR4).
0.89 CCR2 and CCR5 using in silico methodologies and both these structures will be important for modelers as well as experimentalists in the scientific community.
0.88 CCR2/CCR5.
0.87 CCR2 and CCR5 against the modeled receptor structure.
0.87 CCR2 and CCR5.
0.85 CCR2 and CCR5.
0.84 CCR2 and CCR5 models are summarized in Table 1.
0.84 CCR2 and CCR5 was performed.
0.82 CCR2 and CCR5 models is shown in Figure 5.
0.81 CCR2 and CCR5 and their ligands have been implicated in the pathophysiology of a number of diseases, including rheumatoid arthritis and multiple sclerosis.
0.81 CCR2 and CCR5 was done using the crystal structure of CCXR4 as the template.
0.79 CCR2 and CCR5 is shown in Figure 3.
0.78 CCR2 (Compound 2, 14, RS-504393 and Teijin), CCR5 (Maraviroc, SCH351125, TAK779 and Vicriviroc) and dual inhibitors (Compound 19).
0.78 CCR2 and CCR5).
0.77 CCR2 and (b) CCR5 plot shows the variation in potential energy throughout the system for a period of 5 ns.
0.76 CCR2 and CCR5 was selected and refined by simple minimization.
0.72 CCR2 and CCR5 has been proposed.
0.68 CCR2 and CCR5 were compared.
0.64 CCR2 and CCR5 were developed according to previously proposed sites and were in good agreement with already published results.
0.61 CCR2 and (b) CCR5 Calpha from the initial structures throughout the simulation of 5 ns as function of time.
0.60 CCR2 and 90.78 for CCR5 and it is better than those models which were obtained before MDS which indicating the quality of the generated models.
0.60 CCR2 and CCR5.
0.55 CCR2 (UniProtKB: P41597) and CCR5 (UniProtKB: P51681) with the CXCR4 (PDB ID; 3ODU) as template.
0.55 CCR2 and Ile198 of CCR5.
0.51 CCR2 and CCR5.
0.50 CCR2 and CCR5) selected from modeler was further refined by MDS, to improve and access the stability of the model.
24011637 0.97 CCR5 haplogroup (HHF) that is linked to the CCR2-V64I variant shows different frequencies and functions across populations.
0.97 CCR2-CCR5 region in subjects of African, European and Hispanic ancestry.
0.97 CCR2 and CCR5 genes, high LD can be found between SNPs in the two genes that may have functional importance.
0.97 CCR2 and CCR5 show population-specific patterns that may contribute to disparities in disease infection or progression.
0.96 CCR2 and CCR5 at several loci and provide new information about CCR2 that contributes to our understanding of its population-specific genetic variability.
0.96 CCR2 SNPs and CCR5 SNPs were determined in cohort 1.
0.96 CCR5-Delta32, which is carried on haplotype HHG*2, was associated with CCR2 haplotypes H1 and H4 (Supplementary Table S2 and S3).
0.96 CCR2-V64I variant and were heterozygous for CCR5-rs1799987/SNP #11(Supplementary Table S2- S3).
0.96 CCR2 haplotype patterns and confirmed seven of the nine CCR5 haplotypes described originally.
0.95 CCR2 haplotype H3 (the only haplotype with the V64I variant/SNP 4) is associated with the CCR5 HHF haplotype (Supplementary Table S4) defined by Gonzalez as HHF*2.
0.94 CCR2, its functional effects may be related to linked SNPs in CCR5; however little is known about its relationship with other CCR2 SNPs.
0.94 CCR2-V64I and CCR5-Delta32 on delaying AIDS progression.
0.91 CCR2 and CCR5 play a key role in immune and inflammatory responses and have been associated with several diseases, including AIDS.
0.90 CCR2 gene and eight SNPs of the CCR5 gene were genotyped using Sanger sequencing (Table 1; Figure 1).
0.89 CCR2-V64I SNP and several CCR5 haplotypes, there is little information regarding frequencies of other CCR2 SNPs and haplotypes.
0.88 CCR2-V64I (rs1799864) is indicated as SNP #4 on CCR2 exon 2, and CCR5-Delta32 is labeled as SNP #16 on CCR5 exon 3.
0.84 CCR2 and CCR5 genes (including CCR5-Delta32, and CCR2-V64I) in 249 subjects of African, European and Hispanic ancestry.
0.82 CCR2-SNP #6 and CCR5-SNP #13, that were found only in the African and Hispanic groups are in complete LD (Fig 2A and 2C).
0.74 CCR5 HHG*2 haplotype and the CCR2 H1/H1 haplotype.
0.73 CCR2 H1/H1 diplotype but a CCR5 HHG*2/HHC diplotype.
0.64 CCR2-CCR5 region among individuals and populations
0.64 CCR5-Delta32 and CCR2-V64I, other SNPs and haplotypes may be important genetic determinants of disease and should be investigated.
0.57 CCR2-V64I (SNP #4) had the most frequency data available across databases, frequency data on CCR2-SNPs # 2, 3 and 6, and CCR5-SNPs # 9 and #13 were minimal in some of the databases selected for comparison.
0.52 CCR2 SNP #8 and CCR5 SNP #15 are in complete LD in Europeans only (Figure 2B).
0.50 CCR5 gene (rs1800024; -1835C>T) that was associated with slow AIDS progression, is in linkage disequilibrium (LD) with the CCR2-V64I variant.
21747955 0.97 CCR2 and CCR5 Blockade Failed and Why CCR1 Blockade Might Still Be Effective in the Treatment of Rheumatoid Arthritis
0.97 CCR2, and CCR5 as well as other chemokines and receptors involved in monocyte recruitment to the site of inflammation.
0.97 CCR2 and CCR5 receptor blockade has shown positive results in animal models of RA, targeted CCR2 and CCR5 blockade was not effective in RA patients.
0.96 CCR2 or CCR5 blockade on RA monocyte migration in an in vitro model evaluating SF-induced chemotaxis.
0.95 CCR2 nor CCR5 blocking antibodies were able to inhibit SF-induced monocyte chemotaxis, even when both receptors were blocked simultaneously, both anti-CCR1 antibodies and the CCR1 antagonist were able to inhibit SF-induced monocyte chemotaxis.
0.95 CCR2 and CCR5 antagonists.
0.95 CCR2 and CCR5 were blocked simultaneously (similarly at high doses), we were not able to block SF-induced chemotaxis of RA peripheral blood monocytes, suggesting that CCR2 and CCR5 may not be the crucial chemokine receptors promoting monocyte migration towards the inflamed joint.
0.94 CCR2 and CCR5 antibody n = 8; for CCR1 blockade n = 13) were isolated from peripheral blood and pre-incubated with different concentrations of either anti-CCR1, anti-CCR2, or anti-CCR5 blocking antibodies (or medium or isotype controls).
0.94 CCR2 or CCR5 blockade, CCR1 blockade resulted in significant reduction of monocyte migration towards SF (Fig. 4B and 4D) (for anti-CCR1: 5 microg/ml, P = 0.0441; 25 microg/ml, P = 0.0197 compared to isotype control; for small molecule CCR1 antagonist: 5 microg/ml, P = 0.0245; 25 microg/ml, P = 0.0189 compared to CCL5/RANTES).
0.93 CCR2, and CCR5 may have failed in clinical trials in rheumatoid arthritis (RA) patients, using an in vitro monocyte migration system model.
0.93 CCR2 (major ligand CCL2/MCP-1), CCR5 (ligands CCL3/MIP-1alpha, CCL5/RANTES and CCL7/MCP-3) are abundantly expressed by RA monocytes/macrophages suggesting that interference with the migration of these cells by cytokine receptor blockade might be a successful therapeutic approach to reduce synovial inflammation.
