Mouse CXCL1/GRO alpha/KC/CINC-1 Antibody

R&D Systems | Catalog # AF-453-NA

R&D Systems
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Key Product Details

Species Reactivity

Validated:

Mouse

Cited:

Human, Mouse

Applications

Validated:

Western Blot, Neutralization

Cited:

Immunohistochemistry, Immunohistochemistry-Paraffin, Immunohistochemistry-Frozen, Western Blot, Neutralization, Flow Cytometry, Immunocytochemistry, In vivo assay

Label

Unconjugated

Antibody Source

Polyclonal Goat IgG
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Product Specifications

Immunogen

E. coli-derived recombinant mouse CXCL1/GRO alpha /KC/CINC-1
Arg20-Lys96
Accession # P12850

Specificity

Detects mouse CXCL1/GRO alpha /KC/CINC-1 in direct ELISAs and Western blots.

Clonality

Polyclonal

Host

Goat

Isotype

IgG

Endotoxin Level

<0.10 EU per 1 μg of the antibody by the LAL method.

Scientific Data Images for Mouse CXCL1/GRO alpha/KC/CINC-1 Antibody

Chemotaxis Induced by CXCL1/KC and Neutralization by Mouse CXCL1/KC Antibody.

Chemotaxis Induced by CXCL1/KC and Neutralization by Mouse CXCL1/KC Antibody.

Recombinant Mouse CXCL1/KC (453-KC) chemoattracts the BaF3 mouse pro-B cell line transfected with human CXCR2 in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was measured by Resazurin (AR002). Chemotaxis elicited by Recombinant Mouse CXCL1/KC (30 ng/mL) is neutralized (green line) by increasing concentrations of Goat Anti-Mouse CXCL1/KC Antigen Affinity-purified Polyclonal Antibody (Catalog # AF-453-NA). The ND50 is typically 0.3-1.5 µg/mL.
Mouse CXCL1 / GRO alpha / KC / CINC-1 ELISA Standard Curve

Mouse CXCL1 / GRO alpha / KC / CINC-1 ELISA Standard Curve

Recombinant Mouse CXCL1/GRO alpha /KC/CINC‑1 aa 20-96 (Catalog # 453-KC) was serially diluted and captured by Rat Anti-Mouse CXCL1/GRO alpha /KC/CINC‑1 Monoclonal Antibody (Catalog # MAB453) coated on a Clear Polystyrene Microplate (Catalog # DY990). Goat Anti-Mouse CXCL1/GRO alpha /KC/CINC‑1 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF-453-NA) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998)
Detection of jn090xqgax6wba8rkwla.jpg by Western Blot

Detection of jn090xqgax6wba8rkwla.jpg by Western Blot

Effects of OSM on the protein expression of exercise-induced chemokines in the skeletal muscle.A, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of sedentary mice (Sed [1 h] + 2 h) and mice at 2 h after the exercise (Ex [1 h] + 2 h). The apparent molecular weights are indicated on the right. B, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of sedentary mice in the bar graph. C, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of WT and OSM−/− mice at 2 h after the exercise. The apparent molecular weights are indicated on the right. D, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of WT mice in the bar graph. E, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of mice at 2 h after the injection of vehicle (Veh) or OSM. F, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of Veh group in the bar graph. Data are expressed as mean ± SD; n = 5 per group. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. Student’s t test. CCL, CC chemokine ligand; CXCL1, CXC chemokine ligand 1; OSM, oncostatin M. Image collected and cropped by CiteAb from the following open publication (https://linkinghub.elsevier.com/retrieve/pii/S0021925822011292), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of CXCL1/KC by Western Blot

Detection of CXCL1/KC by Western Blot

Effects of OSM on the protein expression of exercise-induced chemokines in the skeletal muscle.A, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of sedentary mice (Sed [1 h] + 2 h) and mice at 2 h after the exercise (Ex [1 h] + 2 h). The apparent molecular weights are indicated on the right. B, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of sedentary mice in the bar graph. C, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of WT and OSM−/− mice at 2 h after the exercise. The apparent molecular weights are indicated on the right. D, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of WT mice in the bar graph. E, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of mice at 2 h after the injection of vehicle (Veh) or OSM. F, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of Veh group in the bar graph. Data are expressed as mean ± SD; n = 5 per group. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. Student’s t test. CCL, CC chemokine ligand; CXCL1, CXC chemokine ligand 1; OSM, oncostatin M. Image collected and cropped by CiteAb from the following open publication (https://linkinghub.elsevier.com/retrieve/pii/S0021925822011292), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of CXCL1/KC by Immunohistochemistry

