• Species Reactivity

  Mouse

• Specificity

  Detects mouse CXCL1/GRO alpha /KC/CINC‑1 in direct ELISAs.    
   

• Source

  Monoclonal Rabbit IgG Clone # 1174A

• Immunogen

  E. coli-derived recombinant mouse CXCL1/GRO alpha /KC/CINC‑1    
  Asn29-Lys96    
  Accession # P12850

• Formulation

  Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.

• Label

  Alexa Fluor 405

Applications

• 
  

  Recommended    
  Concentration

  Sample

• Intracellular Staining by Flow Cytometry

  0.25-1 µg/10    ⁶ cells

  Mouse splenocytes treated with LPS and Brefeldin A were fixed and permeabilized with FlowX FoxP3 Fixation & Permeabilization Buffer Kit (Catalog # )

• 
  

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

Preparation and Storage

• Stability & Storage

  Store the unopened product at 2 - 8 °C. Do not use past expiration date.

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 stimulant for CFU-GM.

• Entrez Gene IDs:

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

• Alternate Names:

  CINC1; CINC-1; CXCL1; GRO alpha; KC; MGSA-alpha