0.93 CCR2 and CCR5 that are responsible for monocyte recruitment to these compartments (via many receptors such as CCR1), this redundancy could have accounted for the observed chemokine receptor blockade failure in both our in vitro model and in the clinical trials.
0.90 CCR2 and CCR5 could not significantly inhibit migration of RA peripheral blood monocytes towards SF in the in vitro chemotaxis model.
0.86 CCR2 ligand), CCL5/RANTES (CCR1 and CCR5 ligand), or by a mix of 5 RA synovial fluids (SFs), and cellular responses compared to chemotaxis in the presence of medium alone.
0.82 CCR2 and CCR5 does not block SF-induced RA monocyte migration.
0.80 CCR2 and CCR5 are not critical for the migration of monocytes towards the synovial compartment in RA.
0.71 CCR2 and CCR5 does not significantly block SF-induced RA monocyte migration
0.65 CCR2 or CCR5, blocking CCR1 may be sufficient to inhibit migration of RA peripheral blood monocytes towards the inflamed synovial compartment in RA.
0.64 CCR2 and CCR5 blockade, ligand-induced RA peripheral blood monocyte migration could be blocked by the respective receptor blocking antibody (CCL2: anti-CCR2 or CCL5: anti-CCR5) but not when RA SF was used as chemoattractant.
0.64 CCR2 antagonists, as CCR2 and CCR5 are very close in homology, and inhibitors often target both.
28208753 0.97 CCR5 and CCR2 Genotypes
0.97 CCR5 (Delta32 CCR5) increases the likelihood of recovery from HB in humans, and given the increased T-cell response to various antigens observed in animal models, we conducted the first study on the human population and hypothesized that both homozygous Delta32/Delta32 of CCR5 gene and homozygous AA of CCR2 gene might be bio-markers for immunological response in subjects after a HBV vaccination.
0.97 CCR2 and CCR5 genes for two SNPs (190G > A CCR2 and Delta32 CCR5) in a group of Polish patients in the context of response to HBV vaccination.
0.95 CCR2 and CCR5, and their polymorphisms: Delta32 and 190G > A, respectively.
0.95 CCR5 and gene CCR2 polymorphisms followed the Hardy-Weinberg equilibrium (chi2 = 0.1605; p = 0.73 and chi2 = 0.4714; p = 0.49, respectively).
0.95 CCR5 and 190G > A CCR2 Allele
0.94 CCR5 and 190G > A CCR2 polymorphisms with a response to a primary course of three HBV vaccinations.
0.94 CCR5: p = 0.34, CCR2: p = 0.81 respectively).
0.93 CCR5 and 190G > A CCR2 polymorphisms and the HBV vaccine immunogenicity are sparse.
0.93 CCR5 and 190G > A CCR2 polymorphisms in the context of a response to HBV vaccination.
0.91 CCR5 and 190G > A CCR2 polymorphisms in the context of HBV vaccination response.
0.90 CCR5 gene and DNA alterations might affect gene expression and then protein function, while the polymorphism G-A transition at position 190 in CCR2 gene, introducing a conservative change into the first transmembrane domain, is not associated with any clinical abnormality.
0.89 CCR2 and CCR5 Genotypes and Anti-HBs Titres
0.62 CCR2 and Delta32 CCR5 Mutations on Decrease of the HBV Vaccine Immunogenicity:A Preliminary Report
27013693 0.97 CCR2, CCR5, and CX3CR1 coordinate monocyte trafficking in homeostatic and inflammatory states.
0.97 CCR2, CCR5, or CX3CR1 with CAD and MI.
0.96 CCR2, CCR5, and CX3CR1 for CAD, MI, and glucometabolic traits.
0.96 CCR2, CCR5, and CX3CR1 and any of the traits studied in European ancestry datasets.
0.95 CCR2, CCR5, and CX3CR1 in the development of experimental atherosclerosis, insulin resistance and cardiometabolic disorders through their modulation of monocyte recruitment and macrophage phenotypes.
0.94 CCR2, CCR5, and CX3CR1 are potential modifiers of both atherosclerosis and glucometabolic traits.
0.94 CCR2 and CCR5 and risk of MI
0.93 CCR2, CCR5, or CX3CR1 in the pathogenesis of atherosclerosis or glucometabolic traits in populations of European ancestry.
0.88 CCR2, CCR5, and CX3CR1, five additional non-coding variants in CX3CR1 were significantly associated with MI after Bonferroni correction (Table 2, Supplemental table 3).
0.65 CCR2, CCR5, and CX3CR1, none approached statistical significance after correction for multiple testing.
0.63 CCR2, CCR5, or CX3CR1 and Risk of Atherosclerotic Coronary Heart Disease and Glucometabolic Traits
0.61 CCR2, CCR5, and CX3CR1.
27965453 0.97 CCR5 chimeric receptors (A) and CCR2 chimeric receptors (B) were measured using DyLight488-LukE in complex with WT LukD. (C) Levels of LukE binding to HEK293T cells transfected with 5555, 2222, 5522, and 2255 were measured using DyLight488-LukE in complex with the pore formation-deficient LukDDN mutant.
0.96 CCR5, we adapted the CCR5/CCR2b chimeric receptor system used to identify the interactions between gp120 and CCR5.
0.94 CCR5 to CCR2b (2252, 2225) resulted in a modest increase in susceptibility, the replacement of both ECL2 and ECL3 (2255) phenocopied WT CCR5 (5555) intoxication by LukED (Fig. 2B).
0.90 CCR5 and CCR2b share 79% amino acid identity.
0.87 CCR5/CCR2b chimeric receptors to elucidate the molecular basis of the interaction between LukED and CCR5.
0.78 CCR2b, and green represents CCR5.
0.74 CCR5 using CCR5/CCR2b chimeric receptors, an approach that has been exploited previously for studying gp120-CCR5 interactions.
0.67 CCR5 and CCR2b chimeras.
0.67 CCR5 was swapped with the corresponding ECLs of CCR2b (CCR5 chimeric receptors 5255 and 5552, where "5" indicates the location of CCR5 sequences and "2" indicates the location of CCR2b sequences), there was no defect in HIV-1 infectivity (Fig. 1B).
0.58 CCR5 were infected with HIV, while those transfected with empty vector, CD4 alone, or CD4 and CCR2b remained uninfected (Fig. 1B and C).
0.58 CCR2 WT (2222) and the CCR2 chimeric receptor containing ECL2 of CCR5 (2252) at similar levels (Fig. 3B), the CCR2 chimeric receptor containing ECL3 of CCR5 (2225) showed increased LukE binding.
0.51 CCR5 to CCR2b (5222, 2522) produced results similar to those seen with WT CCR2b (2222).
23415099 0.97 CCR2 was unaffected by unlabeled CCR5 ligands (MIP-1alpha/CCL3, MIP-1beta/CCL4 and RANTES/CCL5) when CCR2 was expressed alone.
0.97 CCR2 in CCR2/CCR5 coexpressing cells.
0.96 CCR5 and CCR2), blocked migration of cells to CXCL12/CXCR4.
0.95 CCR2, CCR5 and CXCR4 in T lymphoblasts, and similar inhibition of calcium signaling and migration of receptors by antagonists of the orthogonal receptors.
0.94 CCR2 and CCR5 homomers and for the CCR2/CCR5 heteromers suggesting similar propensities for the homo- and hetero-oligomers to form.
