KRAS is member of the Rat sarcoma (RAS) oncogene family and is a small GTPase implicated in various biological processes, such as cell proliferation, cell survival, and cell metabolism. This proto-oncogene is well known to be mutated in many cancer subtypes, inducing uncontrolled proliferation and cell metabolism modifications. It thereby contributes to the Warburg effect in cancer cells. The on/off state of the KRAS protein is determined by nucleotide binding. Only in the GTP bound active state is KRAS able to bind and activate effector proteins. GTP binding can be catalyzed by guanine nucleotide exchange factors for RAS, and GTP hydrolysis can be accelerated by GTPase-activating proteins (GAPs). Identifying new KRAS GTP competitors with a KRAS assay is therefore a relevant strategy to control biological processes involved in cancer growth by reducing the KRAS activity, as well as the associated pathways. KRAS WT GTP assays screen for specific KRAS WT compounds.

Formats

• Our 500 assay point kit allows you to run 500 wells in 96-well or 384-well format, using a 20 µL reaction volume (5 µL of sample).
• Our 5,000 assay point kit allows you to run 5,000 wells in 96-well or 384-well format, using a 20 µL reaction volume (5 µL of sample).

Feature:

• No-wash steps, no separation steps
• ELISA alternative technology
• Sensitive detection
• Small sample volume

AlphaLISA technology allows the detection of molecules of interest in a no-wash, highly sensitive, quantitative assay. In an AlphaLISA assay, a biotinylated anti-analyte antibody binds to the Streptavidin-coated Donor beads while another anti-analyte antibody is conjugated to AlphaLISA Acceptor beads. In the presence of the analyte, the beads come into close proximity. The excitation of the Donor beads causes the release of singlet oxygen molecules that triggers a cascade of energy transfer in the Acceptor beads, resulting in a sharp peak of light emission at 615 nm.