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C8354

Sigma-Aldrich

Anti-CX3CR-1, N-Terminal antibody produced in rabbit

~1 mg/mL, affinity isolated antibody, buffered aqueous solution

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About This Item

MDL number:
UNSPSC Code:
51111800

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 50 kDa

species reactivity

rat, human, mouse

concentration

~1 mg/mL

technique(s)

immunohistochemistry: 2 μg/mL using human heart tissue
western blot: 0.5-1 μg/mL using human spleen tissue lysate

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

Gene Information

human ... CX3CR1(1524)
mouse ... Cx3cr1(13051)
rat ... Cx3cr1(171056)

General description

CX3CR1 is a fractalkaine receptor that regulates chemotaxis and adhesion in white blood cells . Impairment of CX3CR1 function has been associated with defects in hippocampal cognition and neuronal plasticity . Cells expressing CX3CR1 receptors inhibit T-cell proliferation and subsequently prevent intestinal inflammation . Anti-CX3CR-1, N-Terminal antibody is specific for CX3CR1 by immunoblotting using human spleen tissue lysate. The antibody also reacts with mouse and rat CX3CR1.

Immunogen

synthetic peptide corresponding to the N-terminal and amino acids 2-21 of human CX3CR1 (V28, CMKBRL1). This sequence differs from mouse and rat by four amino acids.

Application

Anti-CX3CR-1, N-Terminal antibody is suitable for use in immunoblot (approx. 50kDa), western blot (0.5-1 μg/ml) using human spleen lysate) and immunohistochemistry (~2 μg/mL using human heart tissue).

Physical form

Solution in 0.01 M phosphate buffered saline containing 0.02% sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


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Elif Kervancioglu Demirci et al.
Cell adhesion & migration, 10(1-2), 189-196 (2016-01-09)
Embryo implantation and subsequent placentation require a fine balanced fetal-maternal cross-talk of hormones, cytokines and chemokines. Amongst the group of chemokines, CX3CL1 (also known as fractalkine) has recently attracted attention in the field of reproductive research. It exists both as
Frank Ativie et al.
Frontiers in molecular neuroscience, 11, 295-295 (2018-09-14)
Microglia, the resident immune cells of the brain, play important roles in defending the brain against pathogens and supporting neuronal circuit plasticity. Chronic or excessive pro-inflammatory responses of microglia damage neurons, therefore their activity is tightly regulated. Pharmacological and genetic
Hisako Kayama et al.
Proceedings of the National Academy of Sciences of the United States of America, 109(13), 5010-5015 (2012-03-10)
Adequate activation of CD4(+) T lymphocytes is essential for host defense against invading pathogens; however, exaggerated activity of effector CD4(+) T cells induces tissue damage, leading to inflammatory disorders such as inflammatory bowel diseases. Several unique subsets of intestinal innate
Justin T Rogers et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 31(45), 16241-16250 (2011-11-11)
The protective/neurotoxic role of fractalkine (CX3CL1) and its receptor CX3C chemokine receptor 1 (CX3CR1) signaling in neurodegenerative disease is an intricate and highly debated research topic and it is becoming even more complicated as new studies reveal discordant results. It
Nicholas F Page et al.
Biological psychiatry, 89(9), 896-910 (2021-01-03)
Maternal immune activation (MIA) is a proposed risk factor for multiple neuropsychiatric disorders, including schizophrenia. However, the molecular mechanisms through which MIA imparts risk remain poorly understood. A recently developed nonhuman primate model of exposure to the viral mimic poly:ICLC

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