0.92 CCR2 and CCR5 showed that these receptors were basally associated in the absence of chemokine agonists.
0.91 CCR2/CCR5, CCR2/CXCR4 and CCR2/CCR5/CXCR4) was demonstrated by BRET and ligand binding experiments.
0.91 CCR2 ligands (MCP-1/CCL2 and MCP-2/CCL8) to CCR5 was observed when CCR5 was expressed alone.
0.89 CCR2 and CCR5, especially in their transmembrane domains (78.2% identity, 89.4 similarity).
0.77 CCR5 ligands inhibited binding of 125MCP-1/CCL2 to cells coexpressing both CCR2 and CCR5, and CCR2 ligands inhibited the binding of 125MIP-1beta/CCL4 to the coexpressing cells.
0.65 CCR2 specific ligand 125I-MCP-1/CCL2 to cells coexpressing CCR2 and CCR5 was accelerated significantly by the CCR5 specific ligand MIP-1beta/CCL4 compared to the dissociation rate from cells expressing CCR2 alone.
26397046 0.97 CCR2 190, CCR5 -2459, CCR5 open reading frame, and CXCL12 801 genotypes with HIV acquisition and/or disease progression, we calculated composite full risk scores, considering both protective as well as susceptibility effects of the CXCL12 801 AA genotype.
0.89 CCR2, CCR5, and CXCL12 variation may influence the risk of HIV infection/disease progression in PNG, we first calculated composite partial risk scores, without including CCR5 -2459G>A and considering only the protective effects of the CXCL12 801A allele.
0.87 CCR5 variation in the PNG population, and suggest that the collective variation in CCR2, CCR5, and CXCL12 may elevate the risk of HIV/AIDS as opposed to conferring protection indicated by previous studies.
0.87 CCR2-CCR5 polymorphisms in a total of 41 samples collected from 12 out of 20 total provinces, which were provided by Dr. Mark Stoneking (Max Planck Institute for Evolutionary Anthropology, Germany) for a malaria epidemiological study.
0.74 CCR2, CCR5, and CXCL12 may affect the occurrence of HIV infection and disease in PNG, more so than in the other regions.
0.72 CCR2-CCR5 polymorphisms, including CCR2 190G>A, CCR5 -2459G>A and Delta32, and CXCL12 801G>A in PNG (n = 258), North America (n = 184), and five countries in West Africa (n = 178).
0.69 CCR2 190, CCR5 -2459, CCR5 ORF, and CXCL12 801 genotypes with HIV acquisition and/or disease progression, we calculated composite full risk scores, considering both protective as well as susceptibility effects of the CXCL12 801 AA genotype.
0.67 CCR2 190, CCR5 -2459, CCR5 ORF, and CXCL12 801 genotypes (Table 2), and calculated composite partial/full/simple risk scores (range 2-6, Figures 1-3), could be considered a limitation.
0.66 CCR2 190G>A had a low to moderate prevalence, many of the CCR5 promoter SNPs were rare or absent, CCR5 Delta32 was absent, whereas CCR5 -2459G>A and CXCL12 801G>A were highly prevalent.
0.57 CCR5 Delta32 and the CCR2 190A alleles were associated with protection against HIV infection and/or delayed disease progression, compared with the CCR5 ORF wild type (wt) and the CCR2 190G alleles respectively.
0.54 chemokine (C-C motif) receptor 5 (CCR5), a single nucleotide polymorphism (SNP, 190G>A [Val64Ile], rs1799864) in the ORF of chemokine receptor CCR2, and a SNP (801G>A, rs1801157) in the 3'-untranslated region (3'-UTR) of chemokine (C-X-C motif) 12 (CXCL12 [stromal cell-derived factor 1, SDF-1]) in PNG.
23939622 0.97 C-C chemokine receptor type 5 genes have substantial off-target cleavage, especially within the hemoglobin delta and C-C chemokine receptor type 2 genes, respectively, causing gross chromosomal deletions.
0.96 CCR5 and CCR2 genes, as indicated by indels consistent with NHEJ (Figure 4c).
0.94 CCR2 forward primer and reverse primer downstream of the CCR5 site.
0.92 CCR5 is located ~8 kb upstream of CCR2 on chromosome 3; thus, chromosomal rearrangements may occur with cleavages at both CCR5 and CCR2.
0.92 CCR5 and CCR2 (Supplementary Figure S1h).
0.88 CCR5 and corresponding region in CCR2.
0.81 CCR5 and CCR2 induced by CRISPR/Cas9 systems.
0.75 CCR5 and CCR2 indicate nucleotides that differentiate the two genes.
0.61 CCR5-targeting CRISPR/Cas9 systems also induced off-target cleavage on CCR2, with mutation rates of 5% and 20% (Figure 2c, Supplementary Figure S2).
0.53 CCR2 by the CCR5-targeting CRISPR/Cas9 systems with guide strands R-27 and R-29 that had NTG and NGT PAM substitutions, respectively.
20628649 0.97 CCR5-Delta32 polymorphism is rare among persons of Asian descent, the CCR2-64I-containing HHF*2 haplotype is very common, and has been associated with salutary effects (reduced risk) among persons of Japanese descent for several diseases with immunologic underpinnings including multiple sclerosis, sarcoidosis, and HIV.
0.95 CCR2-CCR5 haplotypes in 133 Japanese KD cases [33 with CAL and 25 with resistance to IVIG] and 312 Japanese controls without a history of KD.
0.93 CCR2, a receptor critically involved in monocyte trafficking and activation, in KD pathogenesis and therapy responses is unclear because the CCR2-64I polymorphism is in linkage disequilibrium with promoter polymorphisms in CCR5 .
0.91 CCR2-64I-bearing CCR5 HHF*2 haplotype with KD-related outcomes may relate either directly or indirectly to inflammation.
0.91 CCR5-Delta32 polymorphism which has been intensively scrutinized in persons of European descent, the CCR2-64I polymorphism has also been associated with variable susceptibility to multiple diseases as well.
0.89 CCR2-64I-bearing CCR5 HHF*2 haplotype was associated with a reduced risk of developing CAL which trended towards statistical significance (OR = 0.44, 95% CI = 0.18-1.07, p = 0.071).
0.88 CCR5 HHF*2 haplotype which bears the CCR2-64I polyrmorphism is associated with a reduced the risk of IVIG-resistance and CAL formation.
0.77 CCR2-CCR5 Haplotypes and CCL3L1 Copy Number with Kawasaki Disease, Coronary Artery Lesions, and IVIG Responses in Japanese Children
0.59 CCR2-64I-containing CCR5-HHF*2 haplotype is associated with a reduced risk of both CAL development and IVIG resistance.
20038229 0.97 CCR5, CCR2, CCL5, CXCL12 and CX3CR1 were explored in a pooled analysis of three case-control studies (San Francisco Bay Area, California; United Kingdom; total: cases N=1610, controls N=1992).
0.97 CCR5, CCR2, CCL5 (RANTES), CXCL12 (SDF-1) and CX3CR1 (fractalkine), and risk of all NHL, diffuse large B-cell, follicular and chronic lymphocytic leukemia/small lymphocytic lymphomas.
0.96 CCR2/CCR5 referent haplotype comprised the common alleles for the CCR2 and CCR5 polymorphisms.
0.96 CCR2, CCR5 and CXCL12 has been associated with hepatocellular carcinoma, cervical, pancreatic and prostate cancers, whereas increased expression of chemokines including CXCL12 (SDF-1) and CCL5 (RANTES) has contributed to tumor angiogenesis, metastasis, progression and survival in breast, prostate and colon cancers.(reviewed in)
0.95 CCR5 Delta32 deletion and no association with the CCR2-64I variant allele among men in our pooled population is consistent with results for AIDS-related B-cell NHL.
0.95 CCR2/CCR5 haplotype that included the CCR5 Delta32 deletion was associated with decreased NHL risk in men and not in women.