Detection of CXCL1/KC by Immunohistochemistry

Pericyte ICAM-1 and CXCL1 expression is increased in vessels with MCs but total expression is not impacted by IL-17A.a–d Cremaster muscles of WT or IL-17AKO mice were stimulated with TNF (300 ng) or PBS for 4 h. Cremaster muscles were collected and immunostained for MCs (avidin), pericytes ( alpha -SMA) and ICAM-1 or CXCL1. a–b Images of venules showing a ICAM-1 or b CXCL1 expression (pseudocolour intensity gradient) on pericytes (purple) and MCs (cyan), dashed lines the limit of MC, scale bars, 5 µm. c, d Quantification of c ICAM-1 MFI (n = 6 WT, n = 5 IL-17AKO mice) and d CXCL1 MFI (n = 5 mice) on pericytes. e, f Cremaster muscles of WT mice were stimulated with TNF (300 ng) or PBS in combination with a blocking anti-IL-17A or control mAbs (50 µg) for 4 h. e, f Quantification of e ICAM-1 MFI (n = 6 PBS Ctrl mAb, n = 9 TNF Ctrl mAb, n = 6 PBS Anti-IL-17A mAb, n = 9 TNF anti-IL-17A mAb mice) and f CXCL1 MFI (n = 4 PBS Ctrl mAb, n = 6 TNF Ctrl mAb, n = 4 PBS Anti-IL-17A mAb, n = 6 TNF anti-IL-17A mAb mice). Mean ± SEM (each mouse represents one independent experiment). c–f two-way ANOVA followed by Sidak’s post-hoc test. *p < 0.05, **p < 0.01, ***p < 0.001 as compared to WT or ctrl mAb (ns = not significant). 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/36396641), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of CXCL1/KC by Western Blot

Detection of CXCL1/KC by Western Blot

Effects of OSM on the protein expression of exercise-induced chemokines in the skeletal muscle.A, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of sedentary mice (Sed [1 h] + 2 h) and mice at 2 h after the exercise (Ex [1 h] + 2 h). The apparent molecular weights are indicated on the right. B, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of sedentary mice in the bar graph. C, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of WT and OSM−/− mice at 2 h after the exercise. The apparent molecular weights are indicated on the right. D, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of WT mice in the bar graph. E, Western blot analysis of CCL2, CCL7, and CXCL1 in the skeletal muscle of mice at 2 h after the injection of vehicle (Veh) or OSM. F, quantitative analysis of the protein expression of CCL2, CCL7, and CXCL1. The band intensities of CCL2, CCL7, and CXCL1 were normalized to beta -tubulin and are represented as the fold induction relative to the intensities of Veh group in the bar graph. Data are expressed as mean ± SD; n = 5 per group. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. Student’s t test. CCL, CC chemokine ligand; CXCL1, CXC chemokine ligand 1; OSM, oncostatin M. Image collected and cropped by CiteAb from the following open publication (https://linkinghub.elsevier.com/retrieve/pii/S0021925822011292), licensed under a CC-BY license. Not internally tested by R&D Systems.

Applications for Mouse CXCL1/GRO alpha/KC/CINC-1 Antibody

Application
Recommended Usage

Western Blot

0.1 µg/mL
Sample: Recombinant Mouse CXCL1/GRO alpha /KC/CINC‑1 aa 20-96 (Catalog # 453-KC)

Neutralization

Measured by its ability to neutralize CXCL1/GRO alpha /KC/CINC‑1-induced chemotaxis in the BaF3 mouse pro‑B cell line transfected with human CXCR2. The Neutralization Dose (ND50) is typically 0.3-1.5 µg/mL in the presence of 30 ng/mL Recombinant Mouse CXCL1/GRO alpha /KC/CINC‑1 aa 20‑96.

Formulation, Preparation, and Storage

Purification

Antigen Affinity-purified

Reconstitution

Reconstitute at 0.2 mg/mL in sterile PBS. For liquid material, refer to CoA for concentration.


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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.

Shipping

Lyophilized product is shipped at ambient temperature. Liquid small pack size (-SP) is shipped with polar packs. Upon receipt, store immediately at the temperature recommended below.

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.

Calculators

The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial. Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.

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Background: CXCL1/GRO alpha/KC/CINC-1

KC, a member of the alpha (CXC) chemokine subfamily, was initially identified as an immediate early gene induced in mouse fibroblasts by platelet-derived growth factor. KC cDNA encodes a 96 amino acid (aa) residue precursor protein with a predicted secretory signal peptide that is removed to yield the mature protein. The protein sequence of mouse KC shows approximately 63% identity to that of mouse MIP-2. KC is also approximately 60% identical to the human GROs. It has been suggested that mouse KC and MIP-2 are the orthologs of the human GROs and rat CINCs. In addition to mouse fibroblasts, KC is expressed in macrophages and endothelial cells. Mouse KC is a potent neutrophil attractant and activator. The functional receptor for KC has been identified as CXCR2. Based on the pattern of KC expression in a number of inflammatory disease models, KC appears to have an important role in inflammation. KC was found to be involved in monocyte arrest on atherosclerotic endothelium and may also play a pathophysiological role in Alzheimer’s disease. Many chemokines are substrates for selective proteolysis at the amino-terminus by various proteases including dipeptidyl peptidase IV or matrix metalloproteases, resulting in truncated chemokine isoforms with different (both enhanced or reduced) bioactivities. The naturally occurring 68 aa N-terminal truncated isoform of mouse KC is reported to be a more potent synergistic growth stimulants for CFU-GM.

Alternate Names

CINC-1, CINC1, GRO alpha, KC, MGSA-alpha

Entrez Gene IDs

2919 (Human); 14825 (Mouse); 81503 (Rat)

Gene Symbol

CXCL1

UniProt

Additional CXCL1/GRO alpha/KC/CINC-1 Products

Product Documents for Mouse CXCL1/GRO alpha/KC/CINC-1 Antibody

Certificate of Analysis

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Product Specific Notices for Mouse CXCL1/GRO alpha/KC/CINC-1 Antibody

For research use only

Citations for Mouse CXCL1/GRO alpha/KC/CINC-1 Antibody

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