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Biotinylated Human CCR8 Protein, His,Flag&Avitag™ (Nanodisc)

分子别名(Synonym)

CC chemokine receptor 8,CD198,ChemR1,CKRL1,CKR-L1,CKRL1,CY6,GPRCL1,GPRCY6,GPR-CY6,TER-1

表达区间及表达系统(Source)

Biotinylated Human CCR8 Protein, His,Flag&Avitag (CC8-H82D4) is expressed from human 293 cells (HEK293). It is a membrane protein, contains complete wild type 7-transmembrane domans (TMD) and extracellular doman (ECD).

Predicted N-terminus: Asp 2

Request for sequence

蛋白结构(Molecular Characterization)

CCR8 Structure

This protein carries a polyhistidine tag, followed by a Flag tag and an Avi tag (Avitag™) at the C-terminus. The protein has a calculated MW of 60.5 kDa.

Nanodiscs are a new class of model membranes that are being used to solubilize and study a range of integral membrane proteins and membrane-associated proteins. The Nanodisc bilayer is bounded by a membrane scaffold protein (MSP1D1) coat that confers enhanced stability and a narrow particle size distribution.

The nanodisc assembles from a mixture of full length membrane protein in detergent, phospholipid micelles and membrane scaffold protein(MSP1D1) upon removal of the detergent.

标记(Labeling)

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

蛋白标记度(Protein Ratio)

Passed as determined by the HABA assay / binding ELISA.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

制剂(Formulation)

Supplied as 0.2 μm filtered solution in 20 mM HEPES, 150 mM NaCl, pH7.5 with trehalose as protectant.

Contact us for customized product form or formulation.

运输(Shipping)

This product is supplied and shipped with dry ice, please inquire the shipping cost.

存储(Storage)

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. The product MUST be stored at -70°C or lower upon receipt;
  2. -70°C for 3 months under sterile conditions.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
*The isotype control of empty/mock nanodisc (Cat. No. APO-H81Q5) is sold separately and not included in protein, you can follow this link for product information.
 

活性(Bioactivity)-ELISA

CCR8 ELISA

Immobilized Biotinylated Human CCR8 Protein, His,Flag&Avitag (Cat. No. CC8-H82D4) at 5 μg/mL (100 μL/well) on streptavidin (Cat. No. STN-N5116) precoated (0.5 μg/well) plate can bind Anti-CCR8 Antibody, Human IgG1 with a linear range of 0.3-20 ng/mL (QC tested).

Protocol

CCR8 ELISA

Immobilized Biotinylated Human CCR8 Protein, His,Flag&Avitag (Cat. No. CC8-H82D4) at 5 μg/mL (100 μL/well) on streptavidin (Cat. No. STN-N5116) precoated (0.5 μg/well) plate can bind Anti-CCR8 Antibody with a linear range of 0.2-5 ng/mL (Routinely tested).

Protocol

 

活性(Bioactivity)-SPR

CCR8 SPR

Anti-CCR8 Antibody captured on Protein A Chip can bind Biotinylated Human CCR8 Protein, His,Flag&Avitag (Cat. No. CC8-H82D4) with an affinity constant of 124 nM as determined in a SPR assay (Biacore 8K) (Routinely tested).

Protocol

 
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背景(Background)

This entry represents CC chemokine receptor 8 (CCR8), which it is expressed predominantly in lymphoid tissues and has also been found in glomerular podocytes and human umbilical vein endothelial cells (HUVECs). CCR8 is associated with Th2 lymphocytes, which are critical for allergy, and has a role in lymphocyte activation, migration, proliferation and differentiation and in allergic diseases. CCR8 binds to CCL1 (also known as I-309) and to CCL16 (also known as liver expressed chemokine). It also exhibits a high affinity for three chemokines of viral origin: vMIP-I, vMIP-II and vMCC-I.