0.60 CCR2/CCR5 haplotypes were associated with risk of all NHL, DLCL or FL.
24792154 0.97 CCR5-specific TALEN pair decreased off-target activity at the closely related CCR2 locus considerably, consistent with fewer genomic rearrangements between the two loci.
0.97 CCR5 and CCR2 loci are indicated below.
0.97 CCR2 allele (674 bp, bottom); C+D, CCR5 allele (300 bp, bottom).
0.95 CCR5 and CCR2 is based on the fact that one of the two TC-NC subunits targets a T in position 0, which is not present in CCR2.
0.94 CCR5-specific ZFN pair in the form of proteins resulted in short persistence in the transduced cells and was associated with reduced off-target activity at CCR2.
0.92 CCR2/CCR5 loci.
0.83 CCR5 and CCR2 induces deletions or inversion of large genomic fragments on chromosome 3, as previously shown, we genotyped a subset of samples transfected with CCR5-specific nucleases by qualitative PCR (Figure 5B).
28108404 0.97 CCR2, and CCR5 in NP and AF cells, and to test if these receptors can respond to their ligands in these cells by cell signaling and migration.
0.96 CCR2, and CCR5 was analyzed using flow cytometry and fluorescently tagged antibodies specific for these proteins.
0.96 CCR2, and CCR5, and respond to the ligands:CCL2, CCL3, and CCL5:through cell signaling and migration.
0.95 CCR2 (0.8% and 1.4%, respectively) on the cell surface, whereas a larger percentage expressed CCR5 (12.7% and 11.6%, respectively).
0.94 CCR2, and CCR5 was evident in human NP and AF cells (n=6).
0.94 CCR2, and CCR5 were detected in both NP and AF cells, yet only CCR5 was detected on the cell surface.
0.94 CCR2, and (Bottom) CCR5:were measured using real-time polymerase chain reaction (PCR) and analyzed relative to control treated samples.
29469805 0.97 CCR5 may partly explain the differences in time between arrest and TEM that we measured for the CCR6+ conventional cells, CCR2-/low MAIT cells and the CCR2+ MAIT cells (Figure 2:figure supplement 2C), because we found differences in the levels of CCR5 expression in the order CCR2+ MAIT cells > CCR2-/low MAIT cells > the CCR2+ subset of CCR6+ conventional cells (Figure 5:figure supplement 1).
0.96 CCR2-/low MAIT cells, in addition to having levels of CCR5 that were lower than on the CCR2+ MAIT cells, the reduced expression of CCR2 presumably also contributed to their delay in initiating TEM.
0.93 CCR5, and CCR2, which played non-redundant roles in trafficking on activated endothelial cells.
0.90 CCR5 on the surface of the CCR6+ conventional cells, we limited the analysis to cells that were CCR2+ because the data in Figure 5A indicated that the CCR2+ cells were those undergoing TEM, and therefore were the cells scored in Figure 2:figure supplement 2C.
0.85 CCR5+CCR2+ subset of CD4+ memory-phenotype T cells that we had studied earlier and discovered that these cells expressed high levels of CEBPD, which encodes C/EBPdelta.
0.79 CCR2 and CCR5 mRNAs in CD8alpha+ T cell subsets after transfections with control or CEBPD siRNAs.
0.73 CCR5, and CCR2 serve sequential and distinct functions in MAIT cell extravasation.
18662820 0.97 CCR2 and CCR5 share some sequence similarity, are located on the same chromosome, and HIV has the potential to use CCR2 as coreceptor.
0.97 CCR2 and CCR5 expression on different T cell subsets.
0.95 CCR2b as its major co-receptor for entry, rather than CCR5 or CXCR4.
0.91 CCR2 may prevent MCP-1/CCR2 binding and lead to a higher affinity of CCR5 binding to its ligands, which might provide fewer opportunities for CCR5/SIVmac251 binding, which could reduce SIVmac251 entry.
0.83 CCR2 has an aminoterminal domain that can bind to HIV-1, indicating a potential role of coreceptor for HIV-1 infection, thus there are reasons to presume that coreceptor usage switch could occur under the pressure of CCR5 inhibitor therapy in HIV-1 infection.
0.74 CCR2b efficiently prevents CCL4 (MIP-1beta) and CCL5 (RANTES) binding to CCR5 on cells expressing both CCR2 and CCR5 receptors and HIV-1 fusion activity could be inhibited by MCP-1.
20548789 0.97 CCR2, CCR1 and CCR5 are activated in patients with liver cirrhosis, likely regulating recruitment (CCR1, CCR5, CCR2) and local differentiation/activation (CCR2) of monocyte subsets in patients with chronic liver diseases.
0.96 ccr2 or ccr5, expression was increased on peripheral monocytes in patients (Fig. 6A), possibly in response to elevated serum levels of CCL3 and CCL4.
0.95 CCR2, CCR1 and CCR5 were expressed at higher levels in fibrotic and cirrhotic livers, while CCL3 and CCL4 were also systemically elevated in CLD-patients.
0.89 CCR2, CCR1 and CCR5 by hepatic monocytes/macrophages, the local upregulation of ccl2 and ccl5 in the whole liver and the systemic elevation of CCL3 (healthy controls compared to CLD patients, p = 0.0387) and CCL4 (healthy controls compared to CLD patients, p = 0.0064) in the circulation, we speculated that peripheral blood monocytes in patients might regulate their chemokine receptor expression, rendering them more prone to accumulate in the diseased liver.
0.88 CCR5 ligands MIP1alpha (CCL3) and MIP1beta (CCL4), but not of the CCR2 ligand MCP-1 (CCL2), were significantly increased in CLD patients (Fig. 5D), suggesting additional systemic actions of these chemokines.
0.68 CCR2, CCR1 and CCR5 was assessed by FACS on monocytes/macrophages (CD14+, green), T- (CD3+CD56-, light orange), NK- (CD3-CD56+, dark orange) and NKT-cells (CD3+CD56+, red) from freshly isolated liver tissue.
23659629 0.97 CCR2 64I, and CX3CR1 (T280M and V249I) co-receptors as well as the levels of CCR5, CXCR4, CX3CR1, and CCR2 mRNA expression in circulating leukocytes were analysed as independent variables.
0.96 CCR5 expression as a predictor of atherosclerosis progression (B = 2.1, OR = 8.1, p = 0.04) and a negligible effect for CXC3R1 and CCR2 expression.
0.96 CCR5 Delta32 was responsible for the increased expression of these receptors, but only CCR2 and CCR5 reached statistical significance (Figure 1).
0.83 CCR2 and CXCR4 in circulating leukocytes from progressors and non-progressors was similar but there were a significant increase in CCR5 and CX3CR1 in patients who showed progression in intima-media thickness.
0.82 CCR2 and CXCR4 did not discriminate between progressors and non-progressors, and the expression of CCR5 and CX3CR1 was significantly higher in the progressors (Figure 2).
0.53 CCR2 V62I gene variant also demonstrated a two-fold higher expression (p = 0.004) of CCR5 compared with non-carriers (data not shown).
29751565 0.97 CCR2, although CCL2 can bind to CCR3 and CCR5 in the absence of the cognate receptor CCR2.
0.97 CCR2 and CCR5 was described previously.
0.95 CCR2, CCR1, CCR3, and CCR5 belong to the same protein sequence homology cluster, i.e., they have high protein sequence identity and can bind the same chemokines.
0.95 CCR2, CCR3, and CCR5 genes reside in the same region at human 3p21.31.
0.94 CCR2B ORF (A) and CCR5 (B) transcripts in the BL cell lines with latency III were detected by RT-duplex-PCR.
0.78 CCR2B and CCR5.
15661933 0.97 CCR5, CXCR3, CXCR4, and CCR2, but lower levels of CCR7, supporting our findings in SF CD4+ T cells.
