Extracellular Signal-Regulated Kinases (ERK) also known as the Mitogen-activated Protein Kinase (MAPK), MAPK/ERK proteins are a family of protein-serine/threonine kinases that are activated via the phosphorylation of tyrosine. MAPK/ERK are activated by diverse mechanisms. In the classical setting, MAPK/ERK is activated by many upstream growth factors/cytokine receptors in response to radiation, hypoxia, physical forces, TNF, RANKL, and toll-like receptors (1).
When gain-of-function mutations occur in Ras/Raf, a commonly observed phenomenon in many types of cancers, MAP/ERK proteins become constitutively activated. MAP/ERK signaling fulfills many cancer hallmarks by the mediation of mitosis and stem cells, production of matrix degrading enzymes, angiogenesis, bone destruction, cytokine production and chromosomal aberrations (2). MAPK/ERK is promiscuous and can phosphorylate a number of substrates. Therefore activation of MAP/ERK can affect a broad array of cellular functions including proliferation, survival, apoptosis, motility, transcription, metabolism and differentiation. Meanwhile phosphates dephosphorylate and inactivate MAP/ERK by shutting off the pathway (3). While aberrant MAP/ERK signaling is in part responsible for oncogenesis, many inhibitors for these pathways are in development. The ubiquitous nature of these MAP/ERK signaling may however result in significant side affects (4). An alternative would be to develop inhibitors that can target the accessory proteins that regulate MAP/ERK functions. Novus Biologicals offers a great selection of tools for your MAP/ERK research needs, including highly specific antibodies, RNAi and protein controls.
