Mouse CX3CL1/Fractalkine Chemokine Domain Antibody

Catalog # Availability Size / Price Qty
AF472
AF472-SP

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Chemotaxis Induced by CX3CL1/Fractalkine and Neutralization by Mouse CX3CL1/Fractalkine Antibody.
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Mouse CX3CL1/Fractalkine Chemokine Domain Antibody Summary

Species Reactivity
Mouse
Specificity
Detects mouse Fractalkine in direct ELISAs and Western blots. In direct ELISAs, less than 40% cross-reactivity with recombinant human Fractalkine and recombinant rat Fractalkine is observed.
Source
Polyclonal Goat IgG
Purification
Antigen Affinity-purified
Immunogen
E. coli-derived recombinant mouse CX3CL1/Fractalkine
Leu22-Lys105
Accession # O35188
Formulation
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.
Endotoxin Level
<0.10 EU per 1 μg of the antibody by the LAL method.
Label
Unconjugated

Applications

Recommended Concentration
Sample
Western Blot
0.1 µg/mL
Recombinant Mouse CX3CL1/Fractalkine Full Length
Neutralization
Measured by its ability to neutralize CX3CL1/Fractalkine-induced chemotaxis in the BaF3 mouse pro‑B cell line transfected with human CX3CR1. The Neutralization Dose (ND50) is typically 0.3-1.5 µg/mL in the presence of 30 ng/mL Recombinant Mouse CX3CL1/Fractalkine aa 25‑105.

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

Scientific Data

Neutralization Chemotaxis Induced by CX3CL1/Fractalkine and Neutralization by Mouse CX3CL1/Fractalkine Antibody. View Larger

Chemotaxis Induced by CX3CL1/Fractalkine and Neutralization by Mouse CX3CL1/Fractalkine Antibody. Recombinant Mouse CX3CL1/Fractalkine (Catalog # 571-MF) chemoattracts the BaF3 mouse pro-B cell line transfected with human CX3CR1 in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by Resazurin (Catalog # AR002). Chemotaxis elicited by Recombinant Mouse CX3CL1/Fractalkine (30 ng/mL) is neutralized (green line) by increasing concentrations of Goat Anti-Mouse CX3CL1/Fractalkine Chemokine Domain Antigen Affinity-purified Polyclonal Antibody (Catalog # AF472). The ND50 is typically 0.3-1.5 µg/mL.

Western Blot Detection of Mouse CX3CL1/Fractalkine by Western Blot View Larger

Detection of Mouse CX3CL1/Fractalkine by Western Blot Cardiomyocyte-specific ADAM10/CX3CL1 signaling regulates neutrophil migration.a Immunofluorescence images and b quantification of CX3CL1, cardiac Troponin T (cTnT, cardiomyocytes, CM) and CD31 (endothelial cells, EC) stained heart tissue sections of sham-operated (Sham) and LAD-ligated (MI) mice 14 days after surgery. Nuclei are stained with DAPI. Representative images are shown. Scale bar, 20 µm. n = 4 per group, mean ± SEM, ns not significant, two-tailed Mann–Whitney test with Dunn’s posttest. c Co-immunoprecipitation of endogenous ADAM10 (A10) and CX3CL1 from whole-cell lysates of HL-1 cells. Representative western blots are shown (n = 4). IgG, immunoglobulin G as a control. WCL, whole-cell lysate. d Western blot analysis of CX3CL1 and e quantification of CX3CL1 expression (n = 6 per group, mean ± SEM, ns not significant, **P < 0.01, ***P < 0.001, one-way ANOVA with Tukey’s posttest) as well as f ectodomain shedding (CX3CL1 levels in supernatant) in normoxic as well as GI254023X (A10i) and DMSO treated hypoxic (1% O2) mouse cardiomyocytes (HL-1) (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest, exact P-values are provided in the Source Data file). g Treatment scheme. HL-1 cells were cultured for 3 h under normoxic or hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3CL1). Supernatants were used in the lower chamber and 3 × 105 freshly isolated mouse bone marrow derived neutrophils or macrophages were seeded in the upper chamber of transwell plates (8 µm pore size) to determine migration capacity. The scheme was created using Servier Medical Art (available online: http://smart.servier.com). h Western blot analysis and i quantification of CX3CL1 expression in HL-1 cells treated for 48 h with unspecific control siRNA (siC) or CX3CL1-specific siRNA (siCX3#1 and siCX3#2). Representative western blots (n = 3 per group, mean ± SEM, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest) are shown. Exact P-values: siC vs. siCX3#1, 0.0043. siC vs. siCX3#2, 0.005. Transwell migration assays of bone marrow derived j neutrophils and k macrophages using the supernatants of HL-1 cells that were cultured under hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3#1 and CX3#2) as chemoattractant (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest). Source data and exact P-values are provided in the Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36496449), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Mouse CX3CL1/Fractalkine by Western Blot View Larger