0.93 CCR2, CCR4, CCR5, CCR7, and CXCR6 expression.
0.88 CCR2, CCR4, CCR5, CCR7, CXCR3, CXCR4, and CXCR6 was determined (Fig. 4).
0.88 CCR5, CXCR3 and CXCR4, and CCR7 and CCR2 (all green).
0.69 CCR2, CCR4, CCR5, CXCR3, CXCR4, and CXCR6 was significantly enriched on rheumatoid SF CD4+ T cells, compared with their circulating CD4+ memory T cell counterparts.
26982176 0.97 CCR5 and CCR2 polymorphisms in the development of the CC have been reported so far .
0.97 CCR2-64Iand CCR5-Delta32 polymorphisms and the presence of cervical lesions (CIN or CC) in HPV infected women from Northeast Region of Brazil.
0.89 CCR2-64I and CCR5-Delta32polymorphisms genotypes in 139 women with cervical lesions (CIN or CC) and 151 HPV+ were according to the Hardy-Weinberg equilibrium.
0.76 CCR2-64I and CCR5-Delta32 polymorphisms were performed using polymerase chain reaction-restriction fragment length polymorphism.
24778447 0.97 CCR5 is at S337, and this corresponds to S341 in CCR1 and S345 in CCR2b.
0.96 CCR2b adjacent to S345 has little homology to either CCR1 or CCR5, and does not contain common sequence elements for a PKC phosphorylation site.
0.95 CCR5 and CCR1, these receptors may both possess PKCbeta-target sequences, while CCR2b does not.
9334377 0.97 CCR5, a series of chimeric receptors was generated by replacing extracellular domains of CCR5 with the corresponding domain of CCR2b, or vice versa, using common restriction sites in regions conserved between the two molecules.
0.97 CCR5 and CCR2b were ideal for this purpose, since these two receptors are closely related but have completely different ligand binding properties.
10037796 0.97 CCR2-transfected HEK-293 cells, neither JAK2 nor JAK3 associates to CCR5 after RANTES or (AOP)-RANTES activation of CCR5-transfected HEK-293 cells (data not shown).
0.90 CCR2-transfected HEK-293 cells, or in any other cell tested that does not express CCR5.
21944757 0.97 CCR5, the CCR2 gene, was directly sequenced in clones isolated by limiting dilution from tcPNA-679 and donor DNA treated THP-1 cells.
0.95 CCR5-targeted zinc finger nucleases, off-target modification the CCR2 gene was determined to occur at a frequency of 5.39%, only 6-fold less than their reported frequency of CCR5 modification (35.6%).
23936229 0.97 CCR5 and the coding polymorphism (V64I) in CCR2, we previously used an evolutionary-based strategy to generate the CCR5 human haplogroups (HH) shown below the CCR5 gene structure.
0.92 CCR5 haplotypes (HHA to HHG*2) were derived after genotyping nine CCR2-CCR5 polymorphisms.
25541967 0.97 CCR5 sgRNAs were tested, off-target mutations at CCR2 sequences that bear one nucleotide mismatch to 6 CCR5 sgRNAs were detected.
0.72 CCR5 in 293 cells co-transfected with DNA plasmids encoding Cas9 and 5 different CCR5 sgRNAs, off-target indels at CCR2 gene were detected in cells transduced with just 2 of 5 CCR5 sgRNAs.
27942440 0.97 CCR2 and CCR5, linkage disequilibrium between variants in the two genes may cause the slow progression as the CCR2 receptor is rarely used for HIV infection.
0.77 CCR5 gene was shown to be in 100% linkage disequilibrium with the CCR2-64I polymorphism; however, the protection provided via linkage of the variants could not be established.
29115572 0.97 CCR2 to have the most similar genomic DNA sequence to CCR5; therefore, the off-target effects of the two TALENs on this gene were investigated.
0.96 CCR2 gene, it is very unlikely that other off-target effects will occur in genes with low homology to CCR5.
24734242 0.97 CCR2, CCR3, CCR5, CCR6, CCR7, CCR9, CCR10, CXCR3, CXCR4, CXCR5, and ChemR23 are involved in control of different subsets of DCs recruitment to periphery tissues and migration to secondary lymphoid tissues or migration within lymphoid tissues.
21429204 0.96 CCR2-CCR5 variants that have previously been implicated in HIV/AIDS and de-emphasized those whose involvement was less predictable from earlier studies.
0.96 CCR2-CCR5 haplotypes consisting of common combinations of SNP alleles spanning those two genes has confirmed a previously reported association of haplotype HHF*2 with favorable response to HIV-1 infection; and our longitudinal analysis of seroconversion in HESN African heterosexual partners has detected probable contributions by the HHD/HHE diplotype to acquisition of infection.
0.94 CCR2-CCR5 haplotypes did not conform to HWE (Table 2).
0.92 CCR2 and CCR5 SNPs/haplotypes/diplotypes on HIV-1 infection or disease progression have shown a wide spectrum of effects in various populations (See Additional File 1; Table S1).
0.92 CCR2-CCR5 haplotypes in Zambian couples
0.91 CCR2-CCR5 on disease progression in a variety of infected populations.
0.89 CCR2 and CCR5 variants resolved nine previously recognized haplotypes.
0.89 CCR2-CCR5 determinants of VL
0.83 CCR2-CCR5 alleles or haplotypes on transmission and acquisition of infection, the highly significant deviation of the distribution of haplotypes from HWE among the index, but not the exposed partners, was strong evidence of a selective effect, and the differential deviation of the seroconverters, but not the persistently seronegatives, corroborated the difference.
0.74 CCR2 and CCR5 with heterosexual transmission of phylogenetically related HIV-1 within discordant partners.
0.58 CCR2-CCR5 diplotype (HHD/HHE and HHF*2) with time to HIV-1 acquisition among initially seronegative partners of HIV-1 discordant Zambian couples.
0.53 CCR2-CCR5 haplotypes were observed in the frequency distribution shown in Table 2.
27169903 0.96 CCR2/CCR5 ligands, proinflammatory cytokines, and biomarkers of bacterial translocation were also evaluated.
0.96 CCR2/CCR5 antagonist activity
0.95 CCR2/CCR5 ligands, cytokines, and bacterial translocation biomarkers were evaluated.
0.95 CCR2/CCR5 blockade in HIV-infected participants in a phase IIb study27 and led to decreases in aspartate aminotransferase (AST)-to-platelet ratio index (APRI), noninvasive hepatic fibrosis index (FIB-4), and enhanced liver fibrosis score.27, 28, 29 Decreases in both APRI and FIB-4 correlated with reductions in soluble CD14 (sCD14, a marker of monocyte activation) levels.
0.93 CCR5 antagonist) requires no dosing adjustment for HI, but no data are available for investigational CCR2 (CCX140-b, JNJ-41443532) or CCR2/5 (BMS-813160, PF-04634817) antagonists.
0.92 CCR2 or CCR5-antagonists PKs.
0.92 CCR2/CCR5 blockade observed here are consistent with previously reported findings.
0.89 CCR2 ligand (CCL2) and CCR5 ligands (CCL3, CCL4, and CCL5) were assessed to determine its antagonistic activity.
0.61 CCR2/CCR5 antagonist, is being evaluated for treatment of nonalcoholic steatohepatitis and liver fibrosis (CENTAUR; NCT02217475).
