HGK, Active(M26-11G)
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Description :Recombinant human HGK (1-328) was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag.
Species :Human
Tag :GST tag
Expression System:Sf9 insect cells using baculovirus
Sequence :1-328
Genbank Number :NP_004825
Specific Activity :Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.
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 :~64 kDa
Gene Aliases :MAP4K4, NIK, FLH21957, FLJ10410, FLJ20373, FLJ90111, KIAA0687
Scientific Background :HGK is the mitogen-activated protein kinase kinase kinase kinase 4(MAP4K4) and a member of the serine/threonine protein kinase family. HGK has been shown to specifically activate MAPK8/JNK (1). The activation of MAPK8 by HGK can be inhibited by dominant-negative mutants of MAP3K7/TAK1, MAP2K4/MKK4, and MAP2K7/MKK7, which suggest that this kinase functions through the MAP3K7-MAP2K4-MAP2K7 kinase cascade and mediates TNF-α signaling. HGK-dependent signaling inhibits PPARγ-responsive gene expression, adipogenesis, and insulin-stimulated glucose transport (2).
References :
1. Yao, Z. et.al: A novel human STE20-related protein kinase, HGK, that specifically activates the c-jun N-terminal kinase signaling pathway. J. Biol. Chem. 274: 2118-2125, 1999.
2. Tang, X. et.al: An RNA interference-based screen identifies MAP4K4/NIK as a negative regulator of PPAR-gamma, adipogenesis, and insulin-responsive hexose transport. Proc. Nat. Acad. Sci. 103: 2087-2092, 2006.
Product Sheets (By Lot #) :
Research Areas :Apoptosis/Autophagy, Cardiovascular Disease, Cellular Stress, Inflammation, JNK/SAPK Pathway, Neurobiology, NfkB Pathway, Ser/Thr Kinases, Neurobiology, Inflammation, Cardiovascular Disease, JNK/SAPK Pathway, NfkB Pathway, Apoptosis/Autophagy, Cellular Stress, Ser/Thr Kinases