Detection of Mouse CX3CL1/Fractalkine by Western Blot Cardiomyocyte-specific ADAM10/CX3CL1 signaling regulates neutrophil migration.a Immunofluorescence images and b quantification of CX3CL1, cardiac Troponin T (cTnT, cardiomyocytes, CM) and CD31 (endothelial cells, EC) stained heart tissue sections of sham-operated (Sham) and LAD-ligated (MI) mice 14 days after surgery. Nuclei are stained with DAPI. Representative images are shown. Scale bar, 20 µm. n = 4 per group, mean ± SEM, ns not significant, two-tailed Mann–Whitney test with Dunn’s posttest. c Co-immunoprecipitation of endogenous ADAM10 (A10) and CX3CL1 from whole-cell lysates of HL-1 cells. Representative western blots are shown (n = 4). IgG, immunoglobulin G as a control. WCL, whole-cell lysate. d Western blot analysis of CX3CL1 and e quantification of CX3CL1 expression (n = 6 per group, mean ± SEM, ns not significant, **P < 0.01, ***P < 0.001, one-way ANOVA with Tukey’s posttest) as well as f ectodomain shedding (CX3CL1 levels in supernatant) in normoxic as well as GI254023X (A10i) and DMSO treated hypoxic (1% O2) mouse cardiomyocytes (HL-1) (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest, exact P-values are provided in the Source Data file). g Treatment scheme. HL-1 cells were cultured for 3 h under normoxic or hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3CL1). Supernatants were used in the lower chamber and 3 × 105 freshly isolated mouse bone marrow derived neutrophils or macrophages were seeded in the upper chamber of transwell plates (8 µm pore size) to determine migration capacity. The scheme was created using Servier Medical Art (available online: http://smart.servier.com). h Western blot analysis and i quantification of CX3CL1 expression in HL-1 cells treated for 48 h with unspecific control siRNA (siC) or CX3CL1-specific siRNA (siCX3#1 and siCX3#2). Representative western blots (n = 3 per group, mean ± SEM, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest) are shown. Exact P-values: siC vs. siCX3#1, 0.0043. siC vs. siCX3#2, 0.005. Transwell migration assays of bone marrow derived j neutrophils and k macrophages using the supernatants of HL-1 cells that were cultured under hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3#1 and CX3#2) as chemoattractant (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest). Source data and exact P-values are provided in the Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36496449), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Mouse CX3CL1/Fractalkine by Western Blot View Larger

