FASTK, Active(F01-10G)
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Description :Recombinant full-length human FASTK 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 :Full Length
Genbank Number :NM_006712
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 :~84 kDa
Gene Aliases :FAST; FLJ13079
Scientific Background :FASTK or Fas-Activated Serine/Threonine Kinase is a member of the serine/threonine protein kinase family that becomes rapidly activated during Fas-mediated apoptosis in Jurkat cells and in response to Fas receptor ligation. FASTK interacts with and phosphorylates TIA1 which is an apoptosis-promoting nuclear RNA-binding protein. FAST K influences alternative pre-mRNA splicing by affecting the activity of TIA-1/TIAR (1). FASTK is a strong inducer of lymphocyte apoptosis. FASTK is the component of the molecular cascade that involved in FAS-mediated apoptosis (2). FASTK is highly expreesed in heart, brain, placenta, lung, liver, skeletal muscle, kidney, and pancreas.
References :
1. Izquierdo, J M. et al: Fas-activated serine/threonine kinase (FAST K) synergizes with TIA-1/TIAR proteins to regulate Fas alternative splicing. J Biol Chem. 2007 Jan 19;282(3):1539-43.
2. Tian. et.al: Fas-activated serine/threonine kinase (FAST) phosphorylates TIA-1 during Fas-mediated apoptosis. J. Exp. Med. 182: 865-874, 1995.
Product Sheets (By Lot #) :
Research Areas :Apoptosis/Autophagy, Cancer, Cardiovascular Disease, NfkB Pathway, Ser/Thr Kinases, Cancer, Cardiovascular Disease, NfkB Pathway, Apoptosis/Autophagy, Ser/Thr Kinases