Key functional receptor for CCL2 but can also bind CCL7 and CCL12. Its binding with CCL2 on monocytes and macrophages mediates chemotaxis and migration induction through the activation of the PI3K cascade, the small G protein Rac and lamellipodium protrusion (Probable). Also acts as a receptor for the beta-defensin DEFB106A/DEFB106B. Regulates the expression of T-cell inflammatory cytokines and T-cell differentiation, promoting the differentiation of T-cells into T-helper 17 cells (Th17) during inflammation. Facilitates the export of mature thymocytes by enhancing directional movement of thymocytes to sphingosine-1-phosphate stimulation and up-regulation of S1P1R expression; signals through the JAK-STAT pathway to regulate FOXO1 activity leading to an increased expression of S1P1R. Plays an important role in mediating peripheral nerve injury-induced neuropathic pain. Increases NMDA-mediated synaptic transmission in both dopamine D1 and D2 receptor-containing neurons, which may be caused by MAPK/ERK-dependent phosphorylation of GRIN2B/NMDAR2B. Mediates the recruitment of macrophages and monocytes to the injury site following brain injury.
Background References
1. Tsutsumi, T. et al. Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice. J. Dent. Res 92: 65-70 (2013).
2. Lee, Y. et al. In vivo MR evaluation of the effect of the CCR2 antagonist on macrophage migration. Magn Reson Med 64: 72-79 (2010).
Sequence Similarity
Belongs to the G-protein coupled receptor 1 family.
Tissue Specificity
Expressed by monocytes and IL2-activated NK cells.
Post-translational Modification
N-glycosylated.; Sulfation increases the affinity for both monomeric and dimeric CCL2 with stronger binding to the monomeric form. Binding of sulfated CCR2 to CCL2 promotes conversion of CCL2 from dimer to monomer.
Western blot analysis of CCR2 on different lysates. Proteins were transferred to a PVDF membrane and blocked with 5% BSA in PBS for 1 hour at room temperature. The primary antibody (ET1611-65, 1/2,000) was used in 5% BSA at room temperature for 2 hours. Goat Anti-Rabbit IgG - HRP Secondary Antibody (HA1001) at 1/50,000 dilution was used for 1 hour at room temperature. Positive control: Lane 1: mouse spleen tissue lysate Lane 2: THP-1 cell lysate
Immunohistochemical analysis of paraffin-embedded human tonsil tissue with Rabbit anti-CCR2 antibody (ET1611-65) at 1/500 dilution.
The section was pre-treated using heat mediated antigen retrieval with Tris-EDTA buffer (pH 9.0) for 20 minutes. The tissues were blocked in 1% BSA for 20 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (ET1611-65) at 1/500 dilution for 1 hour at room temperature. The detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. Tissues were counterstained with hematoxylin and mounted with DPX.
Immunohistochemical analysis of paraffin-embedded human esophagus tissue with Rabbit anti-CCR2 antibody (ET1611-65) at 1/400 dilution.
The section was pre-treated using heat mediated antigen retrieval with Tris-EDTA buffer (pH 9.0) for 20 minutes. The tissues were blocked in 1% BSA for 20 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (ET1611-65) at 1/400 dilution for 1 hour at room temperature. The detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. Tissues were counterstained with hematoxylin and mounted with DPX.
Flow cytometric analysis of THP-1 cells labeling CCR2.
Cells were washed twice with cold PBS and resuspend. Then stained with the primary antibody (ET1611-65, 1ug/ml) (red) compared with Rabbit IgG Isotype Control (green). After incubation of the primary antibody at +4℃ for an hour, the cells were stained with a iFluor™ 488 conjugate-Goat anti-Rabbit IgG Secondary antibody (HA1121) at 1/1,000 dilution for 30 minutes at +4℃. Unlabelled sample was used as a control (cells without incubation with primary antibody; black).
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