Detection of Mouse CX3CL1/Fractalkine by Western Blot Cardiomyocyte-specific ADAM10 KO improves post-MI cardiac function.a–c Echocardiographic assessment of fractional area shortening, ejection fraction and left ventricular end-systolic interior diameter in 8-week-old ADAM10fl/fl (WT) and ( alpha MHC-Cre) ADAM10 KO mice under a basal conditions (WT, n = 7, KO, n = 8, mean ± SEM, ns not significant) as well as b 3 days (WT, n = 8, KO, n = 9, mean ± SEM, ns not significant, *P < 0.05, two-tailed t test) and c 14 days after myocardial infarction (WT, n = 6, KO, n = 9, mean ± SEM, ns not significant, *P < 0.05, two-tailed t test, exact P-values are provided in the Source Data file). d Representative end-systolic B-mode and M-mode echocardiograms of ADAM10 WT and ADAM10 KO mice 14 days after myocardial infarction. e Western blot analysis and f quantification of ADAM10, CX3CL1 and IL-1 beta expression in heart tissue lysates of ADAM10 WT and ADAM10 KO mice 3 days after myocardial infarction (n = 6, mean ± SEM, ns not significant, *P < 0.05, **P < 0.01, two-tailed t test). Exact P-values: ADAM10, 0.0159. CX3CL1, 0.0084. IL-1 beta, 0.0317. g Analysis of leukocyte counts in blood samples of ADAM10 WT (n = 8) and ADAM10 KO (n = 7) mice (mean ± SEM, ns not significant, *P < 0.05, two-tailed t test). Exact P-values: Neutrophils, 0.0404. Eosinophils, 0.7886. Monocytes, 0.3373. Lymphocytes, 0.751. h Analysis of leukocyte counts in the infarcted area/ infarct border zone of ADAM10 WT (n = 8) and ADAM10 KO (n = 7) mice (mean ± SEM, ns not significant, *P < 0.05, two-tailed two-tailed t test). Exact P-values: Neutrophils, 0.0214. Eosinophils, 0.176. Monocytes, 0.639. Macrophages, 0.6064. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36496449), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Mouse CX3CL1/Fractalkine by Western Blot View Larger

Detection of Mouse CX3CL1/Fractalkine by Western Blot Cardiomyocyte-specific ADAM10/CX3CL1 signaling regulates neutrophil migration.a Immunofluorescence images and b quantification of CX3CL1, cardiac Troponin T (cTnT, cardiomyocytes, CM) and CD31 (endothelial cells, EC) stained heart tissue sections of sham-operated (Sham) and LAD-ligated (MI) mice 14 days after surgery. Nuclei are stained with DAPI. Representative images are shown. Scale bar, 20 µm. n = 4 per group, mean ± SEM, ns not significant, two-tailed Mann–Whitney test with Dunn’s posttest. c Co-immunoprecipitation of endogenous ADAM10 (A10) and CX3CL1 from whole-cell lysates of HL-1 cells. Representative western blots are shown (n = 4). IgG, immunoglobulin G as a control. WCL, whole-cell lysate. d Western blot analysis of CX3CL1 and e quantification of CX3CL1 expression (n = 6 per group, mean ± SEM, ns not significant, **P < 0.01, ***P < 0.001, one-way ANOVA with Tukey’s posttest) as well as f ectodomain shedding (CX3CL1 levels in supernatant) in normoxic as well as GI254023X (A10i) and DMSO treated hypoxic (1% O2) mouse cardiomyocytes (HL-1) (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest, exact P-values are provided in the Source Data file). g Treatment scheme. HL-1 cells were cultured for 3 h under normoxic or hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3CL1). Supernatants were used in the lower chamber and 3 × 105 freshly isolated mouse bone marrow derived neutrophils or macrophages were seeded in the upper chamber of transwell plates (8 µm pore size) to determine migration capacity. The scheme was created using Servier Medical Art (available online: http://smart.servier.com). h Western blot analysis and i quantification of CX3CL1 expression in HL-1 cells treated for 48 h with unspecific control siRNA (siC) or CX3CL1-specific siRNA (siCX3#1 and siCX3#2). Representative western blots (n = 3 per group, mean ± SEM, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest) are shown. Exact P-values: siC vs. siCX3#1, 0.0043. siC vs. siCX3#2, 0.005. Transwell migration assays of bone marrow derived j neutrophils and k macrophages using the supernatants of HL-1 cells that were cultured under hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3#1 and CX3#2) as chemoattractant (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest). Source data and exact P-values are provided in the Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36496449), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Mouse CX3CL1/Fractalkine by Western Blot View Larger

