5% Off All Online Orders
Many biological processes such as apoptosis, inflammation, angiogenesis, immune response and migration often accompany changes of cytokine expression levels. Because of the extensive cross-talk between cytokines, a complete analysis of biological responses and functions must be obtained through multiplex assays. Antibody arrays allow a much broader view of protein activity than can be obtained with single-target ELISAs and Western blots. Moreover, antibody array screening improves the chances for discovering key factors, disease mechanisms or biomarkers related to cytokine signaling.
|Design Principle||Sandwich ELISA|
|Solid Support||Glass Slide|
|Design Principle||Sandwich ELISA|
|Design Principle||Competitive ELISA|
|Results||Semi-quantitative or Quantitative|
|Detection||Fluorescent or Chemiluminescent|
|Solid Support||Glass Slide or Membrane|
|Design Principle||Direct Labeling (Biotin)|
|NAME||APPLICATIONS||SOLID SUPPORT||DESIGN PRINCIPLE||OUTPUT||# OF ANALYTES||SPECIES*|
|Quantibody®||protein expression profiling||slide||sandwich-based||quantitative||10 – 440||H, M, R, B, C, F, E, P, L, N|
|C-Series Arrays||protein expression profiling||membrane||sandwich-based||semi-quantitative||10 - 274||H, M, R|
|G-Series Arrays||protein expression profiling||slide||sandwich-based||semi-quantitative||10 - 274||H, M, R|
|L-Series Arrays||protein expression profiling||both||label-based||semi-quantitative||90 - 1000||H, M, R|
|Phospho Arrays||phosphorylation profiling||both||sandwich-based||semi-quantitative||17 - 71||H|
|E-Series Arrays||protein expression profiling||membrane||competition-based||quantitative||10||H|
|Lectin Arrays||protein-lectin interaction.
Meaning?... Which protein-bound sugars are present in my sample?” or “which sugars are bound to my protein of interest?
|Glycome Arrays||glycosylation profiling.
Meaning?... Which proteins in my sample are glycosylated, and to what extent?
|slide||sandwich-based (lectin-ab pair)||semi-quantitative||507||any|
|Protein Arrays||auto-antibody profiling, characterizing antibody specificity, More... Can be adapted for detection of protein-protein interactions, protein modifications, small molecule-protein interactions||slide||label-based||semi-quantitative||48 - 487||H, M|
|Rapid Isotyping Strips||isotyping; hybridoma screening and selection||lateral flow strip||sandwich-based||qualitative||10||M|
|Rapid Isotyping Arrays||isotyping; hybridoma screening and selection||slide||sandwich-based||semi-quantitative||8 - 10||M, R|
*H=human | M=mouse | R=rat | P=porcine | C=canine | F=feline | B=bovine | E=equine | N=rhesus monkey | L=rabbit
|YOUR SPECIFIC NEED||OUR SOLUTION|
|I want to screen as many factors as possible (I need a "big net")||L-Series: Label-based Arrays or larger Quantibody® Arrays|
|I want to focus on a specific pathway or biological process||Pathway-specific arrays (e.g. Inflammation; Apoptosis, etc) or Phosphorylation Arrays|
|I want to choose a specific panel of markers||Custom Array|
|I have a limited sample volume||Glass Slide-based Arrays:
|I don't have a laser scanner||Membrane-based Arrays:
Or use our free glass slide scanning service
|I want quantitative results||Quantibody® Arrays or E-Series Arrays|
|I want to identify antibody isotypes||Isotyping Arrays|
|I want to study protein glycosylation||Glycobiology Arrays (Lectin Arrays, Glycosylation Arrays, Glycan Arrays)|
|I want to screen protein-protein interactions||Protein Arrays|
|I have samples from an uncommon species||L-Series: Label-based Arrays or Quantibody® Arrays|
|I want to do biomarker discovery||Any RayBiotech Array|
|Equipment Needed||CCD, X-ray, gel doc||Laser scanner||CCD, X-ray, gel doc
|Sensitivity||pg to ng||pg to ng||pg to ng||pg to ng|
|Target Density||Low to High||Low to High||Low to High||Low to High|
|Specificity||Very High||Very High||High||Very High|
Straussman R, Morikawa T, Shee K, Barzily-Rokni M, Qian ZR , Du J, et al. Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion. Nature. 2012; 487: 500-504.
The investigators incubated melanoma (skin cancer cells) in vitro with cell-cultured media obtained from multiple stromal cell lines and identified those media that induced the highest degree of stromal-mediated resistance to a RAF inhibitor (recently approved to treat melanoma). They then used both the G-Series 4000 and L-Series 507 Arrays to characterize the expression profiles of secreted factors in stromal cell-cultured media that induced the greatest degree of drug resistance in the cancer cells. They then used statistical analysis of the individual secreted factors detected in the various expression profiles to find those that correlated best with drug resistance.
Scheel C, Eaton EN, Li SH, Chaffer CL, Reinhardt F, Kah K-J, 2, Bell G, Guo W, Rubin J, Richardson AL, Weinberg RA. Paracrine and autocrine signals induce and maintain mesenchymal and stem cell states in the breast. Cell. 2011; 145(6):926-940.
This paper focuses on the mechanism of epithelial-to-mesenchymal transition (EMT), which is an important process in tumor formation. The Human L-Series 507 Array yielded a short list of targets, including the TGFβ and WNT/β-catenin pathways, which are known to antagonize one another. By knowing where to look, they were able to focus their efforts on the right signal pathways, greatly improving their chances of working out the entire mechanism of this process, which netted them a paper in Cell.
Vargas DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo CA. Neuroglial activation and neuroinflammation in the brain of patients with autism. Annals of Neurology. 2005; 57(1):67–81.
The authors of the paper found the first evidence of a neuroinflammatory process in the pathology of autism, even identifying several key factors that pointed to the mechanism of this process. This neuroinflammatory component of autism had been suspected for years, but no one had ever proven it. If the authors had decided to select a few ELISA kits or even a 20-plex bead panel to do this investigation instead of an array kit detecting 120 different cytokines, the authors may have missed identifying the key targets, and we might still be wondering if autism has a neuroinflammatory component.
Coppé J-P, Patil CK, Rodier F, Sun Y, Muñoz DP, Goldstein J, Nelson PS, Desprez P-Y, Campisi J. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biology. 2008; 6(12).
This paper describes the first characterization of the senescence-associated secretory phenotype in stromal–tumor interactions. It uncovers the expression profile of permanently senescent tissues (epithelial and stromal) that secrete a wide range of factors that included pro-inflammatory factors, growth factors, cell-adhesion factors and proteases that restructure the extracellular matrix (ECM). In subsequent inquiries, these various components of this broad secretory profile were shown to work in concert to promote tumorigenesis. The Human Cytokine Array 1000 was instrumental in this discovery.