 

前沿进展

Macrophage-derived CCL1 targets CCR8 receptor in hepatic stellate cells to promote liver fibrosis through JAk/STAT pathway
Diao, Li, Zhang et al
Biochem Pharmacol (2025)
Abstract: Liver fibrosis is caused by liver injury resulting from the wound healing response. According to recent research, the primary factor responsible for liver fibrosis is the activation of hepatic stellate cells (HSCs). C-C motif chemokine ligand 1 (CCL1) is one of several chemokine genes clustered on chromosome 17, which is involved in immune regulation and inflammatory processes. However, the role of CCL1 in liver fibrosis has not been reported. We found that CCL1 secreted by macrophages can target and activate the receptor protein C-C motif chemokine receptor 8 (CCR8) of HSCs, accelerating liver fibrosis progression by activating the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signalling pathway. This suggested that the CCL1-mediated regulation of CCR8 is an important event in liver fibrosis progression. In conclusion, this study identified a novel signalling axis, the CCL1/CCR8/JAK/STAT pathway, which regulates the activation and apoptosis of HSCs, thus providing a novel therapeutic strategy for liver fibrosis.Copyright © 2025. Published by Elsevier Inc.
A multi-omics analysis of effector and resting treg cells in pan-cancer
Chalepaki, Gkoris, Chondrou et al
Comput Biol Med (2025) 189, 110021
Abstract: Regulatory T cells (Tregs) are critical for maintaining the stability of the immune system and facilitating tumor escape through various mechanisms. Resting T cells are involved in cell-mediated immunity and remain in a resting state until stimulated, while effector T cells promote immune responses. Here, we investigated the roles of two gene signatures, one for resting Tregs (FOXP3 and IL2RA) and another for effector Tregs (FOXP3, CTLA-4, CCR8 and TNFRSF9) in pan-cancer. Using data from The Cancer Genome Atlas (TCGA), The Cancer Proteome Atlas (TCPA) and Gene Expression Omnibus (GEO), we focused on the expression profile of the two signatures, the existence of single nucleotide variants (SNVs) and copy number variants (CNVs), methylation, infiltration of immune cells in the tumor and sensitivity to different drugs. Our analysis revealed that both signatures are differentially expressed across different cancer types, and correlate with patient survival. Furthermore, both types of Tregs influence important pathways in cancer development and progression, like apoptosis, epithelial-to-mesenchymal transition (EMT) and the DNA damage pathway. Moreover, a positive correlation was highlighted between the expression of gene markers in both resting and effector Tregs and immune cell infiltration in adrenocortical carcinoma, while mutations in both signatures correlated with enrichment of specific immune cells, mainly in skin melanoma and endometrial cancer. In addition, we reveal the existence of widespread CNVs and hypomethylation affecting both Treg signatures in most cancer types. Last, we identified a few correlations between the expression of CCR8 and TNFRSF9 and sensitivity to several drugs, including COL-3, Chlorambucil and GSK1070916, in pan-cancer. Overall, these findings highlight new evidence that both Treg signatures are crucial regulators of cancer progression, providing potential clinical outcomes for cancer therapy.Copyright © 2025. Published by Elsevier Ltd.
Design and application of CCR8 antagonists
Van Loy, Schols, De Jonghe
Future Med Chem (2025)
Selective depletion of CCR8+Treg cells enhances anti-tumor immunity of cytotoxic T cells in lung cancer via dendritic cells
Chen, Wang, Tang et al
J Thorac Oncol (2025)
Abstract: Accumulation of regulatory T (Treg) cells, an immunosuppressive population, limits the efficacy of immunotherapy in non-small cell lung cancer (NSCLC). C-C Motif Chemokine Receptor 8 (CCR8) is selectively expressed in tumor-infiltrating Treg cells and, thus considered an ideal target. Across four NSCLC-bearing mice models, the combination of CCR8 antibody and programmed cell death protein-1 (PD1) inhibitor significantly reduced tumor growth without obvious mouse body weight drops and systemic cytokine storm. The single-cell RNA and T-cell receptor sequencing analysis demonstrated that anti-CCR8 therapy synergizes with PD1 blockade by remodeling the tumor microenvironment and disrupting CCR8+Treg - CCL5+ dendritic cells (DC) interaction. Mechanistically, therapeutic depletion of CCR8+Treg cells combined with PD1 inhibitor extremely increased interleukin-12 secretion by the JAK-STAT pathway activation on CCL5+ DCs, thereby promoting cytotoxic activity of CD8+ T cells. The therapeutic potential of the CCR8 antibody LM-108 in combination with immunotherapy was observed in clinical patients with advanced NSCLC. Overall, CCR8 expression on tumor-infiltrating Treg cells is correlated with immunosuppressive function on DCs and CD8+ T cells, thus impeding anti-tumor immunity.Copyright © 2025. Published by Elsevier Inc.
Showing 1-4 of 553 papers.
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CCR8靶点信息
英文全称:C-C chemokine receptor type 8
中文全称:CC趋化因子受体8型
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:14详情
最高研发阶段:临床二期
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