Product: CCR5 Antibody
Catalog: AF6339
Description: Rabbit polyclonal antibody to CCR5
Application: WB IF/ICC
Reactivity: Human, Mouse, Rat, Monkey
Prediction: Pig, Bovine, Rabbit, Chicken
Mol.Wt.: 40kDa; 41kD(Calculated).
Uniprot: P51681
RRID: AB_2835195

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

WB 1:500-1:2000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Pig(82%), Bovine(91%), Rabbit(82%), Chicken(88%)
CCR5 Antibody detects endogenous levels of total CCR5.
Cite Format: Affinity Biosciences Cat# AF6339, RRID:AB_2835195.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


AM4 7; C C chemokine receptor type 5; C C CKR 5; C-C chemokine receptor type 5; C-C CKR-5; C-C motif chemokine receptor 5 A159A; CC Chemokine Receptor 5; CC Chemokine Receptor Type 5; CC CKR 5; CC-CKR-5; CCCKR 5; CCCKR5; CCR 5; CCR-5; CCR5; CCR5 chemokine (C C motif) receptor 5; CCR5_HUMAN; CD 195; CD195; CD195 Antigen; Chemokine C C motif receptor 5; Chemokine receptor CCR5; CHEMR13; CKR 5; CKR5; CMKBR 5; CMKBR5; FLJ78003; HIV 1 Fusion Coreceptor; HIV-1 fusion coreceptor; HIV1 fusion coreceptor; IDDM22; MIP-1 alpha receptor;


P51681 CCR5_HUMAN:

Highly expressed in spleen, thymus, in the myeloid cell line THP-1, in the promyeloblastic cell line KG-1a and on CD4+ and CD8+ T-cells. Medium levels in peripheral blood leukocytes and in small intestine. Low levels in ovary and lung.

CCR5 a 7-transmembrane G-linked receptor for a number of inflammatory C-C type chemokines including MIP-1-alpha, MIP-1-beta and RANTES. Transduces a signal by increasing the intracellular calcium ion level. May play a role in the control of granulocytic lineage proliferation or differentiation. Acts as a coreceptor (along with CD4) for HIV-1 R5 isolates. Interacts with PRAF2. Interacts with HIV-1 surface protein gp120.



Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P51681 As Substrate

Site PTM Type Enzyme
S6 O-Glycosylation
S7 O-Glycosylation
T195 Phosphorylation
S336 Phosphorylation A0A024R1D8 (ADRBK2) , P35626 (GRK3)
S337 Phosphorylation P35626 (GRK3) , A0A024R1D8 (ADRBK2)
Y339 Phosphorylation
S342 Phosphorylation P35626 (GRK3) , A0A024R1D8 (ADRBK2)
T343 Phosphorylation
S349 Phosphorylation A0A024R1D8 (ADRBK2) , P35626 (GRK3)

Research Backgrounds


Receptor for a number of inflammatory CC-chemokines including CCL3/MIP-1-alpha, CCL4/MIP-1-beta and RANTES and subsequently transduces a signal by increasing the intracellular calcium ion level. May play a role in the control of granulocytic lineage proliferation or differentiation.

(Microbial infection) Acts as a coreceptor (CD4 being the primary receptor) of human immunodeficiency virus-1/HIV-1.


Sulfated on at least 2 of the N-terminal tyrosines. Sulfation contributes to the efficiency of HIV-1 entry and is required for efficient binding of the chemokines, CCL3 and CCL4.

O-glycosylated, but not N-glycosylated. Ser-6 appears to be the major site. Also sialylated glycans present which contribute to chemokine binding. Thr-16 and Ser-17 may also be glycosylated and, if so, with small moieties such as a T-antigen.

Palmitoylation in the C-terminal is important for cell surface expression, and to a lesser extent, for HIV entry.

Phosphorylation on serine residues in the C-terminal is stimulated by binding CC chemokines especially by APO-RANTES.

Subcellular Location:

Cell membrane>Multi-pass membrane protein.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Highly expressed in spleen, thymus, in the myeloid cell line THP-1, in the promyeloblastic cell line KG-1a and on CD4+ and CD8+ T-cells. Medium levels in peripheral blood leukocytes and in small intestine. Low levels in ovary and lung.

Subunit Structure:

Interacts with PRAF2. Efficient ligand binding to CCL3/MIP-1alpha and CCL4/MIP-1beta requires sulfation, O-glycosylation and sialic acid modifications. Glycosylation on Ser-6 is required for efficient binding of CCL4. Interacts with GRK2. Interacts with ARRB1 and ARRB2. Interacts with CNIH4.

(Microbial infection) Interacts with HIV-1 surface protein gp120.

(Microbial infection) May interact with human cytomegalovirus/HHV-5 protein UL78.


Belongs to the G-protein coupled receptor 1 family.

Research Fields

· Cellular Processes > Transport and catabolism > Endocytosis.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)


1). Huang R et al. CCL5 derived from tumor-associated macrophages promotes prostate cancer stem cells and metastasis via activating β-catenin/STAT3 signaling. Cell Death & Disease 2020 Apr 16;11(4):234 (PubMed: 32300100) [IF=9.0]

Application: WB    Species: human    Sample: prostate cancer cells

Fig. 5 CCL5 promotes prostate cancer invasion and PCSCs self-renewal via activating the CCR5/β-catenin/STAT3 pathway. a–c Heatmaps of 94 metastasis-related DEGs (a), 42 stemness-related DEGs (b), as well as 30 STAT3 pathway-related DEGs (c). RNA-Seq analysis was conducted to characterize the cellular responses of PC3 cells to 40 ng/ml CCL5 treatment. Differential gene expression analysis was conducted to identify the DEGs (n = 3). d Venn diagram of the DEGs in the indicated groups. CTNNB1, also known as β-catenin, was the most significant one of them. e Western blotting assay indicated that the CD133+ PCSCs sorted from PC3 cells by MACS method exhibited increased expression of CCR5, β-catenin, and STAT3 when compared with the CD133- subpopulation (n = 3). f CCL5 treatment significantly elevated the promoter activity of STAT3 in PC3 cells while XAV-939, the specific inhibitor of β-catenin, partly abrogated that (n = 6). g Immunofluorescence assay indicated that CCL5 treatment (40 ng/ ml) could significantly induce the expression and nuclear translocation of β-catenin in prostate cancer cells. Scale bar, 10 μm. h CHIP assay suggested that β-catenin could bind to the promoter region of STAT3, while the specific inhibitor of β-catenin (XAV-939) partly decreased their binding activity. i CCR5 specific siRNAs could significantly abrogate the activation effect of CCL5 on β-catenin/STAT3 pathway (n = 3). All values are presented as the mean ± SD, *p < 0.05, **p < 0.01.

2). Song Q et al. Transcription factor RUNX3 promotes CD8+ T cell recruitment by CCL3 and CCL20 in lung adenocarcinoma immune microenvironment. JOURNAL OF CELLULAR BIOCHEMISTRY 2020 Jan 3 (PubMed: 31898342) [IF=4.0]

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