0.57 CCR2 and CCR5 blockade increased systemic inflammation, levels of proinflammatory cytokines were measured.
9207004 0.96 CCR2 and CCR5, but not cytokine receptors such as interleukin (IL)-2Ralpha, IL-2Rbeta, tumor necrosis factor receptor 1, or transforming growth factor betaR, are redistributed to a pole in T cells that are migrating in response to chemokines.
0.96 CCR2 cDNA (Fig. 1 A), but not with CCR5 cDNA-transfected cells (Fig. 1 B).
0.96 CCR2 and CCR5 was virtually undetectable on freshly isolated peripheral blood T lymphocytes (Fig. 1 C, and data not shown), whereas a significant fraction of IL-2- cultured, PHA-activated T lymphoblasts (>50%) express both receptors (Fig. 1, D and E).
0.95 CCR5-specific antiserum recognizes only CCR5, but not CCR2 cDNA-transfected cells (Fig. 1 B).
0.95 CCR2 mAb MCP-1R03 (A) and mouse anti-CCR5 antibody (B) to the 293 cell line, transiently transfected with human CCR2 (white histogram) and CCR5 (shaded histogram) cDNA.
0.95 CCR2 and CCR5 receptors on migrating T lymphocytes.
0.94 CCR2 or CCR5 to the leading edge of the cell was triggered by the chemokines MCP-1, RANTES, and IL-8, as well as by the cytokines IL-2 and IL-15 (Fig. 5, a and b), known to be chemotactic factors.
0.83 CCR2 (a) or CCR5 (b) receptors were redistributed was calculated as described.
0.62 CCR2 and CCR5 receptors polarize to the leading edge of migrating lymphocytes, a finding that helps to understand the chemotactic response mechanism.
23880174 0.96 CCR5 promoter 59029 A/G and CCR2-64I polymorphism were in equilibrium from generation to generation (the X2 value > 3.84).
0.95 CCR5-Delta32, CCR5 promoter 59029A/G, CCR2-64I and SDF1-3'A were analyzed using polymerase chain reaction (PCR) and restriction fragment length polymorphisms.
0.95 CCR5 promoter 59029 A/G and CCR2-64I in the studied population were in equilibrium (P > 0.05) (Table 5).
0.95 CCR5-Delta32, CCR5 promoter 59029 A/G, CCR2-64I and SDF1-3'A alleles reported in African populations living in different African countries are however sparse.
0.95 CCR5- 32 and CCR2-64I alleles have been shown to have a strong protective effect on progression of HIV-1 infection, but SDF1-3'A homozygosity carried no such protection.
0.88 CCR5 promoter and CCR2 in HIV positive individuals and HIV negative individuals were analyzed.
0.79 CCR5-Delta32, CCR2-64I and SDF1-3'A in Cameroon.
0.70 CCR5, CCR2 and stromal-derived factor 1 (SDF1) have been found to modulate the susceptibility of individuals to HIV-1 infection and/or the pathogenic progression.
0.62 CCR5-Delta32), CCR5 promoter A/G (Adenine/Guanine), CC-Chemokine Receptor 2 mutation 64 isoleucine (CCR2-64I) and the Stromal cell-derived Factor 3'A mutation (SDF1-3'A), are involved in the susceptibility to HIV-1 infection and progression.
15588486 0.96 CCR2 and CCR5-CCRL2), which supports the linkage disequilibrium patterns illustrated in Figure 1.
0.92 CCR2 and CCR5.
0.91 CCR2, CCR5 and CCRL2) on chromosome 3p21, and a cluster of three CC-chemokine genes [MPIF-1 (CCL23) PARC (CCL18) and MIP- 1alpha (CCL3)] on chromosome 17q11-12.
0.86 CCR5 and V64I in CCR2), Gonzalez et al. find that the ancestral haplotype is at high frequency in African populations.
0.58 CCR2 and CCR5, although long-range pairwise linkage disequilibrium across the region appears to remain intact on two common haplotypes.
0.54 CCR2(N260N) and CCR5 (208).
17786209 0.96 CCR2/CCR5 diplotype and HIV mother to child transmission (MTCT) in Malawi.
0.96 CCR2 and CCR5 mutations, including a valine to isoleucine substitution at codon 64 in the CCR2b gene (CCR2-64I), CCR5 mutations -2733A G, -2554 G T, -2459A G, -2135C T, -2132C T, -2086A G, -1835C T, and the delta-32 deletion in the open reading frame of CCR5 (CCR5-ORF).
0.96 CCR2/CCR5 haplotypes are associated with perinatal transmission of HIV-1.
0.94 CCR2/CCR5 Haplotypes and abridged phylogenetic tree.
0.66 CCR2b gene, in linkage disequilibrium with regions of the CCR5 promoter, is associated with delayed disease progression in some, though not all studies.
18845960 0.96 CCR5 promoter, CCR2, CX3CR1, and Stromal cell-derived factor-1 (SDF-1) genes were determined in 980 infants from sub-Saharan Africa using real-time polymerase chain reaction to determine association with MTCT.
0.83 CCR5 promoter, CCR2, CX3CR1, and SDF-1 polymorphisms on the risk of HIV-1 MTCT in 3 sub-Saharan African cohorts of infants.
0.81 CCR5 promoter, CCR2, and CX3CR1 polymorphisms were associated with risk of MTCT likely through their role as an HIV-1 coreceptor or by modulating the early immune response.
21091093 0.96 CCR2 and two non-functional polymorphisms in CCR5.
0.93 CCR5, and a reduced risk of gastric cancer in women in a hospital-based case-control study, but no association with CCR2 V64I genotypes.
0.79 CCR2, CCR5, CX3CR1) genes and one frameshift deletion (CCR5) in blood leukocyte DNA in relation to gastric cancer risk and survival.
24489825 0.96 CCR2B or CCR5 were determined by FACS analysis.
0.93 CCR2B or CCR5 (A2) clearance from the plasma membranes of Jurkat (CXCR4), CEM (CXCR4 or CCR5), K562 (wt or WM CXCR4) cells, fresh PBMCs (CXCR4), or monocytes (CCR2B or CXCR4) in the context of Nef expression.
0.52 CCR2B or CCR5 in fresh monocytes or a CEM cell line co-expressing GFP and Nef or null plasmid (Figure 1A2).
19351767 0.96 CCR2 with MCP-1, and CCR5 with RANTES and MIP-1beta.
0.86 CCR2, CCR3, or CCR5, could affect cell migration.
23076379 0.96 CCR5 gene at frequencies of 0.43% in hematopoietic cells in the spleen, and 0.05% in the bone marrow: off-target modification in the partially homologous CCR2 gene was two orders of magnitude lower.
0.93 CCR2 gene was on the order of 5%, only 7 times less than the on-target modification, ZFNs targeting CCR5 have been approved for use in clinical trials.
25964300 0.96 CCR2 locus we set up a digital-PCR assay, in analogy to the one described above for CCR5 (primer sequences are provided in Supplementary Table S2).
30256641 0.96 CCR2-RA binds with low affinity to CCR5 (KD of 100 nM), suggesting that CCR2-RA-[R] is a nonselective antagonist that can bind several chemokine receptors.
24688285 0.95 CCR2 (CCR2V64I) is tightly linked to certain single nucleotide polymorphisms (SNPs) in the CCR5 cis-regulatory region.
0.94 CCR2, is located close to the CCR5 gene region in chromosome 3.
0.93 CCR2-CCR5 gene loci between the northern and southern parts of the country.
0.92 CCR2-CCR5 haplotypes in Omanis and compared the patterns of genetic diversity with those of other populations.
0.92 CCR2V64I and the majority of CCR5 SNPs in the promoter region.
0.90 CCR2-CCR5 genes in the Omani population.
0.86 CCR5 and CCR2V64I among Ethiopian Jews.
0.84 CCR2-CCR5 haplotypes.
0.79 CCR5 promoter SNPs and CCR2V64I in the Omani population differed from that of Ethiopian Jews.
0.78 CCR2V64I was significantly linked to four promoter SNPs in the CCR5 gene.
0.57 CCR2-CCR5 complex in this region.
20416280 0.95 CCR5-Delta32 allele that widely fluctuates between different populations, the allelic frequency of CCR2b-64I does not vary much between populations and is between 10% and 20%.
