Antibody Arrays

Comparison of Antibody Array Platforms

*H=human | M=mouse | R=rat | B=bovine | C=canine | F=feline | E=equine | P=porcine | L=rabbit | N=rhesus monkey | G=chicken | D=dolphin | O=ovine

How To Choose An Array

How Arrays Can Advance Your Research

Due to the sheer number of secreted factors that could potentially be involved in cell–cell interactions, high-content screens are essential to identifying key secreted factors.

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.

High-density screening arrays help you determine where to focus to get the biggest return on your research efforts.

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.

Using a cytokine array keeps you from missing something important.

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.

Cell–cell signaling pathways are complex, and multiple factors may be working together, in concert. Therefore, screening for a limited number of secreted targets will often give you an incomplete picture.

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 inconcert to promote tumorigenesis. The Human Cytokine Array 1000 was instrumental in this discovery.