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CX3CR1 Membrane Protein Introduction

Introduction of CX3CR1

CX3CR1, also known as the fractalkine receptor or G-protein coupled receptor 13 (GPR13), is a protein encoded by the CX3CR1 gene. The receptor has seven transmembrane domains, belonging to G-protein coupled receptor family. In the periphery, it is expressed on T cells, dendritic cells, and a small subpopulation. In the central nervous system, it is exclusively expressed on microglia. Now, many types of research have shown that CX3CR1 and its ligand - chemokine fractalkine are involved in the pathogenesis of several diseases.

Basic Information of CX3CR1
Protein Name CX3C chemokine receptor 1
Gene Name CX3CR1
Aliases V28, CCRL1, GPR13, CMKDR1, GPRV28, CMKBRL1
Organism Homo sapiens (Human)
UniProt ID P49238
Transmembrane Times 7
Length (aa) 387
Sequence MREPLEALKLADLDFRKSSLASGWRMASGAFTMDQFPESVTENFEYDDLAEACYIGDIVVFGT
VFLSIFYSVIFAIGLVGNLLVVFALTNSKKPKSVTDIYLLNLALSDLLFVATLPFWTHYLINE
KGLHNAMCKFTTAFFFIGFFGSIFFITVISIDRYLAIVLAANSMNNRTVQHGVTISLGVWAAA
ILVAAPQFMFTKQKENECLGDYPEVLQEIWPVLRNVETNFLGFLLPLLIMSYCYFRIIQTLFS
CKNHKKAKAIKLILLVVIVFFLFWTPYNVMIFLETLKLYDFFPSCDMRKDLRLALSVTETVAF
SHCCLNPLIYAFAGEKFRRYLYHLYGKCLAVLCGRSVHVDFSSSESQRSRHGSVLSSNFTYHT
SDGDALLLL

Function of CX3CR1 Membrane Protein

CX3CR1 is a receptor for the fractalkine ligand that is a transmembrane protein involved in the adhesion and migration of leukocytes. Moreover, CX3CR1 also plays a major role in the regulatory mechanism for pancreatic islet beta cell function and insulin secretion. Besides, the results have found that CX3CR1 controls the clearance of entero-invasive pathogens by dendritic cells (DCs). Thus, it is also suggested that CX3CR1 may be associated with the regulation of immunological tolerance and inflammation. In addition, CX3CR1 also is a coreceptor for HIV-1, and the gene variations can lead to an increased susceptibility to HIV-1 infection and rapid progression to AIDS. Recent studies have also shown that CX3CR1 may participate in many pathological processes, including atherogenesis, dysplasia of the hip, amyotrophic lateral sclerosis, pancreatic adenocarcinoma, schizophrenia, autism spectrum disorders, IgA nephropathy.

CX3CR1 Membrane Protein Introduction Introduction of CX3CR1 Fig.1 Biological functions of fractalkine. (Umehara, 2004)

Application of CX3CR1 Membrane Protein in Literature

  1. Imgenberg-Kreuz J., et al. Transcription profiling of peripheral B cells in antibody-positive primary Sjögren's syndrome reveals upregulated expression of CX3CR1 and a type I and type II interferon signature. Scandinavian Journal of Immunology2018, 87(5):e12662. PubMed ID: 29655283

    The study shows that peripheral B cells from patients with anti-SSA antibody-positive primary Sjögren's syndrome increase the expression of CX3CR1, chemokines, and type I and type II interferon signature, while reduce cytokine signaling expression, displaying immune activation.

  2. Leonardi I., et al. CX3CR1+ mononuclear phagocytes control immunity to intestinal fungi. Science. 2018, 359(6372):232-236. PubMed ID: 29326275

    The authors identify that CX3CR1+ mononuclear phagocytes (MNPs) play a key role in the initiation of innate and adaptive immune responses to intestinal fungi. Lacking CX3CR1+ MNPs in mice results in the changes of gut fungal communities and severe colitis. And in Crohn's disease patients, a missense mutation in the gene CX3CR1 is associated with decreased antifungal responses.

  3. Stout M C., et al. Inhibition of CX3CR1 reduces cell motility and viability in pancreatic adenocarcinoma epithelial cells. Biochem Biophys Res Commun. 2018, 495(3):2264-2269. PubMed ID: 29274778

    It has been proved that increased expression of CX3CL1 and CX3CR1 are associated with metastasis of prostate and breast cancer in authors’ previous findings. In this study, authors find that CX3CL1 exposure can increase motility, invasion, and contact-independent growth of pancreatic ductal adenocarcinoma (PDAC) cells and CX3CR1 antagonism can reduce these phenotypes.

  4. Huang L., et al. Fractalkine/CX3CR1 axis modulated the development of pancreatic ductal adenocarcinoma via JAK/STAT signaling pathway. Biochem Biophys Res Commun. 2017, 493(4):1510-1517. PubMed ID: 28986258

    The study indicates the role of FKN/CX3CR1 in the regulation of PDAC growth. Results show that FKN and CX3CR1 expression is significantly increased in pancreatic ductal adenocarcinoma (PDAC) tissues, especially in the metastatic samples, and is highly correlated with the severity of PDAC. Ectopic expression of FKN promotes the proliferation and migration of PDAC, while knockdown of CX3CR1 reverse the function of FKN.

  5. O'Sullivan S A., et al. The chemokine fractalkine (CX3CL1) attenuates HO-induced demyelination in cerebellar slices. J Neuroinflammation. 2017, 14(1):159. PubMed ID: 28810923

    The research shows that chemokine fractalkine signaling may function protective role in demyelination induced by oxidative stress. These also suggest that fractalkine receptor (CX3CR1) may act as a potential target for protecting against oxidative stress-induced demyelination in both inflammatory and non-inflammatory nervous system disorders.

CX3CR1 Preparation Options

To obtain the soluble and functional target protein, the versatile Magic™ membrane protein production platform in Creative Biolabs enables many flexible options, from which you can always find a better match for your particular project. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-CX3CR1 antibody development services.


As a forward-looking research institute as well as a leading custom service provider in the field of membrane protein, Creative Biolabs has won good reputation among our worldwide customers for successfully accomplishing numerous challenging projects including generation of many functional membrane proteins. Please feel free to contact us for more information.

Reference

  1. Umehara H, et al. (2004). Fractalkine in vascular biology: from basic research to clinical disease. Arteriosclerosis Thrombosis & Vascular Biology. 24(1), 34-40.

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