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Description :Rabbit Polyclonal Antibody
Specificity :Recognizes the DRAK2 (STK17B) protein and has no cross responses to DAP or ZIP kinases.
Cited Applications :WB, ELISA, ICC
Cross Reactivity :Human
Host / Isotype / Clone# :Rabbit, IgG
Immunogen :DRAK2 (STK17B) antibody was raised against a peptide corresponding to amino acids 351 to 365 of human DRAK2 (STK17B)
Formulation :PBS + 0.02% sodium azide.
Purification :Affinity chromatography
Stability :Store at 4oC (add 0.1% NaN3) for several months, and at -20oC for longer periods. 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.
Sample Data :Western blot analysis of DRAK2 (STK17B) in Jurkat (1,3) and Raji (2,4) cell lysate in the absence (1,2) or presence (3,4) of blocking peptide with DRAK2 (STK17B) antibody at 1:500 dilution.
Sample Data :Immunocytochemistry of DRAK2 (STK17B) in Jurkat cells with DRAK2 (STK17B) antibody at 10 ug/ml.
Scientific Background :DRAK2 is a member of the serine/threonine kinase family and is related to death-associated protein kinase that triggers apoptosis (1). DRAK2 is selectively important for T-cell survival and inhibition of DRAK2 has therapeutic potential for autoimmune disease (2). T-cell survival depends on a balance of T-cell receptor and co-stimulatory signals and deficiency of DRAK2 can affect autoimmune disease susceptibility without generalized suppression of the immune system (3).
1. Sanjo, H. et.al: DRAKs, novel serine/threonine kinases related to death-associated protein kinase that trigger apoptosis. J. Biol. Chem. 273: 29066-29071, 1998.
2. Ramos, S. J. et.al: Enhanced T cell apoptosis within Drak2-deficient mice promotes resistance to autoimmunity. J. Immun. 181: 7606-7616, 2008.
3. McGargill, M. A. et.al: Drak2 regulates the survival of activated T cells and is required for organ-specific autoimmune disease. J. Immun. 181: 7593-7605, 2008.
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Research Areas :Apoptosis/Autophagy, Metabolic Disorder, Ser/Thr Kinases, Metabolic Disorder, Apoptosis/Autophagy, Ser/Thr Kinases