F1300
Fractalkine, Chemokine Domain human
≥97% (SDS-PAGE), recombinant, expressed in E. coli, lyophilized powder
Synonym(s):
CX3CL-1, Neurotactin
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About This Item
MDL number:
UNSPSC Code:
51111800
biological source
human
recombinant
expressed in E. coli
assay
≥97% (SDS-PAGE)
form
lyophilized powder
potency
1.2 ng/mL
mol wt
~8.5 kDa
storage condition
avoid repeated freeze/thaw cycles
impurities
endotoxin, tested
UniProt accession no.
storage temp.
−20°C
Gene Information
human ... CX3CL1(6376)
General description
CX3CL1 (chemokine (C-X3-C motif) ligand 1) or fractalkine is a membrane protein, which is the only member of CXC3 family. Its chemokine domain (CKD) anchors it to the cell membrane through its mucin-like stalk. It acts as a ligand for the G-protein coupled receptor CX3CR1, which is found on smooth muscle cells, T-cells, natural killer (NK) cells and monocytes. Fractalkine is expressed on epithelial, endothelial and smooth muscle cells and neurons.[1]
Biochem/physiol Actions
CX3CL1 (chemokine (C-X3-C motif) ligand 1) or fractalkine, along with CX3CR1, is involved in various disorders such as atherosclerosis, multiple sclerosis, neuropathic pain and rheumatic disorders. It facilitates the proliferation and survival of primary human vascular smooth muscle cells in an epidermal growth factor receptor (EGR)-dependent manner. It plays an essential role in cell survival and promotes the survival of cells such as monocytes, T-cells and microglia. In humans, it is thought be involved in atherogenesis, and thus, might have potential as a target in treatment of cardiovascular disease.[1] In patients with sickle cell disease (SCD), the serum levels of this chemokine is increased, thus implicating it in the pathogenesis of inflammation associated with SCD.[2]
Leukocyte chemoattractant protein and member of the chemokine superfamily possessing a CX3C motif. The soluble chemokine domain of human fractalkine is reported to chemoattract T cells and monocytes.
Physical form
Lyophilized from a 0.2 μm filtered solution in 30% acetonitrile and 0.1% trifluoroacetic acid containing 1.25 mg bovine serum albumin.
Analysis Note
The biological activity is measured by its ability to flux calcium or chemoattract mouse BaF/3 cells transfected with hCX3CR1 cells with the ec50 range of 0.3-1.5 ng/ml. Fractalkine can also chemoattract freshly isolated peripheral blood lymphocytes.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Murali Ganesan et al.
Biomolecules, 9(12) (2019-12-15)
In an era of improved survival due to modern antiretroviral therapy, liver disease has become a major cause of morbidity and mortality, resulting in death in 15-17% of human immunodeficiency virus (HIV)-infected patients. Alcohol enhances HIV-mediated liver damage and promotes
Gemma E White et al.
Arteriosclerosis, thrombosis, and vascular biology, 34(12), 2554-2562 (2014-11-02)
The CX3C chemokine fractalkine (CX3CL1) has a critical role in the development of atherogenesis because apolipoprotein-E-deficient mice lacking CX3CL1 or its receptor CX3CR1 develop smaller plaques and polymorphisms in CX3CR1 are associated with altered risk of cardiovascular disease. CX3CR1 is
Selma Unal et al.
International journal of hematology, 101(2), 114-118 (2014-12-07)
In the present study, we examined the role of fractalkine (Fkn), a member of the chemokine family, in the pathogenesis of sickle cell disease (SCD). Eighty-seven children with sickle cell disease and 55 healthy children were enrolled in the study.
Takuya Tomita et al.
Nature communications, 11(1), 2019-2019 (2020-04-26)
Retinoblastoma protein (Rb) is a tumor suppressor that binds and represses E2F transcription factors. In cervical cancer cells, human papilloma virus (HPV) protein E7 binds to Rb, releasing it from E2F to promote cell cycle progression, and inducing ubiquitination of
Zhe Sha et al.
The Journal of cell biology, 217(5), 1757-1776 (2018-03-15)
Proteasome inhibitors are used as research tools and to treat multiple myeloma, and proteasome activity is diminished in several neurodegenerative diseases. We therefore studied how cells compensate for proteasome inhibition. In 4 h, proteasome inhibitor treatment caused dramatic and selective
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