Detection of Mouse CX3CL1/Fractalkine by Western Blot Cardiomyocyte-specific ADAM10/CX3CL1 signaling regulates neutrophil migration.a Immunofluorescence images and b quantification of CX3CL1, cardiac Troponin T (cTnT, cardiomyocytes, CM) and CD31 (endothelial cells, EC) stained heart tissue sections of sham-operated (Sham) and LAD-ligated (MI) mice 14 days after surgery. Nuclei are stained with DAPI. Representative images are shown. Scale bar, 20 µm. n = 4 per group, mean ± SEM, ns not significant, two-tailed Mann–Whitney test with Dunn’s posttest. c Co-immunoprecipitation of endogenous ADAM10 (A10) and CX3CL1 from whole-cell lysates of HL-1 cells. Representative western blots are shown (n = 4). IgG, immunoglobulin G as a control. WCL, whole-cell lysate. d Western blot analysis of CX3CL1 and e quantification of CX3CL1 expression (n = 6 per group, mean ± SEM, ns not significant, **P < 0.01, ***P < 0.001, one-way ANOVA with Tukey’s posttest) as well as f ectodomain shedding (CX3CL1 levels in supernatant) in normoxic as well as GI254023X (A10i) and DMSO treated hypoxic (1% O2) mouse cardiomyocytes (HL-1) (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest, exact P-values are provided in the Source Data file). g Treatment scheme. HL-1 cells were cultured for 3 h under normoxic or hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3CL1). Supernatants were used in the lower chamber and 3 × 105 freshly isolated mouse bone marrow derived neutrophils or macrophages were seeded in the upper chamber of transwell plates (8 µm pore size) to determine migration capacity. The scheme was created using Servier Medical Art (available online: http://smart.servier.com). h Western blot analysis and i quantification of CX3CL1 expression in HL-1 cells treated for 48 h with unspecific control siRNA (siC) or CX3CL1-specific siRNA (siCX3#1 and siCX3#2). Representative western blots (n = 3 per group, mean ± SEM, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest) are shown. Exact P-values: siC vs. siCX3#1, 0.0043. siC vs. siCX3#2, 0.005. Transwell migration assays of bone marrow derived j neutrophils and k macrophages using the supernatants of HL-1 cells that were cultured under hypoxic conditions in parallel to A10i or DMSO treatment in combination with unspecific control siRNA (siC) or CX3CL1 depletion (siCX3#1 and CX3#2) as chemoattractant (n = 3 per group, mean ± SEM, ns not significant, **P < 0.01, Kruskal–Wallis test with Dunn’s posttest). Source data and exact P-values are provided in the Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36496449), licensed under a CC-BY license. Not internally tested by R&D Systems.

Reconstitution Calculator

Reconstitution Calculator

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Preparation and Storage

Reconstitution
Reconstitute at 0.2 mg/mL in sterile PBS.
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Shipping
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 6 months, -20 to -70 °C under sterile conditions after reconstitution.

Background: CX3CL1/Fractalkine

CX3CL1/Fractalkine is a transmembrane adhesion protein with a chemokine domain separated from the membrane by a mucin stalk. It is upregulated on many cell types during inflammation. The chemokine and mucin regions can be shed as a soluble chemokine that signals through the receptor CX3CR1. During extravasation, membrane-bound CX3CL1 traps leukocytes, then is cleaved to allow diapedesis. Soluble CX3CL1 protects neurons from microglial neurotoxicity, recruits macrophages for wound healing, recruits osteoclast precursors for bone resorption, and contributes to pathogenesis in coronary artery disease.

