MEK1, Unactive(M02-14H)
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Description :Recombinant full-length human MEK1 was expressed in Sf9 insect cells using an N-terminal His tag.
Species :Human
Tag :HIS tag
Expression System:Sf9 insect cells using baculovirus
Sequence :Full Length
Genbank Number :NM_002755
Purity :Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability and Shipping :Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Applications :Kinase Assay, Western Blot
Molecular Weight :~47 kDa
Gene Aliases :MAP2K1, MKK1, MAPKK1, PRKMK1
Scientific Background :MEK1 is a protein serine/threonine kinase that is an upstream activator of the extracellular signal-regulated kinases (ERKs) which are activated in response to numerous growth factors and cytokines (1). Activation of ERKs by MEK1 involves phosphorylation of both tyrosine and threonine residues. MEK1, like the ERKs is ubiquitously distributed in tissues with the highest expression in heart, brain and spinal cord. MEK plays an important role in the growth and survival of cancer cells. In hepatocellular carcinoma, MEK activity is frequently elevated and inhibitors of MEK activity may be an effective treatment for this disease (2).
References :
1. Sugden, P H. et al: Regulation of the ERK subgroup of MAP kinase cascades through G protein-coupled receptors. Cell Signal. 1997 Aug;9(5):337-51.
2. Huynh, H. et al: Over-expression of the mitogen-activated protein kinase (MAPK) kinase (MEK)-MAPK in hepatocellular carcinoma: its role in tumor progression and apoptosis. BMC Gastroenterol. 2003 Aug 8;3:19.
Product Sheets (By Lot #) :
Research Areas :Cancer, Neurobiology, Cardiovascular Disease, ERK/MAPK Pathway, Apoptosis/Autophagy, Angiogenesis, Invasion/Metastasis, Ser/Thr Kinases, Cancer, Neurobiology, Cardiovascular Disease, ERK/MAPK Pathway, Apoptosis/Autophagy, Angiogenesis, Invasion/Metastasis, Ser/Thr Kinases