B16F10 In Vitro Representational Difference Analysis (RDA) Assay

This assay is to provide B16F10-based In Vitro Representational Difference Analysis (RDA) Assay to accelerate our client's oncology projects. The assay will be customized according to the specific requirements. Please contact our scientists to discuss more details.

B16F10

Mouse

B16F10 cell line (from Mus musculus C57BL/6J strain) is a convenient and widely used experimental model of highly metastatic melanoma to study cytotoxicity, migration, metastatic spread and tissue invasion. B16-F10 is a cell line exhibiting a morphology of spindle-shaped and epithelial-like cells that was isolated from skin tissue of a mouse with melanoma. Use these cells in your skin cancer research.

B16-F10

Melanoma

Oncology

In Vitro Representational Difference Analysis (RDA) Assay

B16F10-cell based In Vitro Representational Difference Analysis (RDA) Assay

This technique can detect sequence differences of two different DNA segments. In representational difference analysis, genomes to be compared are digested by specific restriction enzymes and ligated to specific oligonucleotide linkers, providing two different representations of the two genomes to be generated by PCR with primers specific for oligonucleotide linkers. Following the generation of amplicons, oligonucleotide linkers are removed and a new linker is attached only to test amplicons. These amplicons (tester) are then mixed with driver amplicons, which lack linkers. Amplification only occurs with DNA fragments specific to the tester (with primers specific for linkers).

Genome Alteration Assays

Aberrant or somatic mutations are more commonly found in the DNA of cancer cells compared to normal cells. There is an equilibrium that exists between DNA damage and repair in normal cells. However, in cancer cells these events are disturbed, resulting in mutations and genomic instability. Genomic instability in cancer cells causes chromosomal aberrations, microsatellite instability, aneuploidy and uncontrolled gene amplifications and genetic instability in cancer cells are mainly due to point mutations or chromosomal aberrations such as insertions, deletions and translocation, resulting in mutated proteins.