Entrez Gene IDs
6376 (Human); 20312 (Mouse); 89808 (Rat); 102117496 (Cynomolgus Monkey)
Alternate Names
ABCD-3; C3Xkine; chemokine (C-X3-C motif) ligand 1; CX3C membrane-anchored chemokine; CX3CL1; CXC3; CXC3C; FKN; Fractalkine; Neurotactin; neurotactin); NTNsmall inducible cytokine subfamily D (Cys-X3-Cys), member 1 (fractalkine; NTTSmall-inducible cytokine D1; SCYD1C-X3-C motif chemokine 1; small inducible cytokine subfamily D (Cys-X3-Cys), member-1

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Citations for Mouse CX3CL1/Fractalkine Chemokine Domain Antibody

R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.

18 Citations: Showing 1 - 10
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  1. Glabridin Therapy Reduces Chronic Allodynia, Spinal Microgliosis, and Dendritic Spine Generation by Inhibiting Fractalkine-CX3CR1 Signaling in a Mouse Model of Tibial Fractures
    Authors: Long, J;Liu, H;Qiu, Z;Xiao, Z;Lu, Z;
    Brain sciences
    Species: Mouse
    Sample Types: In Vivo
    Applications: In Vivo
  2. Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction
    Authors: E Klapproth, A Witt, P Klose, J Wiedemann, N Vavilthota, SR Künzel, S Kämmerer, M Günscht, D Sprott, M Lesche, F Rost, A Dahl, E Rauch, L Kattner, S Weber, P Mirtschink, I Kopaliani, K Guan, K Lorenz, P Saftig, M Wagner, A El-Armouch
    Nature Communications, 2022-12-10;13(1):7648.
    Species: Mouse
    Sample Types: Cell Lysates
    Applications: Western Blot
  3. Diet-Induced Obesity Promotes Liver Metastasis of Pancreatic Ductal Adenocarcinoma via CX3CL1/CX3CR1 Axis
    Authors: Y Sun, XX Zhang, S Huang, H Pan, YZ Gai, YQ Zhou, L Zhu, HZ Nie, DX Li
    Journal of Immunology Research, 2022-04-18;2022(0):5665964.
    Species: Mouse
    Sample Types: Whole Cells
    Applications: Bioassay
  4. Compromised fractalkine signaling delays microglial occupancy of emerging modules in the multisensory midbrain
    Authors: Cooper A. Brett, Julianne B. Carroll, Mark L. Gabriele
    Glia
  5. Experimental Trypanosoma cruzi Infection Induces Pain in Mice Dependent on Early Spinal Cord Glial Cells and NF kappa B Activation and Cytokine Production
    Authors: Sergio M. Borghi, Victor Fattori, Thacyana T. Carvalho, Vera L. H. Tatakihara, Tiago H. Zaninelli, Felipe A. Pinho-Ribeiro et al.
    Frontiers in Immunology
  6. Contribution of spinal cord glial cells to L. amazonensis experimental infection-induced pain in BALB/c mice
    Authors: Sergio M. Borghi, Victor Fattori, Felipe A. Pinho-Ribeiro, Talita P. Domiciano, Milena M. Miranda-Sapla, Tiago H. Zaninelli et al.
    Journal of Neuroinflammation
  7. Dynamic changes of CX3CL1/CX3CR1 axis during microglial activation and motor neuron loss in the spinal cord of ALS mouse model
    Authors: Jingjing Zhang, Yufei Liu, Xinyao Liu, Song Li, Cheng Cheng, Sheng Chen et al.
    Translational Neurodegeneration
  8. Absence of CX3CR1 impairs the internalization of Tau by microglia
    Authors: M Bolós, M Llorens-Ma, JR Perea, J Jurado-Arj, A Rábano, F Hernández, J Avila
    Mol Neurodegener, 2017-08-15;12(1):59.
    Species: Mouse
    Sample Types: Whole Tissue