0.95 CCR5 and CCR2 allelic variants, however it is reported to be decreased with longer duration of infection.
0.94 CCR5-Delta32, CCR2b-641, RANTES In1.1C, SDF-1 3'A, IL-10-5'-592A and IL-4-589T may be used as clinical markers to predict progression of HIV-1 infections.
0.84 CCR5-Delta32, CCR2b-641, RANTES In1.1C, SDF-1 3'A, IL-10-5'-592A and IL-4-589T alleles in two unique HIV-1 infected patient cohorts that represent the two distinct stages of disease progression, namely rapid progressors (RPs) and long term non-progressors (LTNPs) (n = 12/group) were recruited.
0.84 CCR5-Delta32, (B) CCR2b-641, (C) RANTES In1.1C and (D) SDF-1 3'A allelic variants in the RP and LTNP groups.
0.78 CCR5-Delta32, CCR2b-641, RANTES In1.1C, SDF-1 3'A, IL-10-5'-592A and IL-4-589T in peripheral blood mononuclear leukocytes (PBML) isolated from patients was performed by real time, quantitative (Q)-PCR using DNA was isolated from PBML.
0.78 CCR2b-641 and the CCR5-Delta32, are associated with delayed progression of HIV-1 disease due to poor binding of HIV-1 to target cells.
0.64 CCR5-Delta32, CCR2b-641, RANTES In1.1C, SDF-1 3'A, IL-10-5'-592A, and IL-4-589T in LTNP and RP subject cohorts
0.55 CCR2 (CCR2-64I) and CCR5 (CCR5-D32).
27458015 0.95 CCR2 could increase 125I-HDL binding by 30% and cell association by 23% compared with those in siRNA-negative control (NC)-transfected cells; however, this reversed effect could not be observed by siRNA-CCR3 and siRNA-CCR5.
0.91 CCR2, CCR3, and CCR5 are expressed in ECs and are the candidate receptors for CCL2.
0.85 CC-chemokine receptor 2 (CCR2), CCR3, and CCR5, which are high affinity receptors for CCL2, are expressed on human endothelial cells.
0.77 CCR2 expression was significantly increased in a dose- and time-dependent manner and by a maximum of 212 and 139%, respectively, after treatment with CCL2 at 80 mug/ml for 18 h and at 40 mug/ml for 12 h. In contrast, CCL2 did not increase or only slightly increased CCR3 or CCR5 expression (Fig. 3, A and B).
0.75 CCR2, CCR3, and CCR5 were detected using Western blotting as described under "Experimental Procedures." The quantitative analysis of protein was performed using ImageJ software.
0.53 CCR2, CCR3, and CCR5 in HDL uptake by HCAECs were further assessed by RNA interference (data not shown).
9841919 0.95 CCR2b, CCR3, CCR4, CCR5, CCR8, CXCR4, STRL33 (Bonzo), and GPR15 (BOB) were tested in the GHOST cell assay (Fig. 1).
0.95 CCR2-based coreceptors in response to the appearance of deleted CCR5 genes at high frequencies in its host.
0.94 CCR5 to CCR2b would require an intermediate coreceptor.
0.89 t-CCR5 or CCR2b derived from humans.
0.88 CCR2-based coreceptors, the closest chemokine coreceptor to CCR5.
24253260 0.95 CCR5 produced off-target effects in the CCR2 gene in human cells at a frequency of 5.4%, more than 1,000-fold higher than what we have found for triplex-forming PNAs.
0.94 CCR2 in 2.8 million reads, an off-target frequency of 0.004%, which is more than three orders of magnitude less as compared with the off-target frequencies in CCR2 reported for ZFNs targeting CCR5.
0.94 CCR5 and CCR2 gene in blank and CCR5-NP-treated PBMCS.
0.63 CCR5 gene and a low off-target frequency of 0.004% in the CCR2 gene, a 216-fold difference.
0.58 CCR5 in the PBMCs was 0.97% after a single treatment, with an off-target frequency of just 0.004% in CCR2, the most closely related gene to CCR5.
28273887 0.95 CCR2 and an increased expression of CCR1 and CCR5.
0.95 CCR2, CCR5, CXCR4, and CX3CR1 and were analyzed by flow cytometry (Supplementary Fig. S1).
0.59 CCR2, CCR5, CXCR4 and CX3CR1), migratory capacity, the influence of chemokines during monocyte maturation and cytokine production, and their relationship with clinical parameters and the development of the disease.
32098198 0.95 CCR5 32 variant and hypertension formed the central focus of a study by Mettimano and co-workers in which the authors investigated polymorphisms within the CCR5 and CCR2 genes in hypertensive patients, respectively.
0.76 CCR5 and CCR2 were studied.
0.71 CCR5 and CCR2 levels/expression increase in AD patients compared to controls.
21376172 0.95 Ccr2) and control of leukocyte movement from blood to brain (Cxcr3 and Ccr5).
25324719 0.95 CCR2, CCR5, CXCR2, CXCR3, and CXCR4 during flavivirus and alphavirus infection, focusing on the effect of therapeutic blockade of these receptors using small molecule receptor antagonists or chemokine neutralizing antibodies.
27151309 0.95 CCR5 directed CRISPR/Cas9 system had a significant off-target occurrence, especially in CCR2 gene locus, due to its sequence similarity to CCR5.
31447666 0.95 CCR5 and CCR2 in the PBMCs of AD patients, while in vitro administration of Abeta increased their expression in PBMCs.
26322257 0.94 CCR5-wt allele is fixed in these populations and also the homozygous genotypes of CCR2 genotype (64I/64I) and SDF1 (3'A/3'A) are not found in the Baiga population.
0.94 CCR5-Delta32, CCR2-64I and SDF1-3'A are recorded low in Gond and very low in the Baiga tribe.
0.93 CCR5-Delta32, CCR2-64I and SDF1-3'A alleles in primitive tribe (Baiga) and a non-primitive tribe (Gond) of central India were investigated.
0.93 CCR5-Delta32, CCR2-64I and SDF1-3'A. Due to the absence of social interactions with modern populations, primitive tribes have not acquired the alleles that reduce the progression of HIV-1 infection making them highly susceptible.
0.92 CCR5 (CCR5-Delta32), CCR2 (CCR2-64I) and SDF1 (SDFA-3'A; the ligand of CXCR4) are known to slow down the HIV-1 progression in infected individual.
0.92 CCR5-Delta32, CCR2-64I and SDF1-3'A were (0, 0.035, 0.080) and (0, 0.110, 0.100) in Baiga and Gond respectively.
0.87 CCR5, CCR2 and SDF1.
19643012 0.94 CCR2 bearing cells were shown towards wells containing CCL2, and CCR5 bearing cells towards those with U83A.
0.93 CCR2 antibody used was linked to PE and CCR5 antibody linked to FITC.
0.92 CCR2, but not CCR5.
0.85 CCR5 or uncultured cells which primarily expressed CCR2.
0.82 CCR2 and CCR5.
0.73 CCR5 but not CCR2, towards 1 nM U83A, was demonstrated, consistent with the binding specificity of U83A (Figure 3).
22046140 0.94 CCR5 and CCR2 variants with HIV-1 pathogenesis is well known, the role of variation in other nearby chemokine receptor genes remain unresolved.