    Applications: IHC
  9. PGI2 Controls Pulmonary NK Cells That Prevent Airway Sensitization to House Dust Mite Allergen
    Authors: Bryan Simons
    J. Immunol, 2016-11-28;0(0):.
    Species: Mouse
    Sample Types: Whole Tissue
    Applications: IHC-P
  10. CXCR4+CD45- cells are niche forming for osteoclastogenesis via the SDF-1, CXCL7, and CX3CL1 signaling pathways in bone marrow
    Authors: Yoh Goto
    Stem Cells, 2016-07-08;0(0):.
    Species: Mouse
    Sample Types: Whole Cells
    Applications: Neutralization
  11. P2RX7 sensitizes Mac-1/ICAM-1-dependent leukocyte-endothelial adhesion and promotes neurovascular injury during septic encephalopathy.
    Authors: Wang H, Hong L, Huang J, Jiang Q, Tao R, Tan C, Lu N, Wang C, Ahmed M, Lu Y, Liu Z, Shi W, Lai E, Wilcox C, Han F
    Cell Res, 2015-05-22;25(6):674-90.
    Species: Mouse
    Sample Types: In Vivo
    Applications: Neutralization
  12. Interaction between CX3CL1 and CX3CR1 regulates vasculitis induced by immune complex deposition.
    Authors: Morimura S, Sugaya M, Sato S
    Am J Pathol, 2013-03-05;182(5):1640-7.
    Species: Mouse
    Sample Types: Whole Tissue
    Applications: IHC
  13. Fractalkine/CX3CL1 protects striatal neurons from synergistic morphine and HIV-1 Tat-induced dendritic losses and death
    Authors: Masami Suzuki, Nazira El-Hage, Shiping Zou, Yun-Kyung Hahn, Mary E Sorrell, Jamie L Sturgill et al.
    Molecular Neurodegeneration
  14. Comprehensive assessment of chemokine expression profiles by flow cytometry.
    Authors: Eberlein J, Nguyen TT, Victorino F, Golden-Mason L, Rosen HR, Homann D
    J. Clin. Invest., 2010-02-08;120(3):907-23.
    Species: Mouse
    Sample Types: Whole Cells
    Applications: Flow Cytometry
  15. Essential involvement of CX3CR1-mediated signals in the bactericidal host defense during septic peritonitis.
    Authors: Ishida Y, Hayashi T, Goto T, Kimura A, Akimoto S, Mukaida N, Kondo T
    J. Immunol., 2008-09-15;181(6):4208-18.
    Species: Mouse
    Sample Types: Whole Cells
    Applications: ICC
  16. Chemokine receptor CX3CR1 mediates skin wound healing by promoting macrophage and fibroblast accumulation and function.
    Authors: Ishida Y, Gao JL, Murphy PM
    J. Immunol., 2008-01-01;180(1):569-79.
    Species: Mouse
    Sample Types: Whole Tissue
    Applications: IHC, IHC-P
  17. Down-regulation of surface fractalkine by RNA interference in B16 melanoma reduced tumor growth in mice.
    Authors: Ren T, Chen Q, Tian Z, Wei H
    Biochem. Biophys. Res. Commun., 2007-10-29;364(4):978-84.
    Species: Mouse
    Sample Types: Cell Lysates, Whole Cells, Whole Tissue
    Applications: Flow Cytometry, ICC, IHC-P, Western Blot
  18. Intervention of MAdCAM-1 or fractalkine alleviates graft-versus-host reaction associated intestinal injury while preserving graft-versus-tumor effects.
    Authors: Ueha S, Murai M, Yoneyama H, Kitabatake M, Imai T, Shimaoka T, Yonehara S, Ishikawa S, Matsushima K
    J. Leukoc. Biol., 2006-10-19;81(1):176-85.
    Species: Mouse
    Sample Types: Whole Tissue
    Applications: IHC

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