0.93 CCR5 and CCR2 since these receptor genes had been previously sequenced in HIV patients, nor did we resequence CX3CR1.
0.93 CCR2-V64I-CCR5-Delta32 composite genotype, CCR5-2459, HLA class 1 homozygosity, HLA-B*35Px, HLA-B*57 and HLA B*27 (without covariates, AIC:1796.32, with 9 covariates, AIC:1737.28).
0.87 CCR5 and CCR2 associations, significant associations were identified for CCR3, CCR8, and CCRL2 on progression to AIDS.
28532213 0.94 CCR5 and all structures of CXCR4 are inactive, and a recent double antagonist bound CCR2 structure has the conformational signature of a deep inactive state.
0.94 CCR5:maraviroc (c) CXCR4:IT1t, and (d) CCR2 in a ternary complex with BMS-681 and CCR2-RA-[R].
0.78 CCR5 inhibitor Maraviroc, and BMS-681, a potent dual affinity CCR2/CCR5 antagonist (Fig. 5b-d).
30596191 0.94 CCR2-64I, CCR5-59029-A/G, TRIM5alpha-136Q, SDF1-3'A respectively in the mothers and 18.8%, 35.9%, 11.3% and 20.5% in the babies.
0.62 CCR5-Delta32, CCR5-59029A/G, CCR2-64I, SDF1-3'A and TRIM5alpha-136Q polymorphisms in a Cameroonian cohort of mother-baby and also to look at their association with the MTCT and acquisition of HIV-1.
0.51 CCR2-64I and CCR5-59029-A/G mutation, there was no difference in the distribution between exposed-infected and exposed-non infected children.
28178200 0.94 CCR2 and CCR5 respond cooperatively to ligands of these receptors.
0.74 CCR2 is co-expressed (and dimerized) with CCR5, CCL4 effectively displaces CCL2 from binding to CCR2 within the heteromer.
9151905 0.94 CCR2b, CCR3, CCR4, CCR5, CXCR1 (IL-8 RA), CXCR2 (IL-8RB), CXCR3, and CXCR4 (fusin/Lestr) were stained with anti-CCR5 mAb 3A9.
19109148 0.94 CCR5 but not CCR1 or CCR2 regulates IL-2 production as well as IL-2-dependent events such as expression of the alpha-chain of the IL-2 receptor (IL-2Ralpha; also known as CD25), transactivation of the NFAT, phosphorylation of STAT5, and cell proliferation during T cell activation.
23493039 0.93 CCR5 32 and CCR2-64I variations and Alzheimer's disease in the Iranian population.
0.91 CCR5 and CCR2 genotypes and allele frequencies in AD compared to healthy controls (P> 0.05).
0.87 CCR2 and CCR5 genes expression increase in AD patients comparing to control subjects.
0.87 CCR2 and CCR5 expression were increased in AD patients compared to controls; but two studies from Italy and two studies from Spain showed no statistically significant differences between AD and control groups.
0.79 CCR2 and CCR5 are chemokine receptors expressed on microglia that mediate accumulation of leukocytes at sites of inflammation.
0.77 CCR5 32 and CCR2-64I variations and AD in the Iranian population.
0.71 CCR2 and CCR5 genes are characterized by polymorphisms in their sequence.
0.70 CCR5 32 and CCR2-64I between the AD patients and healthy controls (P> 0.05).
0.70 CCR5 and CCR2 genotype and allele frequencies of each group are summarized in Table 3.
0.68 CCR2 and CCR5 are two types of CC receptors, which predominantly express on monocytes surfaces.
0.65 CCR2 and CCR5 interaction may be implicated in the in vivo processes that hinder leukocyte rolling on blood vessels and induce leukocyte parking in tissues during inflammatory responses.
0.64 CCR5-Delta32 is a genetic variant of CCR5 and is characterized by the presence of a 32-bp deletion in the coding region of the gene, which leads to the expression of a nonfunctional receptor, and the CCR2-64I has a change of valine to isoleucine at codon 64, in the first transmembrane domain.
0.57 CCR5 32 and CCR2-64I variations were determined in 156 AD patients and 161 control subjects using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods, and the results were compared among AD and healthy controls.
27900346 0.93 CCR5 modification with <20% modification of CCR2 and decreasing levels at the KRR1, FBLX11 and ZCCHC14 loci (Figure 3b).
31261839 0.92 CCR2 ORF SNP 190G > A (Val64Ile), rs1799864; and six CCR5 promoter SNPs -2773A > G (rs2856758), -2554G > T (rs2734648), -2135T > C (rs1799988), -2132C > T (rs41469351), -2086A > G (rs1800023), and -1835C > T (rs1800024).
0.63 CCR2-CCR5 polymorphisms, haplotypes have been organized into seven evolutionarily distinct human haplogroups (HH) designated HHA, -B, -C, -D, -E, -F (F*1 and F*2), and -G (G*1 and G*2) (Table 1).
18757833 0.92 CCR2, and CCR5 expression and begin to express CCR4, CCR7, and CXCR4, allowing for homing to regional lymph nodes.
24508837 0.91 CCR2 and CCR5 cis-regulatory region based on which the human haplotypes (HH) A-E, F*1, F*2, G*1 and G*2 have been defined using evolutionary-based analysis (Figure 1) .
0.74 CCR2-CCR5 polymorphisms and classified into haplotypes.
0.58 CCR5 HH are designated as HHA to HHG*2, with HHF*2 and HHG*2 denoting the haplotypes that bear the CCR2-64I and CCR5-Delta32 polymorphisms, respectively.
19190524 0.91 CCR2-V64I, CCR5-wt/Delta32, CCR5-59029-G/A, CCR5-59353-T/C, CCR5-59356-C/T and SDF1-3'-G/A polymorphisms on the rate of disease progression and neurological impairment.
30305110 0.91 CCR2 are not altered in cell cultures derived from CCR5-null mice.
28484468 0.86 C-C chemokine receptor type 5 (CCR5) and C-X-C chemokine receptor type 4 (CXCR4) are two main co-receptors for HIV-1 infection, though other chemokine receptors including CCR2b and CCR3 may also serve as co-receptors, albeit in rare cases.
22310811 0.85 CCR2 and CCR5 variants
0.73 CCR2 gene to CCR5 on chromosome 3p21.3 suggests that the observed impact of this mutation could possibly be as a result of linkage with highly polymorphic CCR5 promoter region.
9034141 0.81 CCR5, CCR3, CCR2b, or CXCR-4.
0.80 CCR2b, CCR3, CCR4, or CCR5.
0.80 CCR5, CCR3, CCR2b, and CXCR-4.
0.78 CCR5, CCR2b, CCR3, and CXCR-4 in patients with disease progression.
0.59 CCR5, CCR3, CCR2b, and CXCR-4.
30921390 0.81 CCR2 rs1799864 A allele reported by Rigato et al was revealed only when combined with CCR5-D32 polymorphism, what is in contrast with a poorer outcome of AG individuals compared with AA individuals observed in this same study.
0.59 CCR2 polymorphism is in complete linkage disequilibrium with a C to T substitution on CCR5 regulatory region at position 59653.
20169157 0.78 CCR2/CCR5 SNPs and HIV MTCT previously described and based on our replicate analyses, we found that this was not always the case.
17888174 0.72 CCR2, CCL3 binds both CCR1 and CCR5.
0.59 CCR5 expression and decreased CCR2 expression during in vitro monocyte to macrophage differentiation.
26688689 0.54 CCR2, CX3CL1/CX3CR1, and CCL5/CCR5 should be detected simultaneously for the